Author: "Lise Tarnow" - Searchworks@Jio Institute Digital Library Search Results

347 results on '"Lise Tarnow"'

251. 19. Efficacy and Safety of Liraglutide Added to Insulin in Type 1 Diabetes: The LIRA-1 Trial (277-OR)

Author: Sten Madsbad, Filip K. Knop, T. Hansen, Jens J. Holst, Søren A. Urhammer, Henrik U. Andersen, Ulrik Pedersen Bjergaard, Tonny Jensen, Lise Tarnow, Thomas F. Dejgaard, Christian Seerup Frandsen, and Thomas Almdal
Subjects: Type 1 diabetes, medicine.medical_specialty, endocrine system diseases, business.industry, Liraglutide, Insulin, medicine.medical_treatment, Placebo-controlled study, nutritional and metabolic diseases, Type 2 diabetes, medicine.disease, Placebo, Gastroenterology, Endocrinology, Internal medicine, Diabetes mellitus, Medicine, medicine.symptom, business, Weight gain, medicine.drug
Abstract: Weight gain and hypoglycemia are common side effects to insulin therapy in type 1 diabetes (T1D). The combination of insulin and glucagon-like peptide-1 receptor agonist (GLP-1RA) therapy has proven effective in reducing weight gain and insulin dose in type 2 diabetes. This 26-week trial is the first randomized, double-blinded, placebo controlled study to evaluate efficacy and safety of GLP-1RA treatment in poorly controlled, overweight patients with T1D. One hundred patients with T1D, HbA1c > 64 mmol/mol and BMI > 25 kg/m2, were randomized to liraglutide 1.8 mg (LIRA) or placebo added to intensive insulin therapy. Mean baseline characteristics were similar between groups (LIRA; placebo ± SD) age 47 ± 13; 49 ± 12 years, HbA1c 73 ± 8;73 ± 8 mmol/mol, daily insulin dose 75 ± 30; 74 ± 26 IU/day and body weight 93.4 ± 14.2; 94.0 ± 12.5 kg except diabetes duration 20 ± 12; 25 ±12 years. After 12 weeks, LIRA reduced HbA1c, body weight and daily insulin dose compared with placebo. At end of treatment no difference in HbA1c between groups was found. Body weight and daily insulin dose remained reduced in the LIRA group. Frequency of hypoglycemia did not differ between groups. Nausea occurred more frequently with LIRA than placebo (48% vs. 7%). In conclusion, LIRA added to insulin treatment reduced body weight and daily insulin dose in overweight, poorly controlled patients with T1D, but did not improve HbA1c compared with placebo at end of treatment.
Published: 2015
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252. Efficacy and safety of the glucagon-like peptide-1 receptor agonist liraglutide added to insulin therapy in poorly regulated patients with type 1 diabetes--a protocol for a randomised, double-blind, placebo-controlled study: The Lira-1 study

Author: Filip K. Knop, Lise Tarnow, Thomas Almdal, Thomas F. Dejgaard, Christian Seerup Frandsen, T. Hansen, Jens J. Holst, Sten Madsbad, and Henrik U. Andersen
Subjects: Adult, Male, medicine.medical_specialty, Adolescent, medicine.medical_treatment, Type 2 diabetes, Drug Administration Schedule, Helsinki declaration, Young Adult, Clinical Protocols, Double-Blind Method, Internal medicine, Diabetes mellitus, Protocol, medicine, Humans, Hypoglycemic Agents, Insulin, Glucagon-like peptide 1 receptor, Aged, Aged, 80 and over, Type 1 diabetes, Gastric emptying, business.industry, Liraglutide, General Medicine, Middle Aged, Overweight, medicine.disease, Diabetes and Endocrinology, Diabetes Mellitus, Type 1, Treatment Outcome, Endocrinology, Drug Therapy, Combination, Female, business, medicine.drug
Abstract: Introduction Intensive insulin therapy is recommended for the treatment of type 1 diabetes (T1D). Hypoglycaemia and weight gain are the common side effects of insulin treatment and may reduce compliance. In patients with insulin-treated type 2 diabetes, the addition of glucagon-like peptide-1 receptor agonist (GLP-1RA) therapy has proven effective in reducing weight gain and insulin dose. The present publication describes a protocol for a study evaluating the efficacy and safety of adding a GLP-1RA to insulin treatment in overweight patients with T1D in a randomised, double-blinded, controlled design. Methods and analysis In total, 100 patients with type 1 diabetes, poor glycaemic control (glycated haemoglobin (HbA1c) >8%) and overweight (body mass index >25 kg/m 2 ) will be randomised to either liraglutide 1.8 mg once daily or placebo as an add-on to intensive insulin therapy in this investigator initiated, double-blinded, placebo-controlled parallel study. The primary end point is glycaemic control as measured by changes in HbA1c. Secondary end points include changes in the insulin dose, hypoglyacemic events, body weight, lean body mass, fat mass, food preferences and adverse events. Glycaemic excursions, postprandial glucagon levels and gastric emptying rate during a standardised liquid meal test will also be studied. Ethics and dissemination The study is approved by the Danish Medicines Authority, the Regional Scientific-Ethical Committee of the Capital Region of Denmark and the Data Protection Agency. The study will be carried out under the surveillance and guidance of the good clinical practice (GCP) unit at Copenhagen University Hospital Bispebjerg in accordance with the ICH-GCP guidelines and the Helsinki Declaration. Trial registration number NCT01612468.
Published: 2015
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253. Irbesartan treatment reduces biomarkers of inflammatory activity in patients with type 2 diabetes and microalbuminuria: an IRMA 2 substudy

Author: Frederik, Persson, Peter, Rossing, Peter, Hovind, Coen D A, Stehouwer, Casper, Schalkwijk, Lise, Tarnow, and Hans-Henrik, Parving
Subjects: Inflammation, Male, Biphenyl Compounds, Tetrazoles, Irbesartan, Middle Aged, Diabetes Mellitus, Type 2, Double-Blind Method, Albuminuria, Humans, Female, Antihypertensive Agents, Biomarkers, Aged
Abstract: The impact of irbesartan treatment on biomarkers of low-grade inflammation, endothelial dysfunction, growth factors, and advanced glycation end products (AGEs) during the Irbesartan in Patients with Type 2 Diabetes and Microalbuminuria (IRMA 2) study was evaluated. IRMA 2 was a 2-year multicenter, randomized, double-blind trial in patients comparing irbesartan (150 or 300 mg once daily) versus placebo. The primary end point was onset of overt nephropathy. A subgroup (n = 269, 68%) was analyzed for biomarkers at baseline and after 1 and 2 years. High-sensitivity C-reactive protein (hs-CRP), interleukin (IL)-6, fibrinogen, adhesion molecules, transforming growth factor-beta, and AGE peptides were assessed. Irbesartan treatment yielded significant changes in hs-CRP (based on generalized estimating equation regression coefficient) with a 5.4% decrease per year versus a 10% increase per year in the placebo group (P0.001). Fibrinogen decreased 0.059 g/l per year from baseline versus placebo's 0.059 g/l increase per year (P = 0.027). IL-6 showed a 1.8% increase per year compared with placebo's 6.5% increase per year (P = 0.005). Changes in IL-6 were associated with changes in albumin excretion (P = 0.04). There was no treatment effect on the other biomarkers. Irbesartan (300 mg once daily) reduces low-grade inflammation in this high-risk population, and this may reduce the risk of micro- and macrovascular disease.
Published: 2006

254. Analysis of 14 candidate genes for diabetic nephropathy on chromosome 3q in European populations: strongest evidence for association with a variant in the promoter region of the adiponectin gene

Author: Nathalie, Vionnet, David, Tregouët, Gbenga, Kazeem, Ivo, Gut, Per-Henrik, Groop, Lise, Tarnow, Hans-Henrik, Parving, Samy, Hadjadj, Carol, Forsblom, Martin, Farrall, Dominique, Gauguier, Roger, Cox, Fumihiko, Matsuda, Simon, Heath, Alexandre, Thévard, Rachel, Rousseau, François, Cambien, Michel, Marre, and Mark, Lathrop
Subjects: Male, Genotype, Chromosome Mapping, Coronary Disease, Polymorphism, Single Nucleotide, White People, Pedigree, Europe, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Gene Frequency, Reference Values, Risk Factors, Humans, Diabetic Nephropathies, Female, Chromosomes, Human, Pair 3, Obesity
Abstract: Linkage studies have mapped loci for diabetic nephropathy and associated phenotypes on chromosome 3q. We studied 14 plausible candidate genes in the linkage region because of their potential role in vascular complications. In a large-scale study of patients from Denmark, Finland, and France who have type 1 diabetes, 1,057 case and 1,127 control subjects, as well as 532 trios, were investigated for association with diabetic nephropathy. We analyzed 69 haplotype-tagging single nucleotide polymorphisms and nonsynonymous variants that were identified by sequencing. Polymorphisms in three genes, glucose transporter 2 (SLC2A2), kininogen (KNG1), and adiponectin (ADIPOQ), showed nominal association with diabetic nephropathy in single-point analysis. The T-allele of SLC2A2_16459CT was associated with a decreased risk of diabetic nephropathy (odds ratio 0.79 [95% CI 0.66-0.96], P = 0.016), whereas the T-allele of KNG_7965CT and the A-allele of ADIPOQ_prom2GA were associated with increased risk of nephropathy (1.17 [1.03-1.32], P = 0.016; 1.46 [1.11-1.93], P = 0.006, respectively). Analyses of the transmission disequilibrium test showed similar trends only for ADIPOQ_prom2GA with the overtransmission of the A-allele to patients with diabetic nephropathy (1.52 [0.86-2.66], P = NS) and of the G-allele to patients without diabetic nephropathy (0.50 [0.27-0.92], P = 0.026). The overall significance for this variant (nominal P = 0.011) suggests that ADIPOQ might be involved in the development of diabetic nephropathy.
Published: 2006

255. The xylosyltransferase I gene polymorphism c.343GT (p.A125S) is a risk factor for diabetic nephropathy in type 1 diabetes

Author: Claudia Bahr, Lise Tarnow, Christian Prante, Christian Götting, Knut Kleesiek, Sylvia Schön, and Joachim Kuhn
Subjects: Adult, Male, medicine.medical_specialty, Genotype, Endocrinology, Diabetes and Metabolism, Xylosyltransferase, Polymorphism, Single Nucleotide, Nephropathy, Diabetic nephropathy, Gene Frequency, Risk Factors, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Genetic predisposition, Humans, Diabetic Nephropathies, Genetic Predisposition to Disease, Pentosyltransferases, Advanced and Specialized Nursing, Type 1 diabetes, business.industry, Protein xylosyltransferase, Middle Aged, medicine.disease, Endocrinology, Diabetes Mellitus, Type 1, Phenotype, Female, Gene polymorphism, business
Abstract: OBJECTIVE—Xylosyltransferase I (XT-I) is the chain-initiating enzyme in the biosynthesis of proteoglycans in basement membranes. It catalyzes the transfer of xylose to selected serine residues in the core protein. The XYLT-II gene codes for a protein highly homologous to XT-I. Proteoglycans are important components of basement membranes and are responsible for their permeability properties. Type 1 diabetic patients have an altered proteoglycan metabolism, which results in microvascular complications. Thus, genetic variations in the xylosyltransferase genes might be implicated in the initiation and progression of these complications. RESEARCH DESIGN AND METHODS—Genotyping of four genetic variations in the genes XYLT-I and XYLT-II was performed in 912 type 1 diabetic patients (453 with and 459 without diabetic nephropathy) using restriction fragment–length polymorphism. RESULTS—The distribution of the c.343G>T polymorphism in XYLT-I is significantly different between patients with and without diabetic nephropathy (P = 0.03). T-alleles were more frequent in patients with diabetic nephropathy (odds ratio 2.47 [95% CI 1.04–5.83]). The allelic frequencies of the other investigated XYLT-I and XYLT-II variations (XYLT-I: c.1989T>C in exon 9; XYLT-II: IVS6–9T>C and IVS6–14_IVS6–13insG in intron 5; and c.2402C>G: p.T801R in exon 11) were not different between patients with and without diabetic nephropathy. CONCLUSIONS—The XYLT-I c.343G>T polymorphism contributes to the genetic susceptibility to development of diabetic nephropathy in type 1 diabetic patients.
Published: 2006

256. Aldosterone synthase (CYP11B2)-344T/C polymorphism and renoprotective response to losartan treatment in diabetic nephropathy

Author: Parving Hh, Steen Andersen, K. J. Schjoedt, Peter Rossing, Maria Lajer, and Lise Tarnow
Subjects: Aldosterone synthase, Adult, Male, medicine.medical_specialty, Time Factors, Clinical Biochemistry, Urology, Renal function, Blood Pressure, Essential hypertension, Polymorphism, Single Nucleotide, Losartan, Diabetic nephropathy, Renin-Angiotensin System, Internal medicine, Renin–angiotensin system, medicine, Albuminuria, Cytochrome P-450 CYP11B2, Humans, Diabetic Nephropathies, Prospective Studies, biology, business.industry, General Medicine, Middle Aged, medicine.disease, Endocrinology, Blood pressure, Diabetes Mellitus, Type 1, Hypertension, biology.protein, Female, medicine.symptom, business, Angiotensin II Type 1 Receptor Blockers, medicine.drug, Glomerular Filtration Rate
Abstract: It has been suggested that an aldosterone synthase gene polymorphism (CYP11B2 -344T/C) is predictive of the blood pressure lowering effect of angiotensin II receptor blockers in essential hypertension. We investigated whether this polymorphism is predictive of reductions in blood pressure and albuminuria and preservation of glomerular filtration rate (GFR) during short-term and long-term treatment with losartan in 57 hypertensive type-1 diabetic patients with diabetic nephropathy.After a 4-week washout period, patients received losartan (100 mg o.d.) and were followed for a mean follow-up of 36 months. At baseline, after 2 and 4 months, and every 6 months thereafter, GFR (51Cr-EDTA-clearance), albuminuria and 24-h blood pressure were determined. The CYP11B2 -344T/C polymorphism was determined by standard polymerase chain reaction (PCR).The TT, CT and CC genotypes were found in 28 %, 58 % and 14 % of patients, respectively. At baseline albuminuria and blood pressure did not differ between genotype groups. Plasma aldosterone levels (geometric mean (95 % CI)) were similar at baseline: 87 (60-125), 77 (53-112), and 89 (49-161) pg mL(-1) and during follow-up (not significant). After initiation of losartan treatment, comparable mean (SE) reductions in blood pressure and albuminuria were seen in patients with TT, CT and CC genotypes (p0.6 between groups). After long-term follow-up, there was a tendency towards a difference in systolic blood pressure reduction (p = 0.07, one-way ANOVA), suggesting a poorer response in patients with the CC genotype. No significant difference in rate of decline in GFR (median (range)) was seen between groups (TT, CT, CC): 4.2 (-1.0 to 16.0), 3.2 (-1.6 to 13.8) and 2.6 (-0.1 to 11.0) mL min(-1)year(-1), respectively (p = 0.5).Compared to a previous smaller study of angiotensin II receptor blockade in essential hypertension, we could not confirm that CYP11B2 -344T/C genotypes contribute towards explaining the observed variability in response to treatment with angiotensin II receptor blockers, which could be due to lack of power.
Published: 2006

257. Time to consider ACE insertion/deletion genotypes and individual renoprotective treatment in diabetic nephropathy?

Author: Hans-Henrik Parving, Peter Karl Jacobsen, and Lise Tarnow
Subjects: medicine.medical_specialty, Genotype, Ace gene, Angiotensin-Converting Enzyme Inhibitors, Peptidyl-Dipeptidase A, Bioinformatics, Diabetic nephropathy, Asian People, Internal medicine, medicine, Insertion deletion, Humans, Diabetic Nephropathies, Alleles, Polymorphism, Genetic, business.industry, Genetic Variation, medicine.disease, Prognosis, Response to treatment, Survival Analysis, Treatment efficacy, Mutagenesis, Insertional, Endocrinology, Nephrology, business, Gene Deletion
Abstract: One reason for the inadequacy of current renoprotective therapy and the persistent poor renal prognosis in diabetic nephropathy is the large interindividual variation in response to treatment. Genetic as well as non-genetic factors are known to influence treatment efficacy. This Commentary summarizes the impact of the angiotensin-converting enzyme (ACE) insertion/deletion polymorphism in the ACE gene on initiation and progression of diabetic nephropathy.
Published: 2006

258. Cardiac autonomic neuropathy predicts cardiovascular morbidity and mortality in type 1 diabetic patients with diabetic nephropathy

Author: Lise Tarnow, Birgitte V. Hansen, Hans-Henrik Parving, Anne Sofie Astrup, Peter Rossing, and Jannik Hilsted
Subjects: Adult, Male, medicine.medical_specialty, Heart disease, Heart Diseases, Endocrinology, Diabetes and Metabolism, Nephropathy, Diabetic nephropathy, Diabetic Neuropathies, Heart Rate, Risk Factors, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Humans, Diabetic Nephropathies, Prospective Studies, Risk factor, Prospective cohort study, Proportional Hazards Models, Advanced and Specialized Nursing, Type 1 diabetes, business.industry, Middle Aged, medicine.disease, Surgery, Diabetes Mellitus, Type 1, Autonomic Nervous System Diseases, Cardiology, Regression Analysis, Female, business, Kidney disease, Follow-Up Studies
Abstract: OBJECTIVE—Cardiac autonomic neuropathy (CAN) has been associated with a poor prognosis in patients with diabetes. Because CAN is common in patients with diabetic nephropathy, we evaluated the predictive value of CAN in type 1 diabetic patients with and without diabetic nephropathy. RESEARCH DESIGN AND METHODS—In a prospective observational follow-up study, 197 type 1 diabetic patients with diabetic nephropathy and a matched group of 191 patients with long-standing type 1 diabetes and normoalbuminuria were followed for 10.1 years (range 0.0–10.3 years). At baseline, CAN was assessed by heart rate variation (HRV) during deep breathing. HRV was evaluated as a predictor of the primary end point: cardiovascular morbidity and mortality. As secondary end points, all-cause mortality and the influence of HRV on progression of diabetic nephropathy (decline in glomerular filtration rate [GFR]) was evaluated. RESULTS—During the follow-up, 79 patients (40%) with nephropathy reached the combined primary end point vs. 19 patients (10%) with normoalbuminuria (log-rank test, P < 0.0001). The unadjusted hazard ratio (HR) for reaching the primary end point when having an abnormal HRV (≤10 bpm) measured at baseline compared with a normal HRV was 7.7 (range 1.9–31.5; P = 0.004) in patients with nephropathy. Similarly in the normoalbuminuric patients, the unadjusted HR was 4.4 (1.4–13.6; P = 0.009). In patients with nephropathy, abnormal HRV was significantly associated with fatal and nonfatal cardiovascular disease after adjustment for cardiovascular risk factors. The adjusted HR for reaching the primary end point in a patient with nephropathy and an abnormal HRV was 6.4 (1.5–26.3, P = 0.010), as compared with a normal HRV. The unadjusted HR for dying when having an abnormal HRV compared with a normal HRV was 3.3 (95% CI 1.0–10.7; P = 0.043) in patients with diabetic nephropathy. After adjustment for confounding factors, the impact of HRV on all-cause mortality in patients with nephropathy was no longer significant (P = 0.293). There was no relationship between abnormal HRV and rate of decline in GFR. CONCLUSIONS—HRV is an independent risk factor for cardiovascular morbidity and mortality in type 1 diabetic patients with nephropathy.
Published: 2006

259. Urinary connective tissue growth factor excretion correlates with clinical markers of renal disease in a large population of type 1 diabetic patients with diabetic nephropathy

Author: Tri Q. Nguyen, Lise Tarnow, Steen Andersen, Peter Hovind, Hans-Henrik Parving, Roel Goldschmeding, and Frans A. van Nieuwenhoven
Subjects: Advanced and Specialized Nursing, Adult, Blood Glucose, Glycated Hemoglobin, Male, integumentary system, Endocrinology, Diabetes and Metabolism, Connective Tissue Growth Factor, Enzyme-Linked Immunosorbent Assay, Middle Aged, Immediate-Early Proteins, Cross-Sectional Studies, Diabetes Mellitus, Type 1, Reference Values, Internal Medicine, Humans, Intercellular Signaling Peptides and Proteins, Regression Analysis, Diabetic Nephropathies, Female, Biomarkers, Glomerular Filtration Rate
Abstract: OBJECTIVE—Levels of connective tissue growth factor (CTGF; CCN-2) in plasma are increased in various fibrotic disorders, including diabetic nephropathy. Recently, several articles have reported a strong increase of urinary CTGF excretion (U-CTGF) in patients with diabetic nephropathy. However, these studies addressed too small a number of patients to allow general conclusions to be drawn. Therefore, we evaluated U-CTGF in a large cross-sectional study of patients with type 1 diabetes. RESEARCH DESIGN AND METHODS—Subjects were 318 type 1 diabetic patients and 29 normoglycemic control subjects. U-CTGF was measured by sandwich enzyme-linked immunosorbent assay. Groups were compared by Kruskal-Wallis and Mann-Whitney analysis. The relation between U-CTGF and markers of diabetic nephropathy was determined by regression analysis. RESULTS—U-CTGF in patients with diabetic nephropathy (n = 89, median 155 pmol/24 h [interquartile range 96–258]) was significantly higher than in microalbuminuric (n = 79, 100 [65–78]) and normoalbuminuric (n = 150, 85 [48–127]) patients and control subjects (n = 29, 100 [78–114]). U-CTGF correlated with urinary albumin excretion (UAE) (R = 0.31) and glomerular filtration rate (R = −0.38) in patients with diabetic nephropathy. A standardized increase in U-CTGF was associated with diabetic nephropathy (odds ratio 2.3 [95% CI 1.7–3.1]), which was comparable with the odds ratios for diabetic nephropathy of increased HbA1c (2.0 [1.5–2.7]), and blood pressure (2.0 [1.5–2.6]). CONCLUSIONS—This is the first large cross-sectional study addressing U-CTGF in human type 1 diabetes. The observed association of U-CTGF with UAE and glomerular filtration rate might reflect a role of CTGF as progression promoter in diabetic nephropathy.
Published: 2005

260. Plasma N-terminal pro-B-type natriuretic peptide and mortality in type 2 diabetes

Author: Birgitte V. Hansen, Peter Hovind, Lise Tarnow, H.-H. Parving, and M. A. Gall
Subjects: Male, medicine.medical_specialty, Time Factors, medicine.drug_class, Endocrinology, Diabetes and Metabolism, Myocardial Ischemia, Renal function, Type 2 diabetes, Excretion, Predictive Value of Tests, Internal medicine, Diabetes mellitus, Natriuretic Peptide, Brain, Internal Medicine, medicine, Natriuretic peptide, Albuminuria, Humans, Diabetic Nephropathies, cardiovascular diseases, Prospective Studies, Prospective cohort study, Diabetic Retinopathy, business.industry, Middle Aged, medicine.disease, Survival Analysis, Peptide Fragments, Endocrinology, Diabetes Mellitus, Type 2, Creatinine, Cohort, Female, medicine.symptom, business, hormones, hormone substitutes, and hormone antagonists, Diabetic Angiopathies, Follow-Up Studies, Glomerular Filtration Rate
Abstract: Raised N-terminal pro-B-type natriuretic peptide (NT-proBNP) is associated with a poor cardiac outcome in non-diabetic populations. Elevated NT-proBNP predicts excess morbidity and mortality in diabetic patients with an elevated urinary albumin excretion rate. This study investigated the prognostic value of NT-proBNP in a cohort of type 2 diabetic patients.In a prospective observational follow-up study, 315 type 2 diabetic patients with normoalbuminuria (n=188), microalbuminuria (n=80) and macroalbuminuria (n=47) at baseline were followed for a median (range) of 15.5 (0.2-17.0) years. Plasma NT-proBNP concentrations were determined by immunoassay at baseline. Endpoints were overall and cardiovascular mortality.Of the patients, 162 died (51%), 119 of them (74%) due to cardiovascular causes. All-cause mortality was increased in patients with NT-proBNP in the second and third tertiles (hazard ratios [95% CI] compared with the first tertile, 1.70 [1.08-2.67] and 5.19 [3.43-7.88], p0.001). These associations persisted after adjustment for urinary albumin excretion rate, glomerular filtration rate and conventional cardiovascular risk factors (covariate adjusted hazard ratios 1.46 [0.91-2.33] and 2.54 [1.56-4.14], p0.001). This increased mortality was attributable to more cardiovascular deaths in the second and third NT-proBNP tertile (unadjusted hazard ratios 1.63 [0.96-2.77] and 4.88 [3.01-7.91], p0.001; covariate adjusted 1.37 [0.79-2.37] and 2.26 [1.27-4.02], p=0.01). When patients with normo-, micro- and macroalbuminuria were analysed separately, NT-proBNP levels above the median (62 ng/l) were consistently associated with increased overall and cardiovascular mortality in all three groups (p0.001).In patients with type 2 diabetes, elevated circulating NT-proBNP is a strong predictor of the excess overall and cardiovascular mortality, this predictor status being independent of urinary albumin excretion rate and conventional cardiovascular risk factors.
Published: 2005

261. Impact of polymorphisms in the genes encoding xylosyltransferase I and a homologue in type 1 diabetic patients with and without nephropathy

Author: Lise Tarnow, Manuela Schöttler, Christian Prante, Christian Götting, Joachim Kuhn, S. A. H. Müller, Sylvia Schön, and Knut Kleesiek
Subjects: Adult, Male, medicine.medical_specialty, Genotype, type 1 diabetes, Xylosyltransferase, Single-nucleotide polymorphism, Blood Pressure, Biology, Polymorphism, Single Nucleotide, Nephropathy, Diabetic nephropathy, Exon, heparan sulfate proteoglycans, Gene Frequency, DHPLC, Internal medicine, medicine, SNP, Humans, Diabetic Nephropathies, Genetic Predisposition to Disease, Genetic Testing, Pentosyltransferases, Gene, Aged, diabetic nephropathy, Intron, Middle Aged, medicine.disease, Endocrinology, Diabetes Mellitus, Type 1, Phenotype, Nephrology, xylosyltransferase, Female, genetic variations, polymorphisms, SNPs
Abstract: Impact of polymorphisms in the genes encoding xylosyltransferase I and a homologue in type 1 diabetic patients with and without nephropathy. Background Xylosyltransferase I (XT-I) is the chain-initiating enzyme in the biosynthesis of heparan sulfate proteoglycans (HSPGs). It catalyses the transfer of xylose to specific serine residues in the core protein. The XYLT-II gene codes for a protein highly homologous to the XT-I but its biologic function is not yet known. HSPGs are thought to play an important role in the permeability properties of the glomerular basement membrane (GBM) and thus the xylotransferase genes might be potential candidate genes predisposing to diabetic nephropathy in type 1 diabetic patients. Methods We screened all XYLT-I and XYLT-II exons and flanking intron regions in 96 Caucasians with type 1 diabetes (48 with and 48 without diabetic nephropathy) using denaturing high-performance liquid chromatography (DHPLC). We also studied a nondiabetic control group. Results Applying this technique we identified 13 variations in XYLT-I and 20 in XYLT-II . The variations IVS6-9T>C and IVS6-14_IVS6-13insG in XYLT-II were found with a frequency of 5.2% (5/96) in nondiabetic nephropathy patients, while all nephropathy patients were negative ( P = 0.06). Nondiabetic controls also showed the single nucleotide polymorphisms (SNP) at a frequency of 1.1% (5/440). The investigation of the SNPs' influence on clinical characteristics revealed significant associations for c.1989T>C ( XYLT-I ) and c.2402C>G ( XYLT-II ) with patients' blood pressure. Conclusion We detected in our cohort associations between DNA sequence variations of genes encoding xylosyltransferases and the occurrence of altered clinical characteristics.
Published: 2005

262. Mannose-binding lectin as a predictor of microalbuminuria in type 1 diabetes: an inception cohort study

Author: Peter, Hovind, Troels Krarup, Hansen, Lise, Tarnow, Steffen, Thiel, Rudi, Steffensen, Allan, Flyvbjerg, and Hans-Henrik, Parving
Subjects: Adult, Inflammation, Male, Incidence, Mannose-Binding Lectin, Cohort Studies, Diabetes Mellitus, Type 1, Disease Progression, Albuminuria, Humans, Diabetic Nephropathies, Female, Complement Activation, Biomarkers, Diabetic Angiopathies
Abstract: Inflammation and complement activation via the mannose-binding lectin (MBL) pathway have been suggested to play a role in the pathogenesis of diabetic microvascular complications. The association between the complement-activating protein MBL and the development of persistent microalbuminuria was evaluated in an inception cohort of 286 newly diagnosed type 1 diabetic patients consecutively admitted to the Steno Diabetes Center between 1 September 1979 and 31 August 1984. Serum MBL was measured with an immunofluorometric assay in 270 of the patients (159 men) after 3 years of diabetes duration. During the median (range) follow-up period of 18.0 (1.0-21.8) years, 75 patients subsequently progressed to persistent micro- or macroalbuminuria (urinary albumin excretion rate30 mg/24 h). In patients with MBL levels above the median (1,597 microg/l), the cumulative incidence of persistent micro- or macroalbuminuria was 41% (CI 31-50) as compared with 26% (CI 17-34) in patients with MBL levels below the median (log-rank test, P = 0.003). In a Cox proportional hazard model with sex and age as fixed covariates, MBL was independently associated with later development of persistent micro- or macroalbuminuria (hazard ratio 1.21 [CI 1.02-1.42] per 1,000 microg/l increase in MBL; P = 0.03) after adjusting for possible confounders. In our study, high levels of MBL early in the course of type 1 diabetes was significantly associated with later development of persistent micro- or macroalbuminuria, suggesting that complement activation initiated by MBL may be involved in the pathogenesis of diabetic microvascular complications.
Published: 2005

263. [Risk factors for the development of microalbuminuria in type 1 diabetes: an incidence cohort study--a secondary publication]

Author: Peter, Hovind, Lise, Tarnow, Peter, Rossing, Berit Ruud, Jensen, Malene, Graae, Inge, Torp, Christian, Binder, and Hans-Henrik, Parving
Subjects: Adult, Cohort Studies, Male, Diabetes Mellitus, Type 1, Risk Factors, Albuminuria, Humans, Female, Prospective Studies, Diabetic Angiopathies
Published: 2005

264. Cardiac function and mass in asymptomatic type 1 diabetic patients with diabetic nephropathy - and correlation to NT-proBNP. A cardiovascular magnetic resonance study

Author: Anne Sofie Astrup, Won Yong Kim, Lise Tarnow, Erling Falk, Botnar, René M., Cheryl Simonsen, Lau Brix, Peter Riis Hansen, Manning, Warren J., and Hans-Henrik Parving
Published: 2005

265. Increased serum adiponectin levels in type 1 diabetic patients with microvascular complications

Author: Allan Flyvbjerg, Jan Frystyk, Lise Tarnow, Hans-Henrik Parving, and T. Krarup Hansen
Subjects: Male, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Gastroenterology, Nephropathy, Reference Values, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Humans, Risk factor, Aged, Type 1 diabetes, Adiponectin, business.industry, Microcirculation, Type 2 Diabetes Mellitus, Middle Aged, medicine.disease, Endocrinology, Diabetes Mellitus, Type 1, Female, business, Diabetic Angiopathies, Kidney disease, Retinopathy
Abstract: Low serum adiponectin (ADPN) has been associated with increased risk of cardiovascular disease (CVD) and retinopathy in patients with type 2 diabetes mellitus. In type 1 diabetic patients, the relationship between ADPN and the presence of vascular complications is largely unknown. We investigated the relationship between serum ADPN and the presence of retinopathy, nephropathy and CVD in patients with type 1 diabetes, divided into matched groups with normoalbuminuria and no retinopathy (n=67), simplex retinopathy (n=106) or proliferative retinopathy (n=19), and nephropathy with simplex (n=62) or proliferative retinopathy (n=137). Healthy control subjects (n=25) were included. Serum ADPN was increased in subjects with type 1 diabetes compared with control subjects (p
Published: 2004

266. Association of aldose reductase gene Z+2 polymorphism with reduced susceptibility to diabetic nephropathy in Caucasian Type 1 diabetic patients

Author: Lise Tarnow, E. Boel, Parving Hh, Maria Lajer, Birgitte V. Hansen, David Edwards, and Jan Fleckner
Subjects: Male, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Diabetic nephropathy, Endocrinology, Polymorphism (computer science), Aldehyde Reductase, Internal medicine, Diabetes mellitus, Internal Medicine, Medicine, Humans, Diabetic Nephropathies, Genetic Predisposition to Disease, Allele, Allele frequency, Type 1 diabetes, Polymorphism, Genetic, business.industry, Diabetic retinopathy, Middle Aged, medicine.disease, Diabetes Mellitus, Type 1, Case-Control Studies, Female, business, Retinopathy
Abstract: Aims The Z−2 allele of the (AC)n polymorphism in the aldose reductase gene (ALR2) confers increased risk of microvascular diabetic complications, whereas the Z+2 allele has been proposed to be a marker of protection. However data are conflicting. Therefore, we investigated whether this polymorphism is associated with diabetic nephropathy and retinopathy in Type 1 diabetes mellitus in a large case–control study and a family-based analysis. Methods A total of 431 Type 1 diabetic patients with diabetic nephropathy and 468 patients with longstanding Type 1 diabetes and persistent normoalbuminuria were genotyped for the case–control study. In addition, 102 case trios and 98 control trios were genotyped for a family-based study. Results Thirteen different alleles were identified. In the case–control study, the Z+2 allele frequency was significantly higher in the normoalbuminuric diabetic than in patients with diabetic nephropathy (0.17 vs. 0.11, P = 0.008), suggesting a protective function of the Z+2 allele. No significant increase in the frequency of the putative risk allele Z−2 was found in patients with diabetic nephropathy vs. controls (0.39 vs. 0.36). No association with diabetic retinopathy was found. Although the results of the transmission of the Z−2 and Z+2 alleles in the independent family-based study were consistent with the association study, the number of informative families was limited and thus differences were not statistically significant. Conclusions The Z+2 allele of the ALR2 promoter polymorphism is associated with a reduced susceptibility to diabetic nephropathy in Danish Type 1 diabetic patients, suggesting a minor role for the polyol pathway in the pathogenesis of diabetic kidney disease. No association of the ALR2 polymorphism with diabetic retinopathy was found.
Published: 2004

267. Plasma N-terminal pro-brain natriuretic peptide as an independent predictor of mortality in diabetic nephropathy

Author: Knut Borch-Johnsen, Per Hildebrandt, H.-H. Parving, Lise Tarnow, and Birgitte V. Hansen
Subjects: Adult, Male, medicine.medical_specialty, Time Factors, medicine.drug_class, Endocrinology, Diabetes and Metabolism, Blood Pressure, Nerve Tissue Proteins, Gastroenterology, Nephropathy, Diabetic nephropathy, Cohort Studies, Risk Factors, Internal medicine, Diabetes mellitus, Natriuretic Peptide, Brain, Internal Medicine, medicine, Natriuretic peptide, Humans, Diabetic Nephropathies, Type 1 diabetes, business.industry, Hazard ratio, Smoking, Reproducibility of Results, medicine.disease, Brain natriuretic peptide, Prognosis, Peptide Fragments, Endocrinology, Diabetes Mellitus, Type 1, Case-Control Studies, Female, business, Biomarkers, Kidney disease, Follow-Up Studies, Glomerular Filtration Rate
Abstract: Raised N-terminal pro-brain natriuretic peptide (NT-proBNP) is independently associated with an increased risk of death in chronic heart failure and acute coronary syndromes in nondiabetic populations. Diabetic nephropathy is characterised by an increased risk of cardiovascular morbidity and mortality. This study investigated the prognostic value of NT-proBNP in a large cohort of type 1 diabetic patients with and without diabetic nephropathy.In a prospective observational follow-up study, 198 type 1 diabetic patients with overt diabetic nephropathy (122 men, age [mean+/-SD] 41+/-10 years, duration of diabetes 28+/-8 years, GFR 74+/-33 ml min(-1)) and a matched control group of 188 patients with longstanding type 1 diabetes and persistent normoalbuminuria (114 men, age 43+/-10 years, duration of diabetes 27+/-9 years) were followed for 9.3 (0.0-9.5) years. Plasma NT-proBNP concentration was determined by immunoassay at baseline.In patients with diabetic nephropathy, plasma NT-proBNP concentration was elevated to (median [range]) 110 (5-79640) ng l(-1) vs. 27 (5-455) ng l(-1) in normoalbuminuric patients (p0.0001). Among patients with nephropathy, 39 (39%) patients with plasma NT-proBNP concentrations above the median and 12 (12%) with values below the median died from any cause (unadjusted hazard ratio 3.86 [95% CI 2.02-7.37], p0.0001; covariate-adjusted hazard ratio 2.28 [1.04-4.99], p=0.04). This lower mortality rate was attributable to fewer cardiovascular deaths: 31 (31%) and 7 (7%) above and below the median NT-proBNP level respectively (unadjusted hazard ratio 5.25 [2.31-11.92], p0.0001; covariate-adjusted hazard ratio 3.81 [1.46-9.94], p=0.006).Elevated circulating NT-proBNP is a new independent predictor of the excess overall and cardiovascular mortality in diabetic nephropathy patients without symptoms of heart failure.
Published: 2004

268. Predictors for the development of microalbuminuria and macroalbuminuria in patients with type 1 diabetes: inception cohort study

Author: Christian Binder, Peter Rossing, Hans-Henrik Parving, Peter Hovind, Inge Torp, Malene Graae, Lise Tarnow, and Berit R. Jensen
Subjects: Adult, Male, medicine.medical_specialty, endocrine system diseases, urologic and male genital diseases, Cohort Studies, Risk Factors, Internal medicine, Diabetes mellitus, medicine, Albuminuria, Humans, Cumulative incidence, Prospective Studies, Prospective cohort study, General Environmental Science, Type 1 diabetes, Proteinuria, business.industry, General Engineering, nutritional and metabolic diseases, General Medicine, medicine.disease, female genital diseases and pregnancy complications, Surgery, Diabetes Mellitus, Type 1, Papers, General Earth and Planetary Sciences, Microalbuminuria, Female, medicine.symptom, business, Diabetic Angiopathies, Cohort study, Follow-Up Studies
Abstract: ObjectiveTo evaluate baseline predictors for the development of persistent microalbuminuria and macroalbuminuria prospectively in patients with type 1 diabetes. DesignProspective observational study of an inception cohort. SettingOutpatient diabetic clinic in a tertiary referral centre, Gentofte, Denmark. Participants286 patients (216 adults) newly diagnosed with type 1 diabetes consecutively admitted to the clinic between 1 September 1979 and 31 August 1984. Main outcome measuresPersistent microalbuminuria and persistent macroalbuminuria. ResultsDuring the median follow up of 18.0 years (range 1.0-21.5 years), total of 4706 patient years of follow up, 79 of 277 (29%) patients developed persistent microalbuminuria. 27 of 79 progressed further to persistent macroalbuminuria. The cumulative incidence of persistent microalbuminuria and persistent macroalbuminuria was 33.6% (95% confidence interval 27.2% to 40.0%) and 14.6% (8.9% to 20.3%), respectively. Significant predictors for the development of persistent microalbuminuria were a 10-fold increase in urinary albumin excretion rate (relative risk 3.78, 1.57 to 9.13), being male (2.41, 1.43 to 4.06), a 10 mm Hg increase in mean arterial blood pressure (1.38, 1.20 to 1.57), a 1% increase in haemoglobin A1c(1.18, 1.04 to 1.32), and a 1 cm increase in height (0.96, 0.95 to 0.98). 28 patients with microalbuminuria (35%) regressed to normoalbuminuria either transiently (n = 15) or permanently (n = 13). ConclusionsAround one third of patients newly diagnosed with type 1 diabetes develop persistent microalbuminuria within the first 20 years of diabetes. Several potentially modifiable risk factors predict the development of persistent microalbuminaria and persistent macroalbuminuria.
Published: 2004

269. Elevated plasma asymmetric dimethylarginine as a marker of cardiovascular morbidity in early diabetic nephropathy in type 1 diabetes

Author: Lise Tarnow, Coen D.A. Stehouwer, Hans-Henrik Parving, Peter Hovind, and Tom Teerlink
Subjects: Adult, Male, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Renal function, Blood Pressure, Arginine, Gastroenterology, Nephropathy, Diabetic nephropathy, chemistry.chemical_compound, Insulin resistance, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Humans, Diabetic Nephropathies, Endothelial dysfunction, Advanced and Specialized Nursing, Type 1 diabetes, business.industry, Middle Aged, medicine.disease, Endocrinology, Diabetes Mellitus, Type 1, chemistry, Cardiovascular Diseases, Creatinine, Female, Morbidity, Nitric Oxide Synthase, business, Asymmetric dimethylarginine, Biomarkers, Diabetic Angiopathies, Glomerular Filtration Rate
Abstract: OBJECTIVE—Increased plasma concentration of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, has been associated with endothelial dysfunction, insulin resistance, and atherosclerosis in nondiabetic populations. In end-stage renal failure, circulating ADMA is elevated and a strong predictor of cardiovascular outcome. This study investigated the relation between ADMA and diabetic micro- and macrovascular complications in a large cohort of type 1 diabetic patients with and without early diabetic nephropathy. RESEARCH DESIGN AND METHODS—ADMA concentrations in plasma were determined by a high-performance liquid chromatography method in 408 type 1 diabetic patients with overt diabetic nephropathy (252 men; mean age 42.7 years [SD 11.0], mean duration of diabetes 28 years [SD 9], median serum creatinine level 102 μmol/l [range 52–684]). A group of 192 patients with longstanding type 1 diabetes and persistent normoalbuminuria served as control subjects (118 men; mean age 42.6 years [SD 10.2], mean duration of diabetes 27 years [SD 9]). RESULTS—In patients with diabetic nephropathy, mean ± SD plasma ADMA concentration was elevated 0.46 ± 0.08 vs. 0.40 ± 0.08 μmol/l in normoalbuminuric patients (P < 0.001). An increase in plasma ADMA of 0.1 μmol/l increased the odds ratio of nephropathy to 2.77 (95% CI 1.89–4.05) (P < 0.001). Circulating ADMA increased in nephropathy patients with declining kidney function, as indicated by elevated values in the lower quartiles of glomerular filtration rate ( 0.2). However, in 44 patients with nephropathy and history of myocardial infarction and/or stroke, ADMA was significantly elevated at 0.48 ± 0.08 μmol/l compared with 0.46 ± 0.08 μmol/l in patients without major cardiovascular events (P = 0.05). CONCLUSIONS—Elevated circulating ADMA may contribute to the excess cardiovascular morbidity and mortality in early diabetic nephropathy.
Published: 2004

270. 40(th) EASD Annual Meeting of the European Association for the Study of Diabetes : Munich, Germany, 5-9 September 2004

Author: S. Artigas, A V Dreval, Mark I. McCarthy, C Watson, Peter H. Bennett, M Quint, Y Ikeda, E Alpert, F Schiele, H Sekihara, Erik Gylfe, P Lowe, J Kuhlmann, Alain Golay, V Longo, Shahidul Alam Khan Akm., L G Mantovani, M Zawodniak-Szalapska, G Winkler, T Harrity, L Virág, U Johne, Kuo S-W., Linda C Tapsell, J Rodriguez, Michel Komajda, K Kankova, Carole A. Cull, M Sporna, E Estilles, U Ribel, M C Spruce, E Buzzigoli, T Prazak, J K McLaughlin, M K Lingohr, M Lim, F Calara, A Siebenhofer, G Meregalli, Roberto Anichini, A D Baron, R Kurashvili, P C Butler, G I Fantus, T. E. De Gooyer, Park Y-M., R. Walther, S Heinrich, Agnieszka Zawiejska, S Mukherjee, Nikolaos Papanas, G Wong, Ian D. Caterson, David M. Maahs, Shuichi Kaneko, Alexandra E. Butler, Francisco Javier Ampudia-Blasco, O N Kong, Attali J-R., C A Hedman, K Oshinyemi, Nicolle Müller, I C Cranston, N Okumus, M V Vlaiculescu, Balasubramanian Ravikumar, W W Cheatham, K Mukasa, K B Biswas, Annunziata Lapolla, Phil McEwan, G Mader, Gilles Chassot, Dragi Anevski, Werner A. Scherbaum, M Donath, C Hesselmann, R A Gandhi, David E. Moller, Ezio Bonifacio, C Garcia, V Ifandi, P Hornnes, Nieuwenhoven Fav., C Puech, S Pérez-Del-Pulgar, Kim S-R., G Hines, C Rubio Terrés, Michael Gaster, N. Hosszufalusi, A Scholze, Andrew A. Young, Stavros Liatis, F Hariri, S Tan, Paul Valensi, Allan E. Karlsen, J Kim, E. Moberg, J Kaiser, L Berman, G Nelson, A Altkrüger, P Kothare, D B Cook, S Doran, G. van Dijk, Shahnaz Shahinfar, Kim C-S., P Stahl, M Manousaki, S Sigrist, S K Lim, M. P. Stern, A Guberti, C Rezzani, J McKenney, Karl Thomaseth, Sofia Carlsson, M Julia, R Brillante, I Rubesova, T Darkow, E Matsumoto, Wendy M. Macfarlane, M Di Martino, G Bardini, Rossella Menghini, D Duhot, E Farcasiu, Annalisa Natalicchio, I Lindner, J Buvat, Christian L. Brand, Harry Dorchy, Iwona Pietrzak, Z T Luo, P Home, M Ekelund, Jesper Gromada, Kristine Færch, F Piarulli, H Kim, R Mentel, Zsuzsanna K. Zsengellér, Dullaart Rpf., Anton Luger, Thomas A. Pearson, V Manicardi, P Rösen, Feng Y-M., R Morganti, Lars Hansen, Demuth H-U., Haruo Kasai, A Shostak, Rudi Steffensen, G Taylor, Markolf Hanefeld, C Santini, E Hamaguchi, Roberto Miccoli, F Storms, M Cooper, Y Lee, Allison E. Aiello, P Smith, T Suehiro, K Treece, M Waluś, Timothy A Welborn, Simone Baltrusch, E Kontela, S Chai, J Crean, H Yokoyama, Johan G. Eriksson, Rafael Hernández Hernández, J Rodríguez-Saldaña, M P Tornero, G Formoso, D. Lovell, E Bingham, A Mylonakis, M Manteghetti, D Fedele, Antonio Martín-Duce, Ralph A. DeFronzo, D Salcedo, Kurt Højlund, Antonio Petrone, Sheu Whh., C Gutierrez, Flavia Pricci, S Kurita, Z G Abbas, M M Benedetti, Philippe A. Halban, Daniel J. Cox, O Ljungkvist, Justine Davies, J Palsgaard, Lars Sjöström, E Bosi, L Janin-Manificat, W. F. Kelly, M. Fernandez, E Colak, O V Mulyarchik, B Kronshage, F Lang, M Erfurth, Takashi Kadowaki, N Jendrike, U Walter, J Wishart, Y. Neye, D Kim, N Furuhashi, M Barsotti, D Florow, L Ke, L Borgquist, N C Jackson, Ffolliott M. Fisher, V Baskar, K Yoshioka, Bryan A. Wolf, G Chabrier, R Skoumal, Livio Luzi, H Kose, I Pharisien, B. Klein, H Winiarska, M C Johnson, L Griffiths, Nonna Kravchun, C Combe, Baptist Gallwitz, J Zdychova, L Skorda, Jorma Ilonen, W Gao, I N Steen, A Terrinoni, P D Ambery, W Kern, C M Kusminski, Cho M-H., Paolo Pozzilli, Louise G. Grunnet, E Schönle, David R Matthews, Robert W. Taylor, Y Cohen, Kim H-S., M P Eccles, N B Tutuncu, D McDowell, Richard M. Bergenstal, K Takamatsu, T Steiner, Jaan Palgi, Valdemar Grill, N Niculescu, G Federici, S Lehto, P. M. McKeigue, M Barone, Michael E. Trautmann, S Smirnov, J Mannion, M Eto, C Rousseau, M Conti, C S Ernest, Antonio Ceriello, D H Schweitzer, Jung E-D., Andreas Festa, Avijit Lahiri, A Shepelkevich, A Murro, A Kollmann, Jonathan R.S. Arch, R Landgraf, Son H-Y., I Engelsberger, E Agardh, S Rodríguez-Mulero, P J Kraml, K Lee, D. F. Du Toit, E Kim, G Fadini, Williams Ajk., Philip Home, M B Antcieferov, C Perlemoine, D Perrea, Song X-L., D Ruggieri, Krister Bokvist, Heidi Sørensen, Bilbao, G Yoshino, J P Taylor, Shen H-M., S M Furier, R Urquhart, J Wohlgelernter, Jianping Weng, T. Baba, Q Hong, C Silva, Castaigne J-P., M Felaco, X X Zhang, M Jaroň, Milla Rosengård-Bärlund, J G Papp, Toshio Miyata, Lervang H-H., Park M-K., I Kinalska, A Long, Oomen Phn., N Kogawa, Ippolita Patrizia Patera, S. Karadeniz, Dinesh Selvarajah, D S Chung, A Wensaas, Richard Imrich, M Recasens, J Ruxer, O Buchea, E Wilpart, S P Stepanenko, Le Ttd., H Ohgawara, Mariaconsuelo Valentini, A Mondok, M Peltonen, Marianne O. Larsen, K Chatzianagnostou, Agneta Ståhle, A L Ferrari, L Bordier, F Maingrette, A Matsuda, G Vukomanovic, Jakob D. Wikstrom, T Yamakita, E Gorostiaga, J Jin, B Gopalan, Heinz Drexel, S Hewitt, Rury R. Holman, C Dieterle, T L Ruchti, N Asatiani, M Sidira, A Iezzi, A J Sommerfield, D Châtenet, M L Olsen, R Bergemann, C Koehler, T L Kuraeva, B Balas, Christian Berne, E Santos-Mazo, G Smith, A Siejka, R Kožnarová, A Mattina, S Sheikh, A Adomeit, M Rasmussen, J. Fagerudd, N Busciantella Ricci, Nuria Vilarrasa, E Hammar, T L Thoms, L Aydın, Ron G. Rosenfeld, A Nikolajuk, R Gos, C L Morgan, H L Yu, D Dheelchand, S Ramrath, N Boudriga, Jerome I. Rotter, C Jahannault, W M Weston, Folke Lindgärde, M Hertlova, D Knight, A Monroy-Mayorga, E Pardini, A Chamson-Reig, B Franke, Janie McCluskey, Joseph Bryan, C Nikolopoulou, Christie M. Ballantyne, Fausto Santeusanio, L Pegoraro, M Lee, A Klimenko, S Jaiveer, K. Pettersson-Fernholm, Michael A. Nauck, A Ekbom-Schnell, G Deferrari, Riccardo Schiaffini, S. Pampanelli, Khan Aka., David Hopkins, Maija Wessman, M Kamarinos, Noh J-H., O Ebisui, K McCarroll, Jeppe Sturis, Peter Nowotny, N Gorbenko, Åke Sjöholm, David G. Maggs, A E Halseth, B Cresci, A A Ortiz-Gress, A Korakovouni, O Matejkova, C E Mogensen, C J Lin, Ramon Gomis, H Seaman, C Granier, Yang C-H., F Assah, O Sanchez, Fausto Machicao, Peter G. Morris, Alberto Ortiz, A Giardinelli, D Bracaglia, A Gonzalo, S Pavlatos, Andreas Lechner, F Canovic, L Sjolind, Allan Vaag, Birgitte Bruun Nielsen, David A. Ziegler, Vito Lampasona, R Gershoni-Baruch, A. Dei Cas, H Renz, E Mena, Matthew Waltham, Kim D-M., H Levanen, D D Mick, Valentina Alexandrovna Peterkova, E Meskhishvili, Sarah Nutland, R Bustani, John R. Lindsay, M Christoforidou, A Abicht, E Harno, K Cyganek, A Fitchet, S Neelotpol, P Nikishin, P Serradas, J Hinrichsen, M Halvorson, M Chovatia, B Voet, Jinny Willis, E Parretti, M Haslbeck, M Wellard, L Teng, Julio Wainstein, J S Fischer, K. Lalic, D Roggenland, I Gich, R Anwar, Maurizio Cassader, D Serota, X J Li, R J Schotzinger, Vilmundur Gudnason, Björn Zethelius, S A Wootton, W Andrzejewski, R Rezsohazy, R Gao, T Klimentova, T Mazurek, I Bruckner, C Dohrmann, R E James, G daSilva Xavier, Kim S-Y., A Dorca, Stuart J. Pocock, Terri J. Allen, I Giovos, P B Parab, N H Andersen, P Fotinakis, Miriam Cnop, H Lee, Norbert Tennagels, Omorodola I. Abatan, F Ailett, I. Lager, D Manzella, H Hut, Larry A. Distiller, G Lip, Lim S-K., Rong Zhang, T Tsuno, Steen Knudsen, M. Bajardi, Manuel Benito, Dai Sugimoto, Melvin J. Prince, D W Dunstan, D Rankins, K A Majali, G Ozansoy, Isabella Russo, S Uçak, G Annuzzi, R Talar-Wojnarowska, K Lange, S Neugebauer-Baba, Campbell H. Thompson, Eric Renard, P. D. Mountjoy, Z Morrison, Elizabeth A. Davis, Franco Cavallo, C Corvaja, R Antuña, Craig John Currie, H Linnebjerg, He Y-L., A J Palmer, Mariola R. Chacón, H Malinska, M. Jones, R Lichnovská, K Mandes, Paolo Tessari, T Mokhort, A Laina, H. L. Y. Chan, I Schmidt, R Banks, Richard G. IJzerman, L Ksinantova, G Setti, H Vaudry, A Gallo, V Spallone, Chen J-W., Thomas Danne, A Chong, M Hallschmid, S Aczel, S Hulme, N Islam, M Hosoi, P M Ternan, P Di Bartolo, N Bishara, T Shibasaki, Martin A. Osterhoff, Im S-S., M Jecht, T Hamaguchi, S Mattera, K Ways, Elizabeth Northam, U Rajala, Reinhard W. Holl, L Yang, S Panaiotopoulos, K Horvath, R Kluge, Thora B. Bodvarsdottir, Y Dong, Irene Alemanno, C McDougall, Reimar W. Thomsen, M Campbell, W Rabl, John Öhrvik, Yuichiro Yamada, Paola Ungaro, W Benzer, Mike Sampson, Roberto Trevisan, R G Radu, Aas A-M., P E Lobo, Ricardo Scott, S M Son, Josephine M. Forbes, T A Hillier, K L Wyne, Louis L. Nguyen, J Farmer, M H Tan, Kwon H-S., J Yang, L Sandvik, Franco Folli, A K Jenum, M Nguyen, W Pratipanawatr, A L Frederiksen, Rebecca Smith, Lee H-J., A Schäfer, C Manuelli, G S Denver, T Vukovich, B Maceira, K Matsumoto, K. Chokkalingam, Nurcan Üçeyler, P Modi, Timothy M. Morgan, S Mertens, B M Singh, Michaela Riedl, K Iso, C Cucurullo, G. F. Bottazzo, M Calvani, K Hur, J Wetzels, Kazuhiro Takahashi, Y Aso, H Stammer, M G Masding, Fitsum Guebre-Egziabher, J L González-Sánchez, L Armstrong, Alberto Maran, Peter G.F. Swift, S S Popovic, J Starczynski, E Vitacolonna, Luigi Laviola, R W Gelling, Marina Cardellini, D Barilla, Rosa de Diego Martínez, W H Landschulz, Anne Mette Rosenfalck, R K Wong, Kevin E. Schneider, K Peros, Giuseppe Nanni, F Zhang, I Rákóczi, T Iburi, M Nakhjavani, X Q Zhang, S Tournis, Per Lav Madsen, Graham A. Hitman, A. Tura, K Laubner, N D Kostic, Lawrence M. Dolan, R. Sinha Roy, J A Wagner, J. Tuomilehto, J Hauptman, M Abdel-Ghany, D Lacombe, Toralph Ruge, Johannes A Maassen, Triantafyllos Didangelos, K Sasaki, I Argüelles, Klaus Levin, C Popow, Emanuel Christ, R Chetty, L Baillet-Blanco, Jo-Ann Salmon, T Mine, James L. Trevaskis, I Franke, J Gorski, E A Andrianova, A Dayan, A Caballero, Aleksandra Gilis-Januszewska, M Yasujima, Z Kasalová, C.D.A. Stehouwer, F. K. Gorus, G A Nichols, A Glowania, David P. Strachan, P Fredlund, N. F. da Silva, P Reboldi, M Sausbier, K H Groenier, G Stuccio, N Guttman, K R Ahmed, A D Ristic, T Kapellen, J Coutcher, Aldo V. Greco, Oswald Wagner, A Zagayko, Maria Alevizaki, B B Zhang, W F Ferris, Jenny Fredriksson, Lois Jovanovic, J Hänninen, R De Giglio, Kazuo Yagui, O Potterat, P Hamliton, R E Scranton, B Mankovsky, A Stylianou, B Fellström, Abdel-Wahab Yha., M Kitagawa, Katherine L. Baldock, F R Johnson, F Baigts, S D'Addato, F J Sanz, A Mistry, S D Wise, T Pratipanawatr, U R Fölsch, James R.C. Parkinson, Claudia Sommer, C Park, F E Griffiths, M L Martí, R Demirtunc, S Taniguchi, J Lundkvist, T Siegmund, Juan Sztajzel, C Dienesch, F Baumgartner, L Scalone, T M Mckolanis, K Otake, Ullrik Pedersen-Bjergaard, T M Vriesendorp, Michael B. Wheeler, Henry Schmitt, Peter Hovind, S Lange, Stephane Roze, L. Van Gaal, B Klaproth, Anthony E. Civitarese, D Eckland, A Dagar, D F Hopkins, Kari Stefansson, C Gonzalez-Yanes, B Meyboom-de Jong, D. J. Betteridge, K Buhling, M Crepaldi, Ana M. Wägner, L Renna, L Volpe, R McBride, V Corbo, E O Brennesvik, R P Hayes, R Abdollahnia, G Viviani, C F Liew, Francisco Pérez-Bravo, Jeffrey Baron, Brian M. Frier, H H Samira, D Szentendrei, K. J. Schjoedt, W K Waldhäusl, D Gniuli, D Zou, G Tschank, V Urbančič, A L Nolan, Albertini J-P., J Malcomson, M Larbig, C Cheyssac, K Aurich, C M Kesson, S Heller, Maija E. Miettinen, R F Luco, Adrian J. Cameron, Luigi Mattiello, Z. Metelko, X E Zhang, M Parramón, I. G. Obrosova, J Fruchart, M Ilic, Björn Eliasson, Gilles Chatellier, M A Martín, D M Kendall, Holger Luthman, V F Varillas, D Maccubbin, Jang S-A., Amalia Gastaldelli, E Salzsieder, P. de Mol, A Yoshida, H D Lindner, D Gostiljac, M Just, Pan C-Y., J M Fujitaki, G Eiermann, K Bergenheim, A D Frick, A Agacdiken, K Varytimiadis, K Cseh, D A Jackson, S Calderari, Dena G. Hernandez, H M Liebich, K Min, F. de Zegher, Bernd Kulzer, K Han, Ulrich A. Müller, D Marrero, H Hatakeyama, René Koopman, Doo H-K., Petr Wohl, P. Sharp, P Forder, Thor Aspelund, N Meneveau, R M Schmülling, R Aubert, Thom Sam., H Youshikawa, M Ankelo, D Bowden, I Kelly, Frédéric Fumeron, M Sartini, Robert S. Sherwin, L Varadhan, A Criscimanna, John Betteridge, V Jelic, M Bartnik, N Lemke, B Ursø, A Bertoldo, A M Owona, H Okochi, L Pérez-Tamajó, S L Monfre, Daniel Brandhorst, K T Legg, Andries J. Smit, Veronica Sancho, Masashi Hirai, C Klein, Paul J. Thornalley, A Chaidaroglou, K Miura, B Zinman, O M Dvoynishnikova, J Plank, Jan Bolinder, C Lush, B Rubi, R Pozzilli, M Bashir, S A Shtandel, F Mosca, A Naskalska, Josef Vcelak, U Sausbier, P Cavaiani, T U Baehring, Michele Solimena, P Formisano, M Rastaldi, Bernard Thorens, J Ruzzin, E Arbit, M. Hori, Torkel B. Brismar, E Soltes Rak, A Filo, P Heinke, Matthew P. Coghlan, M Masotti, I Perevozskaya, K Ahn, I Moules, K Van Dyck, I Goldstein, Z Mathe, G Z Zhao, S Fajardo, J Taylor, S Chrul, J C Pareja, D Hadjidakis, A J Scheen, N Siddiqua, D C Cavan, R Grella, Krabbe S, H J Rochlitz, A E Hinkkanen, W Wilpshaar, Richard Stevens, M Dreyer, S Hara, X Wang, Melania Manco, D Gillen, Magalie A. Ravier, Olli Simell, John C. Lawrence, Kohnert K-D., Agardh C-D., A Berghold, L Kristensen, Grant Sfa., N Gursoy, Leif Groop, N Freemantle, Anja Schweizer, L Pala, Legros J-J., C. Di Pietro, N. Yamamoto, J Magyar, B Nikolovski, H Ikeda, D Lee, Bruce A. 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Leon, Alberti Gkm., A Opel, S Kokkoris, S B Hong, Philippe Courtois, L Haque, Maria Sörhede Winzell, M C Beauvois, A Szypowska, D Yu, M Gutniak, D Petzinna, B Isomaa, K S Prickett, Maria Felice Brizzi, Pavel Hamet, P J Hammond, K. F. Michelmore, Yumie Takeshita, N Hariharan, Corrado M. Cilio, G Pogatsa, W G Jerome, E Bartley, K Schlembacher, G Blohmó, Guy A. Rutter, Kyung Mook Choi, S. C Tamer, Felix K. Assah, K A Jandeleit-Dahm, M Chan, H Darius, Jørgen F. P. Wojtaszewski, A Papazisi, M Amaya, A Knopff, M Tadayyon, I J Kim, W Russ, T Myrnäs, M. Tryon, S Poonsatha, Noel Cameron, Kim M-H., Alejandra Tomas, F Homo-Dekarche, G. Di Cianni, M Stotzka, C Solimine, Mikhail Borisovich Antsiferov, H Naserke, M Bianchi-Biscay, J I Lara, Moon C-K., Alain Ktorza, Alison N. Jeffery, V Lilla, Eun Seok Kang, Hanley Ajg., J Widder, R Ratner, C Goretti, P J Weston, J Perkins, V Rasmussen, M Evans, T M Gibson, A Jaffe, S I Chisalita, C Owman, L Hiltunen, E Kakishita, C M Mack, H C Potter, M Femerling, M Desai, M Soinio, K Yang, Patricia L. Brubaker, M Meyer, V Dy, J Berden, R Komers, Milos Adamec, R Petzoldt, Alan G. Robinson, R Stevens, A Doi, A Leunda, Eduard Montanya, Alessandra K Cardozo, N Kraenkel, Claudio Cobelli, U A Mueller, S Yamashiro, B R Gedulin, G Francisco, J Dennenmoser, Lesch K-P., Martin G. Bischof, M Ichita, C Fernandes, Jochen Hampe, S Kern, D Kelly, E Zeender, P Perna, J D Best, A C Calkin, Vivian Fonseca, J Prestle, D G Parkes, Satish K. Garg, T Burrell, B M Fischer, D Kruger, J S Skinner, Lin T-M., Jozef Ukropec, Maria Jeziorska, K Arii, David D. D’Alessio, M B Gomes, L Quandt, I Fragaki, M C Brindisi, A Gladkih, E Kitsou, S Di Cola, T Iwasaki, Peter Diem, T Lakka, V V Popova, G Lee, Hannah J. 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Thornalley, P, Babaei jadidi, R, Karachalias, N, Kupich, C, Ahmed, N, Fowler, A, Baker, A, Starczynski, J, O'Hare, P, Szepietowska, B, Szelachowska, M, Puch, U, Glebocka, A, Quinn, D, Mcternan, C, Bonser, R, Idzior walus, B, Woźniakiewicz, E, Dimitriou, K, Apostolou, O, Kontela, E, Devangelio, E, Gould, E, Serri, O, Roussin, A, Buithieu, J, Mamputu, J, Renier, G, Giordanetti, S, De Amici, E, Poggi, G, Turpini, C, Fratino, P, Garzaniti, A, Banu, I, Paries, J, Roman, G, Negrean, M, Bala, C, Nita, C, Kistorp, C, Gustafsson, F, Chong, A, Lip, G, Galatius, S, Ari, N, Sahilli, M, Ceylan isık, A, Ozansoy, G, Karasu yilmaz, C, Matteucci, E, Rosada, J, Pallini, M, Evangelista, I, Cassetti, G, Giusti, C, Giampietro, O, Capaldo, B, Galderisi, M, Cicala, S, Turco, A, Imbroinise, A, Nosso, G, D'Errico, A, De Divitiis, O, Klimontov, V, Korolyova, E, Jeltova, L, Bondar, I, Tarkun, I, Arslan, B, Canturk, Z, Tarkun, P, Agacdiken, A, Komsuoglu, B, Méneveau, N, Pierre justin, E, Alsayed, M, Sabbah, R, Paulin, S, Marcu, S, Tauveron, I, Zimmermann, C, Schiele, F, Seronde, M, Vautrin, P, Lusson, J, Thieblot, P, Bernard, Y, Mistry, A, Pye, M, Peovska, I, Maksimovic Pavlovic, J, Vavlukis, M, Pop Gorceva, D, Bosevski, M, Scognamiglio, R, Negut, C, De Kreutzenberg, S, Madonna, R, De Caterina, R, Willerson, J, Geng, Y, Vahsen, S, Ledwig, D, Ramrath, S, Frantz, S, Schmidt, I, Calvillo, L, Dienesch, C, Elbing, I, Bischoff, H, Ertl, G, Bauersachs, J, Davydov, A, Mkrtum'Yan, A, Baranova, L, Ikeda, Y, Suehiro, T, Osaki, F, Ota, K, Arii, K, Kumon, Y, Hashimoto, K, Doney, A, Morris, A, Palmer, C, Byun, S, Doo, H, Pagnin, E, Calo, L, Fadini, G, Kubaszek, A, Chai, S, Chai, Q, Rasmussen, L, Ledet, T, Wogensen, L, Lengyel, C, Varró, A, Virág, L, Magyar, J, Bíró, T, Jost, N, Skoumal, R, Nánási, P, Tóth, M, Horkay, F, Papp, J, Zacharopoulou, O, Athanaselis, S, Tsokos, N, Doupis, J, Psallas, M, Cokkinos, D, Pavlatos, S, Liatis, S, Akhobadze, T, Dzneladze, L, Samarguliani, I, Taskiran, M, Rasmussen, V, Jensen, G, Fisher, A, Petrovsky, N, Srikusalanukul, W, Budge, M, Trifunovic zamaklar, D, Zivkovic, M, Jelic, V, Vukomanovic, G, Ristic, A, Seferovic, P, Costa, J, Duarte, S, Manley, S, Sailesh, S, Venkataraman, A, Haider, Y, Groza, I, Oprean, M, Ardelean, A, Morosanu, A, Darkow, T, Vanderplas, A, Mamas, M, Mcelduff, P, Burns, J, Edwards, R, Fitchet, A, Young, R, Gibson, J, Lichiardopol, R, Niculescu, N, Totora, A, Pencea, C, Tomescu, I, Cinteza, M, Manicardi, V, Coscelli, C, Navazio, A, Catellani, E, Michelini, M, Dall'Asta, D, Guberti, A, Piazza, A, Gasparini, E, Pantaleoni, M, Guiducci, U, Manari, A, Sejil, S, Janand delenne, B, Avierinos, J, Habib, G, Labastie, N, Vague, P, Lassmann vague, V, Luźniak, P, Tatoń, J, Wojciechowska Luźniak, A, Zairis, M, Lyras, A, Patsourakos, N, Tsirimbis, V, Foussas, S, Lupón, J, Urrutia, A, Herreros, J, González, B, Coll, R, Altimir, S, Prats, M, Valle, V, Abreu padí, C, Rábago, G, Ivanova, L, Brasacchio, D, Harno, E, Keenan, A, Li, H, Lu, Z, Ke, L, Liu, H, Jeong, I, Chae, M, Choi, M, Yoo, H, Kim, C, Yun, M, Na, M, Kang, Y, Kong, O, Son, S, Kim, I, Tanaka, N, Hosoi, M, Matsuyama, Y, Fukumoto, M, Yamakita, T, Yoshioka, K, Ishii, T, Sato, T, Fujii, S, Aoki, T, Shibata, T, Mizutani, N, Suzuki, J, Fowelin, J, Samuelsson, P, Brandrup wogsen, G, Okumura, K, Tokmakova, A, Staroverova, D, Antcieferov, M, Shutichina, I, Kuntchevich, G, Vriesendorp, T, Morélis, Q, Legemate, D, Schaper, F, Mainas, E, Gkioulmpasanis, I, Panagiotou, I, Vassilikos, G, Skorda, L, Sidira, M, Christoforidou, M, Alaveras, A, Artikis, V, Evdemon, E, Lechleitner, M, Koch, T, Ebenbichler, C, Sturm, W, Moretti, L, Moruzzo, D, Boldrini, E, Pandolfo, C, Kameyama, M, Iwasa, R, Cho, M, Nam, J, Huh, K, Kaplar, M, Paragh, G, Erdei, A, Csongradi, E, Garai, I, Varga, J, Galuska, L, Udvardy, M, Higa, M, Kaneko, Y, Hiroi, N, Koziarska, D, Nowacki, P, Majkowska, L, Luzniak, P, Wojciechowska luźniak, A, Tushuizen, M, Nieuwland, R, Snoeck, D, Sturk, A, Diamant, M, Aguiar, L, Bahia, L, Villela, N, Laflor, C, Conde, C, Bottino, D, Dorigo, D, Bouskela, E, Pu, S, Luo, Z, Lam, K, Dan, Q, Xu, A, Shen, J, Cheng, K, Xu, J, Thamer, C, Stefan, N, Haap, M, Heller, E, Tschritter, O, De Prado, A, Ortiz, A, Ybarra, J, Gich, I, Pou, J, Ehren, M, Roggenland, D, Reinsen, B, Klein, H, Rittig, K, Stock, J, Kocher, B, Balletshofer, B, Shon, H, Chung, D, Nakatani, Y, Matsuhisa, M, Kaneto, H, Hatazaki, M, Yoshiuchi, K, Katakami, N, Kawamori, D, Ohtoshi, K, Sakamoto, K, Matsuoka, T, Ozawa, K, Ogawa, S, Hori, M, Yamasaki, Y, Zitouni, K, Harry, D, Nourooz zadeh, J, Earle, K, Olesen, P, Franco, L, Corvaja, C, Semplicini, A, Ceylan işık, A, Arı, N, Rösen, P, Lee, I, Park, K, Jung, E, Shin, D, Jo, S, Obuobie, K, Prakash, P, Hanna, F, Lazarus, J, Varadhan, L, Gurushankar, J, James, D, Sheikh, S, Gaede, P, Zou, D, Vilarrasa, N, Perez maraver, M, Mena, E, Perez, D, Setti, G, Buckingham, R, Urbančič, V, Stefanovska, A, Bernjak, A, Ažman juvan, K, Kocijančič, A, Glowania, A, Filters, T, Fosmark, D, Torjesen, P, Kilhovd, B, Berg, T, Sandvik, L, Hanssen, K, Mentink, C, Donchenko, G, Stepanenko, S, Maingrette, F, Deng, H, Lindenmair, A, Freudenthaler, A, Baumgartner parzer, S, Nizheradze, K, Khoruzhenko, A, Tronko, N, Sheu, W, Ou, H, Shen, H, Lin, T, Wu, H, Yang, C, Mogylnytska, L, Schmoelzer, I, Davies, J, Band, M, Struthers, A, Prázný, M, Škrha, J, Kasalová, Z, Neelotpol, S, Jahan, P, Kauschke, S, Harrop, C, Schäfer, A, Widder, J, Eigenthaler, M, Walter, U, Uchimura, I, Ikebukuro, M, Kaibara, M, Hirata, M, Helal, R, Pervin, F, Yang, X, Jansson, P, Nagaev, I, Jack, M, Carvalho, E, Sunnerhagen, K, Cam, M, Cushman, S, Smith, U, Creely, S, Farmer, J, Gustafson, B, Kusminski, C, Krusinova, E, Wohl, P, Klementova, M, Lanska, V, Mcdougall, C, Kelly, I, Abbas, Z, Lutale, J, Archibald, L, Karunajeewa, H, Stingemore, N, Stuccio, G, Mcgechie, D, Muller, L, Hak, E, Goudzwaard, W, Montorsi, F, Homering, M, Sprenger, K, Goldstein, I, Asnaghi, V, Ferrari, G, Rastaldi, M, Gabellini, D, Dell'Antonio, G, Maestroni, A, Ruggieri, D, Luzi, L, Piemonti, L, Zerbini, G, Anafaroglu, I, Tutuncu, N, Sultana, M, Siddiqua, N, Iwasaki, T, Nakajima, A, Yoneda, M, Mukasa, K, Tanaka, S, and Sekihara, H
Subjects: 0303 health sciences, medicine.medical_specialty, business.industry, EASD, Endocrinology, Diabetes and Metabolism, Human physiology, medicine.disease, 03 medical and health sciences, 0302 clinical medicine, Diabetes mellitus, Family medicine, Internal Medicine, Medicine, business, 030217 neurology & neurosurgery, 030304 developmental biology
Published: 2004

271. Association between mannose-binding lectin and vascular complications in type 1 diabetes

Author: Troels Krarup Hansen, Hans-Henrik Parving, Lise Tarnow, Allan Flyvbjerg, Casper G. Schalkwijk, Steffen Thiel, Rudi Steffensen, and Coen D.A. Stehouwer
Subjects: Adult, Male, medicine.medical_specialty, Genotype, Endocrinology, Diabetes and Metabolism, chemical and pharmacologic phenomena, Biology, Mannose-Binding Lectin, Medical Records, Nephropathy, Diabetic nephropathy, Interquartile range, Internal medicine, Immunopathology, Diabetes mellitus, Internal Medicine, medicine, Odds Ratio, Humans, Diabetic Nephropathies, Genetic Predisposition to Disease, Serum Albumin, Mannan-binding lectin, Type 1 diabetes, Polymorphism, Genetic, Odds ratio, Middle Aged, bacterial infections and mycoses, medicine.disease, Endocrinology, Diabetes Mellitus, Type 1, Cardiovascular Diseases, Case-Control Studies, Female, Diabetic Angiopathies
Abstract: Complement activation and inflammation have been suggested in the pathogenesis of diabetic vascular lesions. We investigated serum mannose-binding lectin (MBL) levels and polymorphisms in the MBL gene in type 1 diabetic patients with and without diabetic nephropathy and associated macrovascular complications. Polymorphisms in the MBL gene and serum MBL levels were determined in 199 type 1 diabetic patients with overt nephropathy and 192 type 1 diabetic patients with persistent normoalbuminuria matched for age, sex, and duration of diabetes, as well as in 100 healthy control subjects. The frequencies of high- and low-expression MBL genotypes were similar in patients with type 1 diabetic and healthy control subjects. High MBL genotypes were significantly more frequent in diabetic patients with nephropathy than in the normoalbuminuric group, and the risk of having nephropathy given a high MBL genotype assessed by odds ratio (OR) was 1.52 (1.02-2.27, P = 0.04). Median serum MBL concentrations were significantly higher in patients with nephropathy than in patients with normoalbuminuria: 2,306 microg/l (interquartile range [IQR] 753-4,867 microg/l) vs. 1,491 microg/l (577-2,944 microg/l), P = 0.0003. In addition, even when comparing patients with identical genotypes, serum MBL levels were higher in the nephropathy group than in the normoalbuminuric group. Patients with a history of cardiovascular disease had significantly elevated MBL levels independent of nephropathy status (3,178 microg/l [IQR 636-5,231 microg/l] vs. 1,741 microg/l [656-3,149 microg/l], P = 0.02). The differences in MBL levels between patients with and without vascular complications were driven primarily by pronounced differences among carriers of high MBL genotypes (P
Published: 2004

272. Progression of nephropathy in type 2 diabetic patients

Author: Kasper Rossing, Peter Hovind, Per K. Christensen, Hans-Henrik Parving, Lise Tarnow, and Peter Rossing
Subjects: Male, medicine.medical_specialty, Urology, Renal function, progression of renal disease, Type 2 diabetes, urologic and male genital diseases, White People, Nephropathy, chemistry.chemical_compound, Internal medicine, Diabetes mellitus, medicine, Albuminuria, Humans, risk factors, Diabetic Nephropathies, Prospective Studies, Risk factor, Creatinine, business.industry, Middle Aged, medicine.disease, female genital diseases and pregnancy complications, Endocrinology, chemistry, Diabetes Mellitus, Type 2, Cardiovascular Diseases, Nephrology, Disease Progression, Kidney Failure, Chronic, nephropathy, Female, type 2 diabetes, medicine.symptom, business, Kidney disease, Follow-Up Studies, Glomerular Filtration Rate
Abstract: Progression of nephropathy in type 2 diabetic patients. Background Nephropathy in type 2 diabetes is the single most common cause of end-stage renal disease (ESRD), but the decline in kidney function varies considerably between individuals, and determinants of renal function loss, early in the course of renal disease, have not been clearly identified. Methods In a prospective observational study, we followed 227 (60 female) Caucasian type 2 diabetic patients with nephropathy for 6.5 (range 3 to 17) years from a baseline glomerular filtration rate (GFR) of 83 (SD30) mL/min/1.73m 2 with 7 (range 3 to 22) measurements of GFR ( 51 Cr-EDTA) per patient. We evaluated determinants of (1) rate of decline in GFR, (2) risk of doubling in serum creatinine or ESRD, and (3) mortality using potential risk factors at baseline and during follow-up. Results The mean (SD) rate of decline in GFR was 5.2 (4.1) mL/min/year. In multivariate regression analysis, higher baseline albuminuria, systolic blood pressure (SBP), hemoglobin A1c, GFR, age, and degree of diabetic retinopathy were significantly associated with increased rate of decline in GFR ( R 2 adj 0.24). During follow-up, elevated mean albuminuria, SBP, hemoglobin A1c, and lower hemoglobin, heavy smoking, and presence of diabetic retinopathy were significantly associated with increased decline in GFR ( R 2 adj 0.26). During follow-up, 63 patients had a doubling in serum creatinine or developed ESRD, and 79 patients died, primarily due to cardiovascular disease. In Cox regression analysis, higher baseline albuminuria, hemoglobin A1c, and SBP, together with lower GFR and hemoglobin, were significantly associated with shorter time to doubling of serum creatinine or ESRD. Higher baseline albuminuria, hemoglobin A1c, SBP, and age were significantly associated with increased mortality. Conclusion Our long-term prospective study of type 2 diabetic patients with nephropathy has revealed several modifiable risk factors of enhanced progression in kidney disease and increased mortality.
Published: 2004

273. Low Birth Weight: A Risk Factor for Development of Diabetic Nephropathy?

Author: Barry M. Brenner, Flemming S Nielsen, Hans-Henrik Parving, Peter Rossing, Birgitte V. Hansen, and Lise Tarnow
Subjects: Adult, Male, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Birth weight, Nephropathy, Diabetic nephropathy, Risk Factors, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Albuminuria, Birth Weight, Humans, Diabetic Nephropathies, Risk factor, Proteinuria, business.industry, Middle Aged, medicine.disease, Body Height, Low birth weight, Diabetes Mellitus, Type 1, Endocrinology, Case-Control Studies, Female, medicine.symptom, business
Abstract: It has been demonstrated that intrauterine growth retardation, defined as birth weight below the 10th percentile, gives rise to a reduction in nephron number. Oligonephropathy has been suggested to increase the risk for systemic and glomerular hypertension in adult life as well as enhance risk for expression of renal disease after exposure to potentially injurious renal stimuli. The aimof this study was to determine if low birth weight is a risk factor for development of diabetic nephropathy. In a case-control study, we investigated 184 (110 men) insulin-dependent diabetes mellitus (IDDM) patients with diabetic nephropathy (persistent albuminuria >300 mg/24 h)(age [mean ± SD] 41.0 ± 9.3 years, duration of diabetes 26.9 ± 8.2 years) and 182 (111 men) normoalbuminuric (
Published: 1995
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274. Decreasing incidence of severe diabetic microangiopathy in type 1 diabetes

Author: Lise Tarnow, Nicolai Larsen, Peter Hovind, Stefanie Eising, Kasper Rossing, Christian Binder, Hans-Henrik Parving, and Peter Rossing
Subjects: Male, medicine.medical_specialty, Time Factors, Endocrinology, Diabetes and Metabolism, Denmark, Diabetic angiopathy, Gastroenterology, White People, Diabetic nephropathy, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Humans, Cumulative incidence, Aged, Advanced and Specialized Nursing, Type 1 diabetes, Diabetic Retinopathy, business.industry, Incidence (epidemiology), Incidence, Microangiopathy, Diabetic retinopathy, Middle Aged, medicine.disease, Surgery, Diabetes Mellitus, Type 1, Female, business, Diabetic Angiopathies, Follow-Up Studies
Abstract: OBJECTIVE—Conflicting evidence of a decline in incidence of microvascular complications in type 1 diabetes during the last decades has been reported. To assess recent trends in the cumulative incidence of diabetic microangiopathy in type 1 diabetes, we analyzed data from long-term prospective observational studies lasting ≥20 years. RESEARCH DESIGN AND METHODS—A total of 600 Caucasian patients with onset of type 1 diabetes between 1965 and 1984 were followed until death or until the year 2000. Patients were divided into four groups based on the year of diabetes onset: group A, 1965–1969 (n = 113); group B, 1970–1974 (n = 130); group C, 1975–1979 (n = 113); and group D, 1979–1984 (n = 244). Group A, B, and C are prevalence cohorts identified in 1984; group D is an inception cohort. RESULTS—In patients followed for ≥20 years, the cumulative incidence (95% CI) of diabetic nephropathy after 20 years of diabetes (urinary albumin excretion >300 mg/24 h) was reduced in patients with more recent diabetes onset (groups A–D): 31.1% (22.5–39.7) vs. 28.4% (19.8–37.0) vs. 18.9% (10.9–26.9) vs. 13.7% (6.2–21.2) (P = 0.015). Similarly, the cumulative incidence of proliferative retinopathy was as follows: 31.2% (22.2–39.8) vs. 30.3% (22.2–38.4) vs. 19.3% (11.2–27.4) vs. 12.5% (5.2–19.8) (P < 0.01). In the latter groups, antihypertensive treatment was started earlier, blood pressure and HbA1c were lower, and fewer patients smoked. CONCLUSIONS—Our study demonstrates a decrease in the cumulative incidence of diabetic microangiopathy in type 1 diabetes over the past 35 years. Improved glycemic control, lower blood pressure (in part due to early aggressive antihypertensive treatment), and reduced prevalence of smoking rates were associated with the improved prognosis.
Published: 2003

275. Birth weight--a risk factor for progression in diabetic nephropathy?

Author: Hans-Henrik Parving, Peter Hovind, Lise Tarnow, Peter Karl Jacobsen, and Peter Rossing
Subjects: Adult, Male, medicine.medical_specialty, Birth weight, Renal function, Kidney Function Tests, Nephropathy, Diabetic nephropathy, Risk Factors, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Humans, Diabetic Nephropathies, Risk factor, Fetal Growth Retardation, business.industry, Infant, Newborn, Infant, Low Birth Weight, medicine.disease, Body Height, Low birth weight, Endocrinology, Diabetes Mellitus, Type 1, Disease Progression, Regression Analysis, Female, medicine.symptom, business, Kidney disease, Follow-Up Studies, Glomerular Filtration Rate
Abstract: Jacobsen P, Rossing P, Tarnow L, Hovind P, Parving H-H (Steno Diabetes Center, Gentofte, Denmark). Birth weight – a risk factor for progression in diabetic nephropathy? J Intern Med 2003; 253: 343–350. Objectives. Intrauterine growth retardation, as seen in individuals with low weight at birth, may give rise to a reduction in nephron number. Oligonephropathy has been linked to hypertension and renal disease in adult life. We tested the concept that low weight at birth acts as a risk factor for progression of diabetic nephropathy. Design and subjects. We performed an observational follow-up study of 161 (97 men) type 1 diabetic patients with diabetic nephropathy [mean age (SD): 35 (11) years, mean duration of diabetes: 22 (8) years]. All patients had been followed for at least 3 years [median (range): 8 (3–20)] with at least three measurements [9 (3–31)] of glomerular filtration rate (GFR) (51Cr-EDTA). Information about birth size was obtained from midwife registrations. Settings. Steno Diabetes Center, a tertiary referral centre. Main outcome measures. Loss of kidney function according to birth weight and weight/length ratio at birth. Results. There was no correlation in univariate analysis between birth weight or weight/length ratio and rate of decline in GFR, neither in men nor in women. Furthermore, the 27 patients with birth weights below the 20th centile had a rate of decline in GFR [median (range)] similar to the 134 patients above: 2.6 (−4.7; 9.6) vs. 3.4 (−2.3; 19.3) mL min−1 year−1, respectively (NS). A multiple regression analysis revealed that albuminuria, arterial blood pressure, and haemoglobin A1C during follow-up showed a significant correlation with the decline in GFR [R2 (adjusted) = 0.34], whereas birth weight and birth weight/length ratio did not. Conclusions. Our study does not suggest that weight at birth is associated with progression of established diabetic nephropathy in type 1 diabetic patients, whilst several other potential modifiable risk factors were identified.
Published: 2003

276. Renoprotective effects of losartan in diabetic nephropathy: interaction with ACE insertion/deletion genotype?

Author: Lise Tarnow, Tina R. Juhl, Hans-Henrik Parving, Peter Rossing, Jaap Deinum, Steen Andersen, Francois Cambien, and Internal Medicine
Subjects: Adult, Male, medicine.medical_specialty, Hypertension and Circulation, hypertension, Genotype, type 1 diabetes, Renal function, Angiotensin II receptor antagonist, Blood Pressure, Peptidyl-Dipeptidase A, Kidney, albuminuria, Losartan, Nephropathy, polymorphism, renoprotection, Diabetic nephropathy, Angiotensin Receptor Antagonists, Hypertensie en circulatie, SDG 3 - Good Health and Well-being, Double-Blind Method, Internal medicine, Diabetes mellitus, medicine, Humans, Diabetic Nephropathies, Prospective Studies, Antihypertensive Agents, Glycated Hemoglobin, business.industry, Sodium, Middle Aged, medicine.disease, Angiotensin II, Endocrinology, angiotensin II receptor antagonism, Nephrology, Albuminuria, Female, medicine.symptom, business, medicine.drug
Abstract: Renoprotective effects of losartan in diabetic nephropathy: Interaction with ACE insertion/deletion genotype?BackgroundThe beneficial short- and long-term renoprotective effects of angiotensin I-converting enzyme (ACE) inhibition are lower in albuminuric diabetic patients homozygous for the deletion compared to the insertion polymorphism of the ACE gene. In an attempt to overcome this interaction, we evaluated the short-term renoprotective effect in diabetic nephropathy of the angiotensin II receptor antagonist losartan in patients homozygous for the insertion or the deletion allele.MethodsFifty-four hypertensive type 1 diabetic patients with diabetic nephropathy homozygous for the insertion (I; N = 26) or the deletion (D; N = 28) allele of the ACE/ID polymorphism were included. After four weeks of washout, the patients received losartan 50 mg daily followed by 100 mg in two treatment periods each lasting two months. Patients and investigators were blinded to ACE genotypes. At baseline and in the end of the treatment periods, 24-hour blood pressure, albuminuria and glomerular filtration rate values were determined.ResultsAt baseline, blood pressure, albuminuria and glomerular filtration rate (GFR) values were similar in the two genotype groups [II vs. DD, 1134 (238 to 5302) vs. 1451 (227 to 8129) mg/24 h, median (range); 156/82 (17/9) vs. 153/80 (17/11) mm Hg, mean (SD); and 86 (22) vs. 88 (24) mL/min/1.73 m2, respectively]. Both doses of losartan significantly lowered blood pressure, albuminuria, and GFR (P < 0.05 vs. baseline). Losartan 100 mg was more effective than 50 mg in reducing albuminuria, 51% (95% CI; 40 to 61) versus 33% (23 to 42), respectively (P < 0.01). No differences in the impact of losartan between the II and DD groups were observed: Losartan 100 mg lowered systolic/diastolic blood pressure by 12/6 and 10/4 mm Hg, whereas albuminuria decreased by 55% (35 to 68) and 46% (28 to 61), in the II and DD groups, respectively (P = NS).ConclusionOur data suggest that losartan offers similar short-term renoprotective and blood pressure lowering effects in albuminuric hypertensive type 1 diabetic patients with the ACE II and DD genotypes. However, the long-term renoprotective effects remain to be evaluated.
Published: 2002

277. Diabetic nephropathy. Pathogenetic aspects and cardiovascular risk factors

Author: Lise, Tarnow
Subjects: Diabetes Mellitus, Type 1, Cardiovascular Diseases, Risk Factors, Humans, Diabetic Nephropathies
Published: 2002

278. Role of Plasma Homocysteine and Plasminogen Activator Inhibitor-1 in the Progression of Diabetic Nephropathy

Author: Jef J. Emeis, Coen D.A. Stehouwer, Peter Rossing, Peter Hovind, Lise Tarnow, and Hans-Henrik Parving
Subjects: medicine.medical_specialty, business.industry, Urology, Renal function, medicine.disease, End stage renal disease, Nephropathy, Diabetic nephropathy, chemistry.chemical_compound, Endocrinology, chemistry, Internal medicine, Diabetes mellitus, Plasminogen activator inhibitor-1, Medicine, business, Plasminogen activator, Cohort study
Abstract: Diabetic nephropathy is a progressive disease and a leading cause of end stage renal disease. However, the decline in glomerular filtration rate (GFR) varies substantially between patients, ranging from 2 to 20 ml/min/year. Thus, identification of predictors of progression in diabetic nephropathy is of importance. Plasma total homocysteine (tHcy) rises with urinary albumin rate in diabetes, and plasminogen activator inhibitor-1 (PAI-1) has been correlated to increased matrix accumulation in various glomerulopathies. The aim of the present prospective observational cohort study was to evaluate the importance of baseline tHcy and PAI-1 as predictors of the rate of decline in GFR. At baseline tHcy and PAI-1 were measured in 157 type 1 diabetic patients with diabetic nephropathy (92 males, age 41 ± 10 years, diabetes duration 28 ± 8 years, GFR (median (range)) 80 (23–143) ml/min/1.73 m2). Hereafter, GFR was measured yearly with a plasma clearance technique for at least 3 years, median 7 (range 3.0 to 8.3) years. The mean rate of decline in GFR was 3.7 (0.3) ml/min/year. A linear regression analysis revealed a borderline significant relation between rate of decline in GFR and tHcy (p=0.069) and PAI-1 (p=0.087), respectively. Analyzing rate of decline in GFR and ter-tiles of tHcy and PAI-1, increasing levels of tHcy was correlated with a faster decline in GFR, p=0.025, whereas PAI-1 was not. However, after adjustment for other risk factors for progression of nephropathy, i.e. progression promoters, in a multiple linear regression analysis, neither tHcy nor PAI-1 was independent predictors of rate of decline in GFR. Our study demonstrates a relation between plasma tHcy and the rate of decline in GFR. Plasma tHcy and PAI-1 were, however, not found to be independent predictors of progression in diabetic nephropathy after adjustment for other well established progression promoters.
Published: 2002
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279. Preventing diabetic nephropathy: an audit

Author: Søren S Lund, Henrik Post Hansen, Flemming S Nielsen, Lise Tarnow, H.-H. Parving, Tonny Jensen, and Peter Rossing
Subjects: Blood Glucose, medicine.medical_specialty, endocrine system diseases, Clinical Biochemistry, Urology, Angiotensin-Converting Enzyme Inhibitors, Blood Pressure, Enzyme-Linked Immunosorbent Assay, urologic and male genital diseases, Nephropathy, Diabetic nephropathy, Internal medicine, medicine, Albuminuria, Humans, Diabetic Nephropathies, Type 1 diabetes, Medical Audit, biology, business.industry, Angiotensin-converting enzyme, General Medicine, medicine.disease, Endocrinology, Diabetes Mellitus, Type 1, ACE inhibitor, biology.protein, Microalbuminuria, medicine.symptom, business, medicine.drug, Kidney disease
Abstract: In type 1 diabetic patients with microalbuminuria not receiving antihypertensive treatment, an increase in urinary albumin excretion rate (AER) of 6% to 14%/year and a risk for the development of diabetic nephropathy of 3% to 30%/year have previously been reported. The aim of the present study was to audit the effect of angiotensin converting enzyme (ACE) inhibition on the progression of microalbuminuria and development of diabetic nephropathy. We consecutively identified 227 type 1 diabetic patients with persistent microalbuminuria (urinary AER between 30 and 300mg/24h, ELISA). According to the level (or = 100 or100mg/24 h) and/or rate of progression in urinary AER (6% oror =6%/year), patients were divided into a high-risk group (n= 177) and a low-risk group (n= 50) for development of diabetic nephropathy. According to international guidelines, all patients at high-risk were recommended ACE-inhibitor treatment. Throughout the study, 67% of the patients were treated with an ACE inhibitor. Urinary AER significantly declined by 8.3%/year (95% CI: 2.8 to 13.9) in the whole group of patients, and the risk for the development of diabetic nephropathy during follow-up was 3.5%/year. Glycaemic control and blood pressure remained unchanged during the study. The implementation of modified international guidelines regarding the use of ACE inhibition in the treatment of microalbuminuric type 1 diabetic patients reduced progression to diabetic nephropathy comparable to what has previously been reported in intervention trials.
Published: 2001

280. Remission of nephrotic-range albuminuria in type 1 diabetic patients

Author: Jeppe Parving, Peter Rossing, Hans-Henrik Parving, Lise Tarnow, Henrik Toft, and Peter Hovind
Subjects: Adult, Male, medicine.medical_specialty, Time Factors, Endocrinology, Diabetes and Metabolism, Remission, Spontaneous, Urology, Renal function, Blood Pressure, Kidney Function Tests, Nephropathy, Diabetic nephropathy, Diabetes mellitus, Internal Medicine, medicine, Albuminuria, Humans, Cumulative incidence, Diabetic Nephropathies, Prospective cohort study, Advanced and Specialized Nursing, Sex Characteristics, business.industry, medicine.disease, Surgery, Proteinuria, Cholesterol, Diabetes Mellitus, Type 1, Nephrosis, Female, medicine.symptom, business, Kidney disease, Follow-Up Studies, Glomerular Filtration Rate
Abstract: OBJECTIVE—To evaluate the cumulative incidence of nephrotic-range albuminuria (NRA), the frequency of remission, and the impact on progression, we analyzed data from a prospective cohort study of type 1 diabetic patients with diabetic nephropathy. RESEARCH DESIGN AND METHODS—All of the albuminuric type 1 diabetic patients (n = 321, 121 women), who had at least yearly measurements of glomerular filtration rate (GFR) with a 51Cr-EDTA plasma clearance technique and were followed for at least 3 years, were evaluated. NRA, defined as persistent albuminuria >2,500 mg/24 h, occurred in 126 patients (35 women) aged (mean ± SD) 34 ± 8 years, with duration of diabetes 22 ± 8 years and follow-up time from onset of NRA (median [range]) 8.7 (3.0–20.9) years. Remission of NRA was defined as sustained albuminuria RESULTS—The cumulative incidence of NRA was 39%. Remission was induced in 28 of 126 (22%) patients; 21 were predominantly treated with ACE inhibitors, 7 with non–ACE inhibitor medications. Remission lasted 3.6 (1.0–18.1) years. More women (37%) than men (16%) obtained remission (P = 0.01). In the remission group compared with the no-remission group, mean arterial blood pressure (mean ± SEM) was reduced (102 ± 1 vs. 106 ± 1 mmHg, P < 0.01), the rate of decline in GFR was diminished (3.8 ± 0.6 vs. 7.5 ± 0.5 ml · min–1 · year–1, P < 0.001), and serum cholesterol was lower (5.3 ± 0.2 vs. 6.1 ± 0.1 mmol/l, P < 0.01) during the whole follow-up period. No difference in glycemic control was found between groups (HbA1c 9.2 vs. 9.4%, NS). CONCLUSIONS—In contrast to observations made before the use of antihypertensive treatment, our prospective observational study suggests that aggressive antihypertensive treatment with and without ACE inhibitors can induce long-lasting remission in a sizeable fraction of type 1 diabetic patients with NRA. The group of patients obtaining remission is characterized by slow progression of diabetic nephropathy and improved cardiovascular risk profile.
Published: 2001

281. Progression of diabetic nephropathy

Author: Peter Hovind, Peter Rossing, Lise Tarnow, Ulla M Smidt, and Hans-Henrik Parving
Subjects: Adult, Male, medicine.medical_specialty, renal failure, Urology, Renal function, Blood Pressure, Nephropathy, antihypertensive treatment, Diabetic nephropathy, Internal medicine, Diabetes mellitus, medicine, Albuminuria, Humans, Diabetic Nephropathies, Edetic Acid, Glycated Hemoglobin, Proteinuria, business.industry, diabetic nephropathy, blood pressure control, Middle Aged, medicine.disease, Endocrinology, Blood pressure, Cholesterol, Nephrology, glycemic control, Disease Progression, Female, medicine.symptom, proteinuria, business, type 1 diabetes mellitus, Kidney disease, Glomerular Filtration Rate
Abstract: Progression of diabetic nephropathy.BackgroundDiabetic nephropathy is a major cause of renal failure. The decline in glomerular filtration rate (GFR) is highly variable, ranging from 2 to 20, with a median of 12 mL/min/year. The risk factors of losing filtration power (progression promoters) have not been clearly identified. Furthermore, information on optimal arterial blood pressure, glycemic control, and cholesterol levels are lacking.MethodsWe measured GFR with 51Cr-EDTA plasma clearance technique, blood pressure, albuminuria, glycosylated hemoglobin A1c, and serum cholesterol every year for seven years (range 3 to 14 years) in 301 consecutive type 1 diabetic patients with diabetic nephropathy recruited consecutively during 1983 through 1997. Diabetic nephropathy was diagnosed clinically if the following criteria were fulfilled: persistent albuminuria> 200 μg/min, presence of diabetic retinopathy, and no evidence of other kidney or renal tract disease. In total, 271 patients received antihypertensive treatment at the end of the observation period.ResultsMean arterial blood pressure was 102 ± 0.4 (SE)mm Hg. The average decline in GFR was 4.0 ± 0.2 mL/min/year and even lower (1.9 ± 0.5 mL/min/year) in the 30 persistently normotensive patients, none of whom had ever received antihypertensive treatment (P < 0.01). A multiple linear regression analysis revealed a significant positive correlation between the decline in GFR and mean arterial blood pressure, albuminuria, glycosylated hemoglobin A1c, and serum cholesterol during follow-up = 0.29, P ≤ 0.001). No threshold level for blood pressure, glycosylated hemoglobin A1c, or serum cholesterol was demonstrated. A two-hit model with mean arterial blood pressure and glycosylated hemoglobin A1c below and above the median values (102mm Hg and 9.2%, respectively) revealed a rate of decline in GFR of only 1.5 mL/min/year in the lowest stratum compared with 6.1 mL/min/year in the highest stratum (P < 0.001).ConclusionsThe prognosis of diabetic nephropathy has improved during the past decades, predominantly because of effective antihypertensive treatment. Genuine normotensive patients have a slow progression of nephropathy. Several modifiable variables have been identified as progression promoters.
Published: 2001

282. An Orally Administered Ghrelin Agonist (TZP-102) Decreases the Overall Severity of Symptoms of Diabetic Gastroparesis (GP): Phase 2 Proof of Concept Study - Preliminary Results

Author: Tuba Esfandyari, Gordana Kosutic, Rayaz A. Malik, Niels Ejskjaer, M. Mazen Jamal, Per M. Hellström, John M. Wo, Laura Shaughnessy, Lise Tarnow, Philippa A. Charlton, Georg Dimcevski, Richard W. McCallum, and Robert P. Venuti
Subjects: Agonist, medicine.medical_specialty, Endocrinology, Hepatology, medicine.drug_class, business.industry, Diabetic gastroparesis, Internal medicine, Gastroenterology, medicine, Ghrelin, business
Abstract: An Orally Administered Ghrelin Agonist (TZP-102) Decreases the Overall Severity of Symptoms of Diabetic Gastroparesis (GP) : Phase 2 Proof of Concept Study - Preliminary Results
Published: 2010
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283. SERUM PLACENTAL GROWTH FACTOR (PLGF) PREDICTS ALL-CAUSE AND CARDIOVASCULAR MORTALITY BUT NOT DETERIORATION OF KIDNEY FUNCTION IN TYPE 1 DIABETIC PATIENTS WITH DIABETIC NEPHROPATHY: PP.6.254

Author: Simone Theilade, Lise Tarnow, A. Jorsal, Hans-Henrik Parving, Maria Lajer, and Peter Rossing
Subjects: Placental growth factor, medicine.medical_specialty, Physiology, business.industry, Renal function, medicine.disease, Diabetic nephropathy, Endocrinology, Internal medicine, Internal Medicine, medicine, Cardiology and Cardiovascular Medicine, business, All cause mortality, Cardiovascular mortality
Published: 2010
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284. Genetic polymorphisms of the renin-angiotensin system and complications of insulin-dependent diabetes mellitus

Author: Ab J.M. Donker, Eline Slagboom, Henk J. G. Bilo, Peter de Knijff, Yvo M. Smulders, Frans J. van Ittersum, Coen D.A. Stehouwer, Lise Tarnow, Angelique M. E. de Man, and Sandra Thijssen
Subjects: Adult, medicine.medical_specialty, Angiotensinogen, Coronary Disease, Diabetic angiopathy, Peptidyl-Dipeptidase A, Receptor, Angiotensin, Type 2, Receptor, Angiotensin, Type 1, Diabetic nephropathy, Renin-Angiotensin System, Diabetes mellitus, Internal medicine, medicine, Albuminuria, Humans, Diabetic Nephropathies, Aged, Transplantation, Diabetic Retinopathy, Polymorphism, Genetic, Receptors, Angiotensin, business.industry, Odds ratio, Diabetic retinopathy, Middle Aged, medicine.disease, Angiotensin II, Endocrinology, Diabetes Mellitus, Type 1, Nephrology, Hypertension, DNA Transposable Elements, Gene polymorphism, business, Diabetic Angiopathies, Gene Deletion, Retinopathy
Abstract: OBJECTIVE: Patients with insulin-dependent diabetes mellitus (IDDM) have a high risk of developing diabetic nephropathy, retinopathy and cardiovascular diseases. The contribution of gene polymorphisms of the renin angiotensin system to these complications is controversial and may differ among populations. METHODS: In 257 Dutch IDDM patients (188 with urinary albumin excretion (UAE)
Published: 2000

285. Renoprotective effects of angiotensin II receptor blockade in type 1 diabetic patients with diabetic nephropathy

Author: Steen Andersen, Birgitte V. Hansen, Hans-Henrik Parving, Lise Tarnow, and Peter Rossing
Subjects: Adult, Male, medicine.medical_specialty, Angiotensin receptor, hypertension, Hypertension, Renal, Bradykinin, Angiotensin-Converting Enzyme Inhibitors, Receptor, Angiotensin, Type 2, Losartan, Receptor, Angiotensin, Type 1, Renin-Angiotensin System, chemistry.chemical_compound, Angiotensin Receptor Antagonists, Double-Blind Method, Enalapril, Internal medicine, medicine, Humans, IDDM, Diabetic Nephropathies, Antihypertensive Agents, Angiotensin II receptor type 1, Cross-Over Studies, biology, business.industry, Angiotensin-converting enzyme, Angiotensin II, Proteinuria, Endocrinology, Diabetes Mellitus, Type 1, chemistry, Nephrology, ACE inhibitor, biology.protein, Female, business, medicine.drug, Glomerular Filtration Rate
Abstract: Renoprotective effects of angiotensin II receptor blockade in Diabetic nephropathy is a serious long-term complica- type 1 diabetic patients with diabetic nephropathy. tion in type 1 diabetes mellitus. Diabetic nephropathy, Background. Angiotensin I-converting enzyme (ACE) in- characterized by persistent albuminuria, a relentless de- hibitors reduce angiotensin II formation and induce bradykinin cline in glomerular filtration rate (GFR), and raised arte- accumulation. Animal studies suggest that bradykinin may play rial blood pressure, develops in 30 to 40% of all type 1 a role for the effects of ACE inhibition on blood pressure diabetic patients (1). Previous studies have documented and kidney function. Therefore, we compared the renal and hemodynamic effects of specific intervention in the renin- that inhibition of the renin-angiotensin system by angio- angiotensin system by blockade of the angiotensin II subtype-1 tensin I-converting enzyme (ACE) inhibitors consis- receptor to the effect of ACE inhibition. tently reduces albuminuria and retards renal injury (2, 3). Methods. A randomized, double-blind, cross-over trial was However, the principal mechanism of action of these performed in 16 type 1 diabetic patients (10 men), age 42 6 renal effects is not completely understood. ACE is not 2 years (mean 6 sem). The study consisted of five periods, each lasting two months. The patients received losartan 50 mg, a very specific enzyme and has other substrates such as losartan 100 mg, enalapril 10 mg, enalapril 20 mg, and placebo bradykinin. Therefore, ACE inhibitors not only decrease in random order. At the end of each period, albuminuria, 24- the production of angiotensin II, but also cause accumu- hour blood pressure, and glomerular filtration rate (GFR) were lation of bradykinin. Bradykinin is a potent vasodilator determined. acting through the release of prostacyclin, nitric oxide, Results. Both doses of losartan and enalapril reduced albu- and endothelial-derived factors (4). Recent animal and minuria (P , 0.05) and mean arterial blood pressure (MABP; P , 0.05), whereas GFR remained stable. Albuminuria was human studies have suggested that bradykinin may play reduced by 33% (95% CI, 12 to 51) on losartan 50 mg, 44% a role in the effects of ACE inhibition on blood pressure (95% CI, 26 to 57) on losartan 100 mg, 45% (95% CI, 23 to 61) and kidney function (5, 6). Furthermore, angiotensin II on enalapril 10 mg, and 59% (95% CI, 39 to 72) on enalapril is not only generated by the ACE pathway, but also 20 mg, and MABP fell by 9 6 2, 8 6 2, 6 6 3, and 11 6 3 through alternative pathways such as the chymase path- mm Hg (mean 6 sem), respectively. No significant differences way (7). These alternative pathways are not affected by were found between the effects of losartan 100 mg and enalapril 20 mg. HbA1C and sodium intake remained unchanged through- ACE inhibition. Therefore, ACE inhibitors will not com- out the study, whereas a significant rise in serum potassium pletely block the formation of angiotensin II. Specific occurred during ACE inhibition. intervention in the renin-angiotensin system by angio- Conclusion. The angiotensin II subtype 1 receptor antago- tensin II receptor blockade has no effect on bradykinin nist, losartan, reduces albuminuria and MABP similar to the metabolism, but antagonizes angiotensin II generated by effect of ACE inhibition. These results indicate that the reduc- tion in albuminuria and blood pressure during ACE inhibition any pathway. This may result in a more effective block- is primarily caused by interference in the renin-angiotensin ade of the renin-angiotensin system, but eliminates the system. Our study suggest that losartan represents a valuable possibility of a positive contribution to the renal and new drug in the treatment of hypertension and proteinuria in hemodynamic effects from bradykinin accumulation. It type 1 diabetic patients with diabetic nephropathy. has previously been shown that the angiotensin II recep- tor antagonist losartan induces changes in blood pressure and proteinuria similar to the changes induced by ACE
Published: 2000

286. The Trp64Arg amino acid polymorphism of the beta3-adrenergic receptor gene does not contribute to the genetic susceptibility of diabetic microvascular complications in Caucasian type 1 diabetic patients

Author: Lise Tarnow, Bente Mottlau, Oluf Pedersen, Birgitte V. Hansen, Hans-Henrik Parving, and Søren A. Urhammer
Subjects: Adult, Male, medicine.medical_specialty, Gene mutation, White People, Nephropathy, Diabetic nephropathy, Internal medicine, Diabetes mellitus, Receptors, Adrenergic, beta, Medicine, Humans, Genetic Predisposition to Disease, Transplantation, Polymorphism, Genetic, business.industry, Microcirculation, Diabetic retinopathy, Middle Aged, medicine.disease, Endocrinology, Diabetes Mellitus, Type 1, Nephrology, Albuminuria, Female, medicine.symptom, business, Diabetic Angiopathies, Kidney disease, Retinopathy
Abstract: Objective. The b 3 -adrenergic receptor is involved in regulation of microvascular blood flow. A missense Introduction mutation ( Trp64Arg) in the b 3 -adrenergic receptor gene has been suggested as a risk factor for proliferative Stimulation of the b 3 -adrenergic receptor increases retinopathy in Japanese type 2 diabetic patients. The cutaneous [1] and pancreatic islet [2] blood flow. aim of the present study was to evaluate the contribu- Impaired receptor function, i.e. due to gene mutation, tion of this polymorphism to the development of might lead to altered blood flow in the microvascumicroangiopathic complications in Caucasian type 1 lar beds of the kidney and eye. Therefore, the b 3 diabetic patients. adrenergic receptor gene can be considered a candidate Subjects and methods. We studied the relationship gene for the development of diabetic microangiopathic between the Trp64Arg polymorphism in type 1 diabetic complications. Recently a missense mutation patients with nephropathy (204 men/132 women, age ( Trp64Arg) of the b 3 -adrenergic receptor gene was 42.8±11.0 years, diabetes duration 28±9 years) and identified [3] and several, but not all, subsequent in type 1 diabetic patients with persistent normoalbum- studies have reported associations of this genetic inuria (118 men/73 women, age 42.6±10.2 years, variant with obesity and insulin resistance in diVerent diabetes duration 27±8 years). Proliferative retinopa- ethnic populations [4‐9]. Interestingly, a recent study thy was present in 254 patients (48%), while 66 patients in Japanese type 2 diabetic patients [10] demonstrated (13%) had no diabetic retinopathy. an association between the Trp64Arg substitution and Results. There were no diVerences in Trp64Arg geno- proliferative retinopathy. type distribution between type 1 diabetic patients with The aim of the present study was to evaluate the diabetic nephropathy and type 1 diabetic patients with contribution of the Trp64Arg polymorphism to the normoalbuminuria: 295 (88%)/38 (11%)/3 (1%) vs 161 development of microangiopathic complications in (84%)/30 (16%)/‐ had Trp/Trp, Trp/Arg or Arg/Arg Caucasian type 1 diabetic patients. genotype respectively. Odds ratio (95% CI ) of nephropathy in carriers of the mutation was 0.75 (0.45‐1.25). No associations between the Trp64Arg polymorphism Subjects and methods and simplex or proliferative retinopathy were revealed either. The frequency of the Arg‐allele was 0.069 in We studied the genotype distribution of the Trp64Arg patients with proliferative retinopathy, 0.066 in polymorphism in 336 type 1 diabetic patients with diabetic patients with simplex retinopathy and 0.090 in patients nephropathy, diagnosed clinically based on the following with no signs of diabetic retinopathy, NS. criteria: persistent albuminuria greater than 300 mg/24 h in at least two of three consecutive 24-h urine collections, presence of retinopathy and no clinical or laboratory evidence
Published: 1999

287. Effects of nisoldipine and lisinopril on left ventricular mass and function in diabetic nephropathy

Author: Peter Rossing, Lise Tarnow, Flemming S Nielsen, A. Sato, S. Ali, and Hans-Henrik Parving
Subjects: Adult, Male, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Diastole, Nisoldipine, Angiotensin-Converting Enzyme Inhibitors, Blood Pressure, Left ventricular hypertrophy, Ventricular Function, Left, Diabetic nephropathy, Double-Blind Method, Lisinopril, Diabetes mellitus, Internal medicine, Internal Medicine, medicine, Humans, Diabetic Nephropathies, Advanced and Specialized Nursing, business.industry, Blood Pressure Monitoring, Ambulatory, Middle Aged, medicine.disease, Calcium Channel Blockers, Blood pressure, Endocrinology, Diabetes Mellitus, Type 1, Echocardiography, ACE inhibitor, Cardiology, Female, business, medicine.drug
Abstract: OBJECTIVE: To compare the effects of the calcium channel blocker, nisoldipine, and the ACE inhibitor, lisinopril, on left ventricular mass (LVM) and systolic function in type 1 diabetic patients with diabetic nephropathy. RESEARCH DESIGN AND METHODS: M-mode echocardiography was performed in 50 hypertensive type 1 diabetic patients with diabetic nephropathy enrolled in a 1-year, randomized, double-blind, parallel study of antihypertensive treatment with nisoldipine CC (20-40 mg/day) or lisinopril (10-20 mg/day). Ambulatory 24-h blood pressure was measured with the Takeda TM 2420 device (A & D, Tokyo, Japan) every 3 months. Three patients dropped out and seven patients were excluded due to technical difficulties. RESULTS: The 24-h diastolic blood pressure was reduced from 83 to 80 mmHg in the nisoldipine group (P = 0.06) and from 85 to 80 mmHg in the lisinopril group (P = 0.02). The decline in systolic blood pressure was not significant with any of the two treatments, and no difference in reduction of blood pressure was seen between groups. LVM corrected for body surface area (LVMI) was comparable between groups at baseline and increased from 96 +/- 5 to 107 +/- 6 g/m2 (mean +/- SEM; P = 0.007) in the nisoldipine group and from 95 +/- 4 to 103 +/- 5 g/m2 (P = 0.03) in the lisinopril group. The mean difference between the change in LVMI in the two groups was 2.9 (95% CI 6.8 to 12.7) g/m2. The prevalence of left ventricular hypertrophy rose from 18 (95% CI 6-30) to 30% (16-44) during the study period. A multiple linear regression analysis revealed that after 1 year of treatment, LVMI increased with higher systolic blood pressure level and declining glomerular filtration rate (R2 = 0.25). Fractional shortening was within normal range at baseline, 42 +/- 1 vs. 41 +/- 1% with nisoldipine and lisinopril, respectively, and did not change during follow-up. CONCLUSIONS: Antihypertensive treatment with nisoldipine or lisinopril to bring diastolic blood pressure level within the normal target range does not hinder a rise in LVMI in type 1 diabetic patients with diabetic nephropathy.
Published: 1999

288. Prevalence of left ventricular hypertrophy in Type I diabetic patients with diabetic nephropathy

Author: Hans-Henrik Parving, A. Sato, and Lise Tarnow
Subjects: Adult, Male, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Denmark, Diastole, Left ventricular hypertrophy, Sudden death, Ventricular Function, Left, Nephropathy, Diabetic nephropathy, chemistry.chemical_compound, Internal medicine, Diabetes mellitus, Internal Medicine, Prevalence, Medicine, Albuminuria, Humans, Diabetic Nephropathies, Creatinine, business.industry, Middle Aged, medicine.disease, Lipids, Echocardiography, Doppler, Diabetes Mellitus, Type 1, chemistry, Cardiology, Female, Hypertrophy, Left Ventricular, business, Isovolumic relaxation time
Abstract: The increased mortality of patients with diabetic nephropathy is mainly due to cardiovascular disease and end stage renal failure. Left ventricular hypertrophy is an independent risk factor for myocardial ischaemia and sudden death. The aim of our cross-sectional study was to evaluate left ventricular structure and function in Type I (insulin-dependent) diabetic patients with diabetic nephropathy. M-mode and Doppler echocardiography were done on 105 Type I diabetic patients with diabetic nephropathy [61 men, age (means ± SD) 44 ± 9 years, and albuminuria [median(range)] 567(10–8188) mg/24 h, serum creatinine 109 (53–558) μmol/l], and 140 Type I diabetic patients with persistent normoalbuminuria [79 men, 47 ± 10 years, urinary albumin excretion rate 8 (0–30) mg/24 h, and serum creatinine 81 (55–121) μmol/l]. Patients with and without nephropathy were comparable with respect to sex, body mass index, and duration of diabetes. Arterial blood pressure was slightly higher in patients with nephropathy: 140/79 ± 17/9 mm Hg vs 134/78 ± 15/8 mm Hg, p < 0.01, and the majority of proteinuric patients received antihypertensive drugs, 84 vs 17 %, respectively, p < 0.001. Left ventricular mass index was increased in the nephropathic group (means ± SD) 100.6 ± 23.9 g/m2 compared with the normoalbuminuric group 91.4 ± 21.9 g/m2, p = 0.002. Left ventricular hypertrophy was found more often in patients with nephropathy 23 (14–31)% compared with patients with normoalbuminuria 9 (5–14)%, p < 0.005. Diastolic function, assessed by the ratio between the peak diastolic velocity and the peak atrial systolic velocity (E/A ratio) and isovolumic relaxation time, was reduced in patients with vs without nephropathy: 1.17 ± 0.29 vs 1.34 ± 0.32, and 81.7 ± 16.5 vs 74.6 ± 14.5, p < 0.001 and p = 0.002, respectively. Systolic function was about the same and normal in both groups. Our study suggests that an increase in left ventricular mass index and a decrease in diastolic function occurs early in the course of diabetic nephropathy. [Diabetologia (1999) 42: 76–80]
Published: 1999

289. Plasma renin and prorenin and renin gene variation in patients with insulin-dependent diabetes mellitus and nephropathy

Author: Hans-Henrik Parving, Jeanette M.G. van Gool, Jaap Deinum, René J.A. de Bruin, Lise Tarnow, Maarten A.D.H. Schalekamp, Frans H.M. Derkx, and Internal Medicine
Subjects: Adult, Male, medicine.medical_specialty, Population, Plasma renin activity, Nephropathy, Diabetic nephropathy, SDG 3 - Good Health and Well-being, Diabetes mellitus, Internal medicine, Renin–angiotensin system, Renin, medicine, Humans, Diabetic Nephropathies, education, Transplantation, education.field_of_study, Enzyme Precursors, Diabetic Retinopathy, Polymorphism, Genetic, business.industry, Genetic Variation, Middle Aged, medicine.disease, Angiotensin II, Endocrinology, Diabetes Mellitus, Type 1, Nephrology, Female, Gene polymorphism, business
Abstract: Background. The most striking abnormality in the renin‐angiotensin system in diabetic nephropathy (DN ) is increased plasma prorenin. Renin is thought to be low or normal in DN. In spite of altered Introduction (pro)renin regulation the renin gene has not been studied for contribution to the development of DN. A major cause of morbidity and death in insulinMethods. We studied plasma renin, prorenin, and four dependent diabetes mellitus (IDDM ) is diabetic polymorphic markers of the renin gene in 199 patients nephropathy (DN ), characterized by proteinuria, with IDDM and DN, and in 192 normoalbuminuric steady decline of kidney function, hypertension and IDDM controls matched for age, sex, and duration of cardiovascular disease [1]. Although poor metabolic diabetes. Plasma renin and total renin were measured control plays a role in the development of DN, it by immunoradiometric assays. Genotyping was PCR- appears that 60‐70% of the diabetic population is based. protected from nephropathy despite inadequate metaResults. Plasma renin was increased in patients with bolic control [2]. It has therefore been suggested that nephropathy (median (range), 26.3 (5.2‐243.3) vs 18.3 susceptibility to DN is innate and determined by (4.2‐373.5) mU/ml in the normoalbuminuric group, genetic factors. This hypothesis is supported by reports P
Published: 1999

290. Amadori albumin in type 1 diabetic patients: Correlation with markers of endothelial function, association with diabetic nephropathy, and localization in retinal capillaries

Author: C.D.A. Stehouwer, Hans-Henrik Parving, H. Twaalfhoven, N. Ligtvoet, A. Jager, Reinier Schlingemann, H. G. T. Blaauwgeers, Victor W.M. van Hinsbergh, Casper G. Schalkwijk, Lise Tarnow, Gaubius instituut TNO, and Other departments
Subjects: Glycation End Products, Advanced, Adult, medicine.medical_specialty, Glycosylation, Endocrinology, Diabetes and Metabolism, Serum albumin, Enzyme-Linked Immunosorbent Assay, Diabetic nephropathy, chemistry.chemical_compound, Glycation, Reference Values, Amadori rearrangement, Diabetes mellitus, Internal medicine, Internal Medicine, medicine, Humans, Glycated Serum Albumin, Diabetic Nephropathies, Serum Albumin, Aged, Aged, 80 and over, Diabetic Retinopathy, biology, Chemistry, Albumin, Retinal Vessels, Middle Aged, medicine.disease, Human serum albumin, Capillaries, Endocrinology, Diabetes Mellitus, Type 1, biology.protein, Biological Markers, Glycated hemoglobin, Endothelium, Vascular, Biomarkers, medicine.drug
Abstract: Nonenzymatic glycation is increased in diabetes. Most studies so far have focused on the role of advanced glycation end products (AGEs) in vascular complications, whereas the role of early glycation Amadori-modified proteins, which is the predominant form of glycated proteins, has not been systemically investigated in humans. We developed an antiserum against glycated human serum albumin (HSA) and used this to study the role of early glycation products in vascular complications in type 1 diabetic patients. Amadori albumin was determined to be the recognition epitope of the antiserum. The antibody recognized a specific glucose adduct and a conformational component specific for human albumin in Amadori albumin, with no recognition of AGEs. Plasma Amadori albumin levels were significantly higher in type I diabetic patients (n = 55) than in healthy control subjects (n = 60) (39.2 ± 9.9 vs. 20.9 ± 4.0 U/ml, P < 0.0005). Amadori albumin correlated with levels of plasma markers of endothelial function von Willebrand factor (r = 0.29, P < 0.05) and vascular cell adhesion molecule-1 (r = 0.41, P < 0.005), but not soluble E-selectin. In addition, Amadori albumin immunoreactivity was detected in the capillaries of retinas of diabetic patients. Plasma levels of Amadori albumin were determined in a second group of type 1 diabetic patients with long-standing diabetes with (n = 199) or without (n = 192) diabetic nephropathy. Patients with nephropathy had higher Amadori albumin levels than did those without it (50.9 ± 9.5 vs. 45.1 ± 6.3 U/ml, P < 0.0005). Age-, sex-, and diabetes duration-adjusted analyses showed that nephropathy was significantly associated with Amadori albumin with an odds ratio (OR [95% CI]) of 1.11 [1.08-1.15] per U/ml increase. After additional adjustment for levels of creatinine, glycated hemoglobin, cholesterol, triglycerides, blood pressure, preexistent retinopathy, and cardiovascular disease, Amadori albumin continued to be significantly associated with nephropathy (OR 1.06 [1.01-1.11]) per U/ml increase. Our results are consistent with a proposed pathophysiological role of Amadori albumin in microvascular complications of type 1 diabetic patients. Chemicals/CAS: Biological Markers; glycosylated serum albumin; Serum Albumin
Published: 1999

291. Predisposition to essential hypertension and development of diabetic nephropathy in IDDM patients

Author: Svante Stenman, Hans-Henrik Parving, Lise Tarnow, J. Fagerudd, Peter Karl Jacobsen, Carola Grönhagen-Riska, K. Pettersson-Fernholm, Flemming S Nielsen, and Per-Henrik Groop
Subjects: Adult, Male, Parents, medicine.medical_specialty, Ambulatory blood pressure, Endocrinology, Diabetes and Metabolism, Blood Pressure, Essential hypertension, Gastroenterology, Nephropathy, Diabetic nephropathy, Cohort Studies, Internal medicine, Internal Medicine, medicine, Humans, Diabetic Nephropathies, business.industry, Incidence, Age Factors, Blood Pressure Monitoring, Ambulatory, medicine.disease, Circadian Rhythm, Endocrinology, Blood pressure, Diabetes Mellitus, Type 1, Case-Control Studies, Hypertension, Albuminuria, Microalbuminuria, Female, medicine.symptom, business, Diabetic Angiopathies, Kidney disease
Abstract: Conflicting results have been reported on the relationship between familial predisposition to hypertension and development of diabetic nephropathy in IDDM. In our case-control study, we assessed the prevalence of hypertension among parents of 73 IDDM patients with diabetic nephropathy (DN+; persistent albuminuria > 200 microg/min or > 300 mg/24 h) and 73 IDDM patients without diabetic nephropathy (DN-; urinary albumin excretion < 20 microg/min or < 30 mg/24 h). Arterial hypertension, defined as antihypertensive therapy or a 24-h ambulatory blood pressure (SpaceLabs 90207) > or = 135/85 mmHg, was present in 57% of parents of DN+ patients compared with 41% of parents of DN- patients (P = 0.034; difference 16% [95% CI 1.3-29.6%]). In addition, the cumulative incidence of hypertension was higher among parents of DN+ patients (log-rank test P < 0.001), with a shift toward younger age at onset of hypertension in this group. However, the difference in prevalence of parental hypertension was not evident using office blood pressure measurements (64 vs. 57%; NS; difference 7% [-5.8-20%). Furthermore, patients with DN+ and with antihypertensive therapy in both parents were themselves more frequently treated for hypertension than were patients with DN+ and without parental treatment for hypertension (100 vs. 61%; P = 0.034; difference 39% [21-57%]). In conclusion, familial predisposition to essential hypertension increases the risk of diabetic nephropathy and may also contribute to the development of systemic hypertension in patients with IDDM and diabetic nephropathy.
Published: 1998

292. Differences between nisoldipine and lisinopril on glomerular filtration rates and albuminuria in hypertensive IDDM patients with diabetic nephropathy during the first year of treatment

Author: Hans-Henrik Parving, Lise Tarnow, Berit R. Jensen, Flemming S Nielsen, Peter Rossing, and Søren Boelskifte
Subjects: Adult, Male, medicine.medical_specialty, Ambulatory blood pressure, Time Factors, Endocrinology, Diabetes and Metabolism, Urology, Nisoldipine, Renal function, Angiotensin-Converting Enzyme Inhibitors, Blood Pressure, Diabetic nephropathy, Double-Blind Method, Lisinopril, Internal medicine, Renin, Internal Medicine, medicine, Albuminuria, Humans, Diabetic Nephropathies, Antihypertensive Agents, Chi-Square Distribution, business.industry, medicine.disease, Calcium Channel Blockers, Blood pressure, Endocrinology, Diabetes Mellitus, Type 1, ACE inhibitor, Hypertension, Patient Compliance, Female, medicine.symptom, business, Diabetic Angiopathies, medicine.drug, Glomerular Filtration Rate
Abstract: Our objective was to compare the effect of a long-acting calcium antagonist (nisoldipine) versus an ACE inhibitor (lisinopril) on albuminuria, arterial blood pressure, and glomerular filtration rate (GFR) in hypertensive IDDM patients with diabetic nephropathy. We performed a 1-year, double-blind, doubledummy, randomized, controlled study comparing nisoldipine (20–40 mg once daily) with lisinopril (10–20 mg once daily) in 52 hypertensive IDDM subjects with diabetic nephropathy. Three patients dropped out, and results for the remaining 49 (25 nisoldipine, 24 lisinopril) are presented. Diuretics were required in 10 nisoldipineand 8 lisinopril-treated patients. Every 3 months, 24-h ambulatory blood pressure (TM2420, A&D, Tokyo, Japan) and albuminuria in three 24-h samples (enzyme immunoassay) were measured; GFR (51Cr-EDTA plasma clearance) was recorded every 6 months. Mean arterial blood pressure (24 h) was reduced from (mean ± SE) 108 ± 3 mmHg at baseline to 101 ± 2 in average during treatment in the lisinopril group and from 105 ± 2 to 103 ± 2 in the nisoldipine group (P = 0.06 comparing changes in the two groups). Albuminuria was reduced 47% (95% CI 21–65) in the lisinopril group versus an increase of 11% (−3 to 27) in the nisoldipine group (P = 0.001). Fractional albumin clearance was reduced 37% (95% CI 4–59%) in the lisinopril versus an increase of 35% (8–69%) in the nisoldipine group (P < 0.01). GFR decreased from 85 ± 5 ml · min−1 · 1.73 m−2 to 73 ± 5 in the lisinopril group and from 84 ± 6 to 80 ± 7 in the nisoldipine group (P < 0.05). The effect of study medication on albuminuria and GFR was independent of changes in systemic blood pressure and baseline variables in multiple regression analyses. In summary, lisinopril reduced albuminuria, but also GFR, to a greater extent than did nisoldipine in hypertensive IDDM patients with diabetic nephropathy during the 1st year of treatment. Longer follow-up is required to clarify whether these drugs have different renoprotective effects.
Published: 1997

293. The prevalence of coeliac disease in adult Danish patients with type 1 diabetes with and without nephropathy

Author: H. Skovbjerg, H. Locht, Hans-Henrik Parving, and Lise Tarnow
Subjects: medicine.medical_specialty, Malabsorption, Denmark, Endocrinology, Diabetes and Metabolism, Gastroenterology, Asymptomatic, Coeliac disease, Nephropathy, Diabetic nephropathy, Internal medicine, Diabetes mellitus, Prevalence, Internal Medicine, medicine, Humans, Diabetic Nephropathies, Type 1 diabetes, business.industry, medicine.disease, Celiac Disease, Diabetes Mellitus, Type 1, Endocrinology, Kidney Failure, Chronic, medicine.symptom, business, Kidney disease
Abstract: To the Editor: Coeliac disease causes malabsorption due to small bowel villous atrophy, which normalises when gluten, which is found in wheat, rye and barley, is withdrawn from the diet. Coeliac patients should be treated with a gluten-free diet that corrects the intestinal malabsorption and protects against the development of osteoporosis and intestinal lymphoma. As shown in several studies (review [1]), type 1 diabetes is associated with a high prevalence (2–10%) of coeliac disease. This has, in part, been explained by genetic factors, in particular by increased frequencies of HLA-DR3 and HLA-DQ2 [2]. Coeliac symptoms are often absent or atypical in type 1 diabetic patients and the diagnosis is therefore often delayed. Diabetic nephropathy is the leading cause of end-stage renal disease and develops in approximately one-third of type 1 diabetic patients within the first 20 years of diabetes. The pathogenesis of diabetic nephropathy is only partially understood. In addition to genetic factors, haemodynamic, metabolic and growth factors are generally accepted to contribute [3]. As in diabetic nephropathy [4], reduced final height is a significant clinical manifestation of coeliac disease. In this study we investigated the prevalence of coeliac disease in adult Danish type 1 diabetes patients, with the specific aim of studying whether undiagnosed coeliac disease is more prevalent in type 1 diabetic patients with diabetic nephropathy than in type 1 diabetic patients without nephropathy. We studied 967 type 1 diabetic patients [5]. The patient population comprised a group of 462 patients with overt diabetic nephropathy (defined as persistent macroalbuminuria [>300 mg/24 h], retinopathy and no signs of other kidney or urinary tract disease; 284 men, median age 41 [range: 17–78] years, median serum creatinine 103 [range: 52–706] μmol/l) and a group of 505 patients with longstanding (23 [range: 10–63] years) type 1 diabetes and persistent normoalbuminuria (275 men, age 46 [range: 20– 81] years). Median age at onset of diabetes was 12 (range: 0–47) and 18 (range: 0–64) years in the nephropathy and normoalbuminuric groups respectively (p
Published: 2005
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294. Mo2090 Gastric Emptying, Glycemia, and Upper GI Symptoms Are Independent Factors in Diabetic Gastroparesis

Author: Elsa Mondou, Tuba Esfandyari, Rayaz A. Malik, John M. Wo, Franck Rousseau, Georg Dimcevski, M. Mazen Jamal, Joseph B. Quinn, Per M. Hellström, Niels Ejskjaer, Richard W. McCallum, and Lise Tarnow
Subjects: Gi symptoms, medicine.medical_specialty, Hepatology, Gastric emptying, business.industry, Diabetic gastroparesis, Internal medicine, Gastroenterology, medicine, business
Published: 2013
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295. Influence of Erythropoietin on Cognitive Performance during Experimental Hypoglycemia in Patients with Type 1 Diabetes Mellitus: A Randomized Cross-Over Trial

Author: Niels Vidiendal Olsen, Jens Faber, Jens J. Holst, Troels W. Kjaer, Ulrik Pedersen-Bjergaard, Peter Lommer Kristensen, Birger Thorsteinsson, Flemming Dela, and Lise Tarnow
Subjects: Blood Glucose, Male, Pediatrics, Anatomy and Physiology, medicine.medical_treatment, lcsh:Medicine, law.invention, Cognition, Endocrinology, Randomized controlled trial, law, lcsh:Science, Cross-Over Studies, Hematologic Tests, Multidisciplinary, Clinical Pharmacology, Electroencephalography, Middle Aged, Medicine, Female, Research Article, medicine.drug, Adult, Drugs and Devices, medicine.medical_specialty, Clinical Research Design, Cognitive Neuroscience, Endocrine System, Hypoglycemia, Diabetes mellitus, Internal medicine, medicine, Humans, Clinical Trials, Effects of sleep deprivation on cognitive performance, Biology, Erythropoietin, Aged, Monitoring, Physiologic, Diabetic Endocrinology, Type 1 diabetes, Endocrine Physiology, business.industry, Insulin, lcsh:R, Diabetes Mellitus Type 1, medicine.disease, Crossover study, Hormones, Electrophysiological Phenomena, Diabetes Mellitus, Type 1, Glucose Clamp Technique, lcsh:Q, business, Neuroscience
Abstract: Introduction The incidence of severe hypoglycemia in type 1 diabetes has not decreased over the past decades. New treatment modalities minimizing the risk of hypoglycemic episodes and attenuating hypoglycemic cognitive dysfunction are needed. We studied if treatment with the neuroprotective hormone erythropoietin (EPO) enhances cognitive function during hypoglycemia. Materials and Methods Eleven patients with type 1 diabetes, hypoglycemia unawareness and recurrent severe hypoglycemia completed the study. In a double-blind, randomized, balanced, cross-over study using clamped hypoglycemia they were treated with 40,000 IU of EPO or placebo administered intravenously six days before the two experiments. Cognitive function (primary endpoint), hypoglycemic symptoms, and counter-regulatory hormonal response were recorded. Results Compared with placebo, EPO treatment was associated with a significant reduction in errors in the most complex reaction time task (−4.7 (−8.1 to −1.3), p = 0.01) and a less reaction time prolongation (−66 (−117 to −16) msec, p = 0.02). EPO treatment did not change performance in other measures of cognition. Hypoglycemic symptoms, EEG-changes, and counter-regulatory hormone concentrations did not differ between EPO and placebo treatment. Conclusion In patients with type 1 diabetes and hypoglycemia unawareness, treatment with EPO is associated with a beneficial effect on cognitive function in a complex reaction time task assessing sustained attention/working memory. Hypoglycemic symptoms and hormonal responses were not changed by EPO treatment. Trial Registration ClinicalTrials.gov NCT00615368
Published: 2013
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296. Genetics of diabetic nephropathy

Author: Hans-Henrik Parving, Peter Rossing, and Lise Tarnow
Subjects: Genetic Markers, Peptidyl-Dipeptidase A, Bioinformatics, Antiporters, Nephropathy, Diabetic nephropathy, Risk Factors, Diabetes mellitus, medicine, Genetic predisposition, Humans, Diabetic Nephropathies, business.industry, General Medicine, DNA, medicine.disease, Angiotensin II, Blood pressure, Diabetes Mellitus, Type 1, Phenotype, Diabetes Mellitus, Type 2, Nephrology, Albuminuria, medicine.symptom, business, Kidney disease
Abstract: Diabetic nephropathy is a clinical syndrome characterized by persistent albuminuria, a relentless decline in GFR, raised arterial blood pressure, and increased relative mortality for cardiovascular diseases. Diabetic nephropathy is a leading cause of end-stage renal failure. The pathogenesis of diabetic nephropathy is multifactorial, with contributions from metabolic abnormalities, hemodynamic alterations, and various growth factors and genetic factors. Epidemiologic and family studies have demonstrated that only a subset of the patients develop this complication that family clustering of nephropathy is present, and that ethnicity plays an important role in the risk of developing this kidney disease. Short stature and low birth weight are both associated with increased risk of developing diabetic nephropathy, supporting the hypothesis that genetic predisposition or factors operating in utero, in early childhood, or both contribute to the development of diabetic nephropathy. Studies elucidating phenotypic markers such as parenteral hypertension and systemic blood pressure elevation have yielded conflicting results. The contribution from elevated blood pressure only plays a minor role in the majority of the patients developing diabetic nephropathy. The majority of the studies have demonstrated increased sodium/lithium countertransport activity in insulin-dependent diabetes mellitus patients with nephropathy, whereas studies of this phenotypic marker in parents of patients with and without nephropathy have yielded conflicting results. Recently, studies of genetic markers involved in the regulation of blood pressure and levels of cardiovascular risk factors have been conducted. Several studies have demonstrated that the deletion polymorphism in the angiotensin-I-converting enzyme acts as a risk factor for cardiovascular disease in diabetic patients. However, a meta-analysis does not support the suggestion that this factor plays any role for the initiation of diabetic nephropathy. Similar negative results have been obtained in relation to polymorphisms of the genes encoding for angiotensinogen and the angiotensin II Type 1 receptor. However, studies in diabetic and non-diabetic glomerulopathies have clearly demonstrated a deleterious effect of the deletion polymorphism in the angiotensin-converting enzyme on the progression of kidney function.
Published: 1996

297. Circadian rhythm of arterial blood pressure and albuminuria in diabetic nephropathy

Author: Hans-Henrik Parving, Lise Tarnow, Henrik Post Hansen, Berit R. Jensen, Flemming S Nielsen, and Peter Rossing
Subjects: Adult, Male, medicine.medical_specialty, Ambulatory blood pressure, Hemodynamics, Renal function, Blood Pressure, Nephropathy, Diabetic nephropathy, Internal medicine, Diabetes mellitus, medicine, Albuminuria, Humans, Diabetic Nephropathies, business.industry, Middle Aged, medicine.disease, Circadian Rhythm, Endocrinology, Blood pressure, Diabetes Mellitus, Type 1, Nephrology, Female, medicine.symptom, business, Extracellular Space
Abstract: Circadian rhythm of arterial blood pressure and albuminuria in diabetic nephropathy. The aim of our study was to evaluate the diurnal relationship between arterial blood pressure and albuminuria, and some potential mechanisms responsible for impaired nocturnal blood pressure reduction (non-dippers, groups I and II) in diabetic nephropathy (DN). Twenty-four-hour ambulatory blood pressure, heart rate (HR) variation (autonomic nervous function) and extracellular fluid volume (ECV) were measured, and urine samples were collected three times during the corresponding day- and nighttimes in 47 insulin-dependent diabetic (IDDM) patients with DN. Mean arterial blood pressure (MABP) during the daytime [mm Hg, median (range)] was identical in group I [105 (96–137)], group II [109 (86–124)] and group III [dippers; average blood pressure reduction from day to night > 10%, 107 (93–132), P = NS], while the nighttime MABP differed [group I, 106 (95–144); group II, 100 (78–118); group III, 91 (76–118); P < 0.001]. No significant difference between the groups concerning the daytime or nighttime albuminuria [μg/min; median (range)] was observed; [Day: group I, 1467 (235–3933); group II, 695 (170–6719); group III, 875 (228–3173). Night: group I, 1079 (279–4665); group II, 572 (113–3807); group III, 659 (81–2493)]. A significant correlation between MABP and albuminuria was demonstrated during day- (ρ = 0.50, P < 0.0005) and nighttime (ρ = 0.46, P < 0.005), while neither the absolute nor the relative changes in MABP from day to night correlated significantly with absolute or relative changes in albuminuria from day to night. The night/day ratio of HR was higher in group I [0.93 (0.76–1.09), median (range)] compared to group III [0.83 (0.74–1.02), P < 0.005] and a significant correlation between this ratio and the night/day ratio of MABP was found (ρ = 0.54, P < 0.0005). ECV was about the same in the three groups. Our study indicated an association between blood pressure and albuminuria, but the mechanisms involved in the reduction of albuminuria from day to night was not unraveled. A relative lack of sympathetic withdrawal during sleep seems to be an important feature of nocturnal hypertension in diabetic nephropathy.
Published: 1996

298. Development of enzyme-linked immunoassays for human angiotensin I converting enzyme suitable for large-scale studies

Author: Fran oise Savoie, Michel Azizi, Lise Tarnow, Xavier Jeunemaitre, Fran ois Alhenc-Gelas, Bertrand Lenoir, and Sergei M. Danilov
Subjects: Male, Genotype, Physiology, medicine.drug_class, Population, Enzyme-Linked Immunosorbent Assay, Peptidyl-Dipeptidase A, Monoclonal antibody, Sensitivity and Specificity, law.invention, Mice, law, Internal Medicine, medicine, Animals, Humans, education, chemistry.chemical_classification, education.field_of_study, Polymorphism, Genetic, biology, business.industry, Antibodies, Monoclonal, Angiotensin-converting enzyme, Molecular biology, Enzyme, chemistry, Polyclonal antibodies, biology.protein, Recombinant DNA, Alkaline phosphatase, Female, Antibody, Cardiology and Cardiovascular Medicine, business, Gene Deletion
Abstract: Objective To develop and validate a simple immunological assay for human angiotensin converting enzyme (ACE) based on monoclonal antibodies. Methods Microtitre plates were coated with mouse monoclonal antibody (MoAb) to human ACE (9B9) and incubated with diluted samples of human plasma. In the sandwich enzyme-linked immunosorbent assay (ELISA), the plasma ACE, bound to MoAb 9B9, was revealed using polyclonal anti-ACE antibodies and alkaline phosphatase conjugated to goat anti-rabbit immunoglobulin G. In the plate precipitation assay the ACE activity, quantitatively precipitated from human plasma by MoAb 9B9, was measured by enzymatic fluorimetric assay with p-benzyloxycarboxyl-glycyl-L-histidyl-L-leucine or p-benzyloxycarboxyl-L-phenylalanyl-L-histidyl-L-leucine as substrate, directly in the wells. Results These assays are specific for the amino-terminal domain of ACE and recognize differences in the conformations of native and recombinant ACE. The sensitivity of the sandwich ELISA was 200 pg/ml assay medium; it quantifies the ACE in 10 microliters human plasma or less. Intra- and inter-assay variability coefficients were 6.2 and 13.6%, respectively. Both variants of the assay determined the plasma ACE concentration in the presence of ACE inhibitors or EDTA. The ACE concentrations were determined by sandwich ELISA in a population of 138 middle-aged healthy Caucasian subjects. They were strongly correlated with the ACE gene insertion/deletion (I/D) polymorphism, which accounted for 20% of the variance of plasma ACE concentration in this population and 16-24% of the variance in plasma ACE activity as measured with three different enzymatic assays. Conclusion The ACE concentration (but not inhibition) can be determined by this ELISA which is suitable for large-scale studies of plasma ACE levels.
Published: 1996

299. 54 EFFECT OF ONE YEAR TREATMENT WITH INSULIN AND ORAL GLUCOSE-LOWERING AGENTS ON LIPID LEVELS IN NON-OBESE PATIENTS WITH TYPE 2-DIABETES

Author: H.-H. Parving, Birgitte V. Hansen, M. Frandsen, S. Søgaard Lund, Oluf Pedersen, Allan Vaag, Birgitte Bruun Nielsen, and Lise Tarnow
Subjects: medicine.medical_specialty, business.industry, Insulin, medicine.medical_treatment, General Medicine, Type 2 diabetes, medicine.disease, Endocrinology, Non obese, Internal medicine, Internal Medicine, medicine, Oral glucose, Cardiology and Cardiovascular Medicine, business
Published: 2011
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300. TZP-102, Ghrelin Agonist Phase 2 Data: The Improvement in Symptoms of Gastroparesis (Nausea, Early Satiety, Bloating and Abdominal Pain) Significantly Correlated With Patient Rating of Overall Treatment Effect

Author: Lise Tarnow, Gordana Kosutic, M. Mazen Jamal, Robert P. Venuti, Richard W. McCallum, John M. Wo, Rayaz A. Malik, Philippa A. Charlton, Tuba Esfandyari, Niels Ejskjaer, Georg Dimcevski, Laura Shaughnessy, and Per M. Hellström
Subjects: Agonist, Abdominal pain, Hepatology, medicine.drug_class, business.industry, Nausea, Gastroenterology, medicine.disease, Bloating, Anesthesia, Diabetes mellitus, medicine, Ghrelin, Treatment effect, Gastroparesis, medicine.symptom, business
Abstract: * Percentage of patients with a score ≥ 1 **Where 0=none,1=very mild, 2=mild, 3=moderate, 4=severe, and 5=very severe for individual symptoms. TZP-102, Ghrelin Agonist, Phase 2 Data: The Improvement in Symptoms of Gastroparesis (Nausea, Early Satiety, Bloating and Abdominal Pain) Significantly Correlated with Patient Rating of Overall Treatment Effect R McCallum1, J Wo2, R Venuti3, T Esfandyari4, M Jamal5, G Dimcevski6, L Tarnow7, R Malik8, PM Hellstom9, L Shaughnessy3, P Charlton3, G Kosutic3, N Ejskjaer10 1Texas Tech Univ Health Sci Ctr El Paso TX, 2Univ Louisville, Louisville KY, 3Tranzyme, Inc., Durham NC, 4Univ Kansas Med Ctr, Kansas City KS; 5Long Beach VA Med Ctr, Long Beach CA, 6Haukeland Univ Hosp, Bergen NO, 7Steno Diabetes Ctr, Gentofte DK, 8Univ Manchester, Manchester UK, 9Uppsala Univ Hosp, Uppsala SE, 10Aarhus Univ Hosp, Aarhus DK
Published: 2011
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