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Malnutrition is one of the most common disorders observed in patients who are being treated for various diseases. In cancer patients with a palliative profile, compared with patients without malignant neoplasms, anemia, lymphopenia, decreased glomerular filtration rate were significantly more often detected, and a tendency to lower albumin levels was revealed. There was a significant decrease in PNI, BMI, shoulder circumference, thickness of the skin‑fat fold of the scapula and shoulder, and a tendency to reduce lean body weight in patients with palliative malignancies. The logistic regression analysis revealed the relationship between the presence of a malignant tumor in palliative patients and the presence of trophic status disorders: PNI (β = –0.37, p = 0.021), weight (β = –0.41, p = 0.001), BMI (β = –0.36, p = 0.001), shoulder circumference (β =–0.65, p = 0.001), thickness of the scapular skin‑fat fold (β = –0.66, p = 0.001).

Background The dexamethasone suppression test (DST) is the recommended first-tier test for suspected Cushing syndrome (CS). Missed dexamethasone intake or insufficient dexamethasone serum exposure may yield false positive results. Quantification of serum dexamethasone in DST samples may therefore improve test performance. Methods Simultaneous quantification of dexamethasone and cortisol by liquid chromatography-tandem mass spectrometry in 400 DST serum samples (100 overt CS, 200 excluded CS, 100 adrenal incidentalomas with (possible) autonomous cortisol secretion, AI-ACS) randomly selected within the indication groups. The 2.5th percentile of dexamethasone in patients with excluded CS was considered the lower limit of normal (LLN). Results Serum dexamethasone varied from undetectable to 20.2 ng/mL with a median of 4.8 ng/mL (95% CI 4.5-5.1 ng/mL). Dexamethasone was undetectable in only 16 patients (4%), suggesting non-compliance. The dexamethasone LLN was 1.8 ng/mL (4.6 nmol/L). Decreased glomerular filtration rate and diabetes mellitus were associated with higher serum dexamethasone concentration, while body mass index, sex, age, nicotine, and oral contraceptives had no significant effect. By excluding the 27 samples with dexamethasone Conclusions Quantification of dexamethasone and method-specific cortisol cutoffs in DST samples may reduce the false positive rate and lower the proportion of patients requiring further workup.

Background. The discussed topic is worth attracting attention because of its high mortality rate in patients with acute renal damage which is caused by urological and surgical diseases. The membrane-destructive component in damaged renal tissues is manifested with decreased glomerular filtration rate, increased endotoxin level and lipid aberrations. The standard infusion and antibacterial therapy does not fully compensate the severity of pathological changes.Purpose. To study the effectiveness of low-level laser irradiation at endotoxicosis and lipid metabolism indicators in acute renal damage in acute experimental peritonitis.Material and methods. Lipid peroxidation, membrane-destructive processes in renal tissues as well as lipid metabolism and endotoxicosis were studied in the experiment with dogs. The effectiveness of infusion and antibiotic therapy and combined therapy with laser light were compared.Basic results: the experiment has demonstrated that acute renal damage was caused by systemic inflammatory diseases of non-urological profile. The applied low-level laser irradiation (LLLI) promoted more rapid correction of pathological processes which were manifested with increased concentration of cholesterol esters, total phospholipids, phosphatidylserine; LLLI decreased levels of cholesterol, phosphatidylcholine, triacylglycerol, phosphatidylinositol, triacylglycerol, phosphatidylinositol, diacylglycerol, lysophospholipids, free fatty acids and endotoxicosis parameters.Conclusion: the obtained results reliably indicate a LLLI positive effect at the organism’s potentials to recover when LLLI is included into the comprehensive therapy (under experiment). This is evidently seen in the restoration of lipid component in elements of renal parenchyma and in the decrease of lipid peroxidation activity.

Introduction. Percutaneous interventions used in the treatment of acute coronary syndrome (ACS) may be complicated by the recurrence of the ischemia clinical picture due to the late lumen loss of the stent. Factors influencing the risk of the restenosis developing may differ depending on the clinical situation and stent characteristics.Objective. To identify risk factors for repeated revascularization in patients with ACS without ST-segment elevation after placement of everolimus-eluting stents. Materials and methods. The study included 126 patients with ACS, who received platinum-chromium containing everolimus-eluting stents. The main clinical and laboratory parameters of the patients were analyzed. After 12 months, the combined endpoint (death, myocardial infarction in the basin of the stented artery, repeated revascularization of the stented vessel) was assessed.Results. During the followup, 18 of 126 patients (14.3 %) reached the combined endpoint. Among patients who reached the endpoint, there were more women (10 (24.4 %) and 8 (9.4 %); p=0.02). In patients who reached the endpoint, the level of highly sensitive troponin was significantly higher (0.032 (0.007; 0.32) ng/ml versus 0.005 (0.002; 0.022) ng/ml; p=0.005), there was a lower left ventricular ejection fraction (52.2±12.3 % vs 58.6±8.9 %; p=0.02) and glomerular filtration rate (68.5±15.7 ml/min vs 76.3±18.2 ml/min; p=0.04), and there was also a significantly lower level of triglycerides (1.3±0.4 mmol/L and 1.8±0.9 mmol/L, p=0.004) and VLDL (0.6±0.2 mmol/L and 0.8±0.4 mmol/L, p=0.006). According to multivariate regression analysis, the leading factors influencing the risk of repeated revascularization were diabetes mellitus (OR 4.25; 95 % CI: 1.12–16.15; p=0.03), glomerular filtration rate and triglyceride level (OR 0.25; 95 % CI: 0.07–0.93; p=0.03).Conclusions. When using everolimus-eluting stents, diabetes mellitus, decreased glomerular filtration rate and low blood triglyceride levels are among the main factors affecting the risk of in-stent restenosis.

ObjectivesWe studied the association between long working hours and decreased kidney function, which was determined using estimated glomerular filtration rate (eGFR), among the working population in South Korea.MethodsWe analysed nationally representative cross-sectional data for 20 851 Korean workers ≥20 years of age. A negative binomial regression model was used to test differences in the prevalence of chronic kidney disease (eGFR 2) among workers divided into groups according to weekly working hours (ResultsA 1-hour increase in weekly working hours was associated with 0.057 mL/min/1.73 m2 (95% CI 0.005 to 0.109) decrease in eGFR among participants who worked ≥52 hours/week. Among participants without hypertension or diabetes, a 1-hour increase in weekly working hours was significantly associated with 0.248 and 0.209 mL/min/1.73 m2 decrease in eGFR among participants who worked 30–40 hours/week and 41–51 hours/week, respectively.ConclusionLong working hours are associated with decreased kidney function. We expect that our findings could call for more research regarding this association and provide policy-oriented perspectives.

Clinicopathologic evaluation of renal function and renal disease in sick adult horses remains grounded in detection of azotemia, assessment of serum and urine electrolyte concentrations, and evaluation of urinalysis findings, including specific gravity, reagent strip analysis, and sediment examination. Because increases in serum or plasma urea nitrogen and creatinine concentrations are insensitive indicators of a decreased glomerular filtration rate, there is considerable interest in identifying novel biomarkers of renal function or injury in blood and urine, with serum symmetric dimethylarginine concentration being the most recent addition to the commercial market.

Aim. To assess the effect of immunosuppressive cyclophosphamide therapy and its regimens on the rate of progression of chronic kidney disease in mesangioproliferative glomerulonephritis. Methods. 72 patients with mesangioproliferative glomerulonephritis and indications for immunosuppressive therapy with disease activation were included in the comparative analysis: 56 patients received cyclophosphan in conventional doses (26 patients with daily or every other day, 30 patients with in pulse mode 1 time per month), and 16 patients did not receive cyclophosphan. Duration of the disease before observation ranged from 0 to 33.58 years, a median follow-up was 6.00 (interquartile range 1.6313.17) years, and after observation from 0 to 5 years with the median follow-up was 2.00 (1.003.50) years. The examination included nephrobiopsia with a morphological diagnosis, activity index/sclerosis, and glomerulonephritis progression rate for decreased glomerular filtration rate (ml/min/1.73 m per year). Results. The progression rate of chronic kidney disease was higher in the group of patients not receiving immunosuppressive therapy, 5.57 (3.277.95) ml/min/1.73 m2 per year compared with of the treated patients group, 3.05 (2.046.78) ml/min/1.73 m2 per year (p=0.040). There were no differences in the rate of decrease in glomerular filtration rate between groups depending on the treatment regimen: 4.86 (2.126.77) ml/min/1.73 m2 per year with regular and 3.67 (2.04 6.91) ml/min/1.73 m2 per year with a pulse mode (p=0.720). The rate of glomerulonephritis also did not differ significantly: 1.0 (1.02.0) and 2.0 (1.02.0) relapses over 5 years, respectively (p=0.691) in both treatment regimens. Conclusion. The treatment of patients with mesangioproliferative glomerulonephritis with cyclophosphane, in combination with prednisone or without it, regardless of the treatment regimen induces a slowdown in the progression of chronic kidney disease, improving the long-term prognosis and without affecting the frequency of relapses of the disease.

This study determined the prevalence and associated factors of decreased estimated glomerular filtration rate (eGFR) in patients who had type 2 diabetes for at least 5 years.A cohort study was conducted in 467 outpatients in a community-based hospital in Ho Chi Minh City, Vietnam. Serum creatinine were tested twice, at two occasions at least 3 months apart. The confirmatory eGFR was the average of the two eGFR of which the difference was ≤20%. The mean urine albumin-to-creatinine ratio was calculated from two consecutive early morning specimens.Most patients were female with a mean age of 61.7 (8.0) years. Albuminuria was found in 40% of participants, and the prevalence of decreased eGFR was 7.5% (n=35). Individuals with declined eGFR were older (p0.001), had duration of diabetes longer (p=0.025), higher systolic blood pressure (p=0.010) and higher acid uric level (p0.001), increased albumin excretion (p=0.009), and more proliferative retinopathy (p=0.011) than those with non-declined eGFR.Although decreased eGFR in type 2 diabetes patients was not prevalent, the strategies to prevent the progressive decline of GFR should be done to prevent patients from progressing to advanced renal disease.

BackgroundMoonseed vine (Triclisia gilletiiStaner) in the family Menispermaceae is a robust creeper of up to 10 cm diameter, of the lowland dense rain forest. In Ondo State, located in the South Western part of Nigeria, the plant which is usually called Peshe is used for the management of renal-related ailments. The present study was undertaken to explore the efficacy ofTriclisia gilletii, a folkloric therapy in the management of renal-related ailment.ResultsPhenols, steroids, saponins, and flavonoids are present in the TGME with a total antioxidant capacity of (30.36 ± 1.90 (mg GAE/g extract), LD50greater than 5000 mg/kg b.w., and in vitro anti-nucleation activity (iC50 = 7.09 mg/mL). Calcium oxalate stone formation as a result of oxalate from ethane-1,2-diol was evident by hypocalcemia, and further electrolyte imbalance and decreased glomerular filtration rate. The enhanced oxidative milieu in hyperoxaluria was evident by increased MDA and PC and decreased enzymatic and non-enzymatic antioxidants as well as renal membrane enzymes activities. The renal histopathological study further emphasized oxalate-induced damage and the ameliorative potential of TGME.ConclusionThe abnormal biochemical, redox electrolyte, membrane integrity, and histological alterations were attenuated by TGME which affirms its usage as nephroprotectant.

Serum cystatin C levels (CysC) are used in human medicine to document progressive kidney failure. Although CysC are not thought to be useful for the diagnosis of kidney dysfunction in dogs, there has been no specific consideration of body weight as a confounding issue. The aim of this study was to assess that the utility of CysC for the diagnosis of decreased glomerular filtration rate (GFR) in smaller vs. larger dogs. In clinically healthy dogs, serum creatinine (Cre) and CysC correlate directly with body weight; we found that dogs weighing

Several metals have nephrotoxic properties. In this chapter we discuss various methods for assessing nephrotoxicity, different forms of proteinuria, and methods of estimating the glomerular filtration rate. Metals may affect renal glomeruli, resulting in a decreased glomerular filtration rate, sometimes associated with massive albuminuria. Effects on renal tubular function are more common, affecting the reabsorption of minerals, sugars, amino acids, and low molecular weight proteins from filtered primary urine. Various biomarkers, especially proteinuria, are also discussed. The most important nephrotoxic metals are lead, cadmium, and mercury. Acute nephrotoxic effects are sometimes seen, especially in suicide attempts or as side effects when metals (e.g. gold, platinum, and antimony) are used in treatment of certain diseases. Long-term exposure is far more common, e.g. via diet, drinking water, or occupational exposure. For example, long-term exposure to cadmium sometimes causes chronic kidney disease, and in rare cases the development of end-stage renal disease with uremia.

Background Heart failure (HF) is a major health problem. Cardiac and renal diseases interact in a complex bidirectional manner in both acute and chronic settings. Renal dysfunction in the setting of heart failure, termed the cardio renal syndrome (CRS), has been considered consequence of left ventricular dysfunction (LVD), whereby decreasing cardiac output (COP) results in renal under perfusion and consequent decreased glomerular filtration rate (GFR). Main body of the abstract This study showed that 500 patients were admitted to internal care unit (ICU), and out of them, 100 (20%) patients developed acute kidney injury (AKI) while 400 (80%) patients did not develop AKI. It is also showed that 67 (67%) of those with AKI and 100 (25%) of those with no-AKI had baseline ventricular systolic dysfunction, left ventricular dysfunction (LVD), right ventricular dysfunction (RVD), and biventricular dysfunction (BiVD)presented in 23 (23%), 16 (16%), and 28 (28%) patients of AKI group, respectively, and presented in 60 (15%), 30 (7.50%), and 10 (2.50%) patients, respectively, in patients without acute kidney injury (AKI) Short conclusion Our study revealed that AKI has highest incidence in patient with biventricular dysfunction followed by left ventricular dysfunction and lastly those with right ventricular dysfunction.

The clinical study enrolled 120 patients, who were hospitalized to the Therapeutic Department of Republican Clinical Hospital No. 5 of Saransk. The patients were divided into 2 groups: Group I (n = 60) included patients with metabolic syndrome; Group II (n = 60) included patients with arterial hypertension. The paper presents data on the assessment of the functional state of kidneys in the analysed groups, defines the role of metabolic disorders in the progression of renal dysfunction in patients with metabolic syndrome and arterial hypertension. It is noted that more pronounced functional changes in the kidneys (microalbuminuria, increased cystatin C levels, decreased glomerular filtration rate) are detected in patients with arterial hypertension and metabolic syndrome, as compared with patients without metabolic disorders. Cystatin C and microalbuminuria have been shown to be one of the earliest markers of kidney damage in hypertension, especially in combination with metabolic disorders. Cystatin C and microalbuminuria level is significantly higher in patients with arterial hypertension and metabolic syndrome, as compared with patients with arterial hypertension, who have no metabolic disorders. Significant correlations were found between cystatin C, microalbuminuria levels and lipid and carbohydrate metabolism in patients with arterial hypertension in combination with metabolic disorders.

Decreased glomerular filtration rate (GFR) is linked to poor survival. The predictive value of creatinine estimated GFR (eGFR) and cystatin C eGFR in critically ill patients may differ substantially, but has been less studied. This study compares long-term mortality risk prediction by eGFR using a creatinine equation (CKD-EPI), a cystatin C equation (CAPA) and a combined creatinine/cystatin C equation (CKD-EPI), in 22,488 patients treated in intensive care at three University Hospitals in Sweden, between 2004 and 2015. Patients were analysed for both creatinine and cystatin C on the same blood sample tube at admission, using accredited laboratory methods. During follow-up (median 5.1 years) 8401 (37%) patients died. Reduced eGFR was significantly associated with death by all eGFR-equations in Cox regression models. However, patients reclassified to a lower GFR-category by using the cystatin C-based equation, as compared to the creatinine-based equation, had significantly higher mortality risk compared to the referent patients not reclassified. The cystatin C equation increased C-statistics for death prediction (p p = 0.013 vs. combined equation). In conclusion, this data favours the sole cystatin C equation rather than the creatinine or combined equations when estimating GFR for risk prediction purposes in critically ill patients.

To evaluate the frequency of unindicated CT Angiograms (CTAs) obtained at our institution and the association between contrast-induced nephropathy (CIN) and decreased glomerular filtration rate (GFR).Retrospective case series SETTING: Academic Level 1 trauma center PATIENTS/PARTICIPANTS: Patients aged 18 years and older with CTAs following lower-extremity (LE) trauma between 2010-2018.CTAs performed in 257 LEs and corresponding pre- and post-contrast renal function labs in these LE trauma patients.The primary outcome was vascular injury requiring intervention. Secondary outcomes were CIN and the association of CIN with decreased GFR and injury severity score (ISS).There was no indication (no hard signs of vascular injury, ABI0.9) for CTA in 121 patients (61%) of the total 199 patients. Of the 78 patients with signs of vascular injury or ABI0.9, 35 (45%) had positive CTAs and 15 (19.2%) required vascular intervention. Of the 121 unindicated patients, 26 (21%) had positive CTAs and 1 (0.008%), a knee dislocation, required vascular intervention. In 155 patients with renal function labs, initial GFR60ml/min was a risk factor for CIN as compared to GFR60ml/min (p=0.001). Rate of CIN did not correlate with Injury Severity Score (ISS).CTAs are obtained more often than indicated and initial GFR60ml/min is a risk factor for developing CIN, irrespective of the trauma burden. CTAs should be reserved for when hard signs of vascular injury or ABI0.9, especially in those patients with decreased renal function.Level IV.

Background: Hyperglycemia during hospital stay is associated with adverse outcomes. Aim: To characterize the frequency of hyperglycemia in a tertiary hospital and to correlate it with length of hospital stay (LOS). Material and Methods: Review of medical records of hospitalized patients. Demographic data and laboratory data, previous diabetes mellitus (DM) history, current main diagnosis, unit of hospitalization and the two highest capillary blood glucose values from the analyzed period were recorded for each patient. LOS was obtained from electronic clinical records. Results: 210 subjects, aged 60 ± 19 years (104 women) were included. 113 patients (54%) developed hyperglycemia ≥ 140 mg/L. Thirty one percent of these had a previous history of diabetes and 29% had stress hyperglycemia (SHG). Patients with a history of DM had a higher average blood glucose than those with SHG (238.9 and 178.2 mg/dL, respectively, p < 0.01) and a greater percentage of cases with a blood glucose above 180 mg/dL (72 and 40.0%, respectively, p < 0.01). Hospital LOS was significantly longer in patients with hyperglycemia ≥ 140 mg/dL as compared with those with normoglycemia (29.3 and 12.8 days, respectively, p < 0.01). This association remained significant when introduced in a linear regression analysis including diagnosis, decreased glomerular filtration rate (GFR) and hospitalization unit (p < 0.01). Conclusions: Hyperglycemia during hospitalization affects more than half of hospitalized patients and is associated with a longer length of stay.

The Apolipoprotein L1 (APOL1) gene plays an important role in determining risk for chronic kidney disease (CKD) and is prevalent in countries with large populations of African ancestry.1,2 The effects of the presence of high risk variants pose a challenge when considering kidney transplantation in endemic populations due to the potential detrimental effects on recipients and donors alike. For recipients, grafts from both living and deceased donors with two APOL1 risk variant alleles are associated with shorter graft survival and decreased glomerular filtration rate (GFR) in comparison to those with zero or one variant.3 Similarly, living donors with two risk variant APOL1 alleles experience significantly decreased pre- and post-donation GFR when compared to those with zero or one variant, precipitating the introduction of APOL1 risk variant screening of potential living kidney donors (pLKDs) across many institutions in resource-rich settings such as the United States.4,5 This is the first study to screen for APOL1 risk variants in pLKDs located in Nigeria, and Antigua & Barbuda, countries with large populations of African descent.

Hyperkalemia is a frequent complication among kidney transplant recipients that can lead to fatal arrhythmias. The causes of hyperkalemia post kidney transplant are multifactorial and often are drug-induced, and include decreased glomerular filtration rate, tubular dysfunction, and impaired sodium delivery in the distal nephron. This review will discuss pathophysiology and recent updates in the management of both acute and chronic hyperkalemia with a focus on kidney transplant recipients.

Hyperkalemia is a frequent complication among kidney transplant recipients that can lead to fatal arrhythmias. The causes of hyperkalemia post kidney transplant are multifactorial and often are drug-induced, and include decreased glomerular filtration rate, tubular dysfunction, and impaired sodium delivery in the distal nephron. This review will discuss pathophysiology and management of both acute and chronic hyperkalemia in kidney transplant recipients.

Background IgA nephropathy (IgAN) is characterized by proteinuria, hypertension, and decreased glomerular filtration rate at the time of diagnosis. However, the underlying mechanism is still obscure. The impact of haptoglobin (Hp) phenotype, as a genetic risk factor, on the progression of IgAN has not been studied yet. The current study examines whether Hp phenotype influences IgAN progression and response to treatment. Materials and methods The study included 40 patients with IgAN, 26 non-IgAN chronic kidney disease (CKD), 114 patients on hemodialysis, and 150 healthy subjects. Blood and urine samples were collected at baseline and 6 months after initiation therapy. Serum creatinine, total proteinuria, and Hp phenotype were determined in all patients and healthy controls. Results Approximately 17% of IgAN patients were Hp 1-1, 40% Hp 2-1, and 42.5% Hp 2-2. In contrast, in non-IgAN CKD patients, the prevalence of Hp 1-1, Hp 2-1, and Hp 2-2 was 8%, 19%, and 73%, respectively. In hemodialytic patients, prevalence of Hp 1-1, Hp 2-1, and Hp 2-2 was 10.5, 49.1, and 40.4%, respectively. In healthy subjects, the distribution of Hp 1-1, Hp 2-1, and Hp 2-2 was 7, 39, and 54%, respectively. Interestingly, IgAN Hp 2-2 and Hp 2-1 patients were more stable and responded better to treatment with routine therapy than other patients with Hp phenotype. Conclusion The prevalence of Hp 1-1 phenotype is higher in IgAN patients than in the general population in Israel, and even more than in patients with CKD or subjects on hemodialysis. Patients with Hp 2-2 exhibited a better renal response to the routine therapies.

Chronic kidney disease (CKD) is characterized by decreased glomerular filtration rate (GFR) due to a variety of causes. Most patients remain undiagnosed at early stage of CKD and proceed to end stage CKD due to unawareness and lacking of efficient biomarkers. Trimethylamine-N-oxide (TMAO) and its predecessor products: choline, l-carnitine and betaine are associated with reduced renal function. However, whether the combined variation of the four metabolites could contribute in prediction and stratification of impaired glomerular function in Chinese CKD patients is unknown. Our aim is to investigate the associations of plasma TMAO, choline, l-carnitine and betaine with glomerular filtration in CKD patients. A total of 65 CKD patients and 64 healthy controls were enrolled in this study. Fasting plasma metabolites were detected using liquid chromatography-based method. Plasma TMAO, choline, betaine and l-carnitine levels were differentially correlated with eGFR. The four metabolites were independently associated with CKD after adjustment for multiple traditional risk factors. The combination of the four metabolites had good performance at discriminating CKD from healthy controls (AUC = 0.96) as well as discriminating low eGFR from high eGFR in CKD (AUC = 0.96). Combinations of TMAO and its precursors were associated with glomerular function and might be utilized in evaluation of CKD.

Purpose Variability in tacrolimus levels has been associated with increased rejection, graft loss, and de novo donor-specific antibody (dnDSA) development in kidney transplant recipients (KTRs); however, limited data on alemtuzumab induction or infection exist. We sought to determine the impact of tacrolimus variability in KTRs on dnDSAs, graft outcomes, and infections 3 years posttransplant after alemtuzumab induction. Methods Adult KTRs from January 1, 2013, to December 31, 2017, receiving alemtuzumab and tacrolimus-based immunosuppression at a single center were included. Tacrolimus variability was calculated using coefficient of variability (CV), and high CV was defined as ≥30%. Graft and infectious outcomes were assessed between high and low CV groups. Results Two hundred fourteen KTRs were included. The median tacrolimus CV from 0 to 3 months and from 3 to 12 months was 28.1% and 25.8%, respectively. Recipients with high CV had decreased glomerular filtration rate at 3 and 12 months (67.7 ± 35.48 vs 80.7 ± 29.3, P = .01 and 70.9 ± 35.4 vs 83.3 ± 30.2, P = .015). High CV was also associated with increased cytomegalovirus viremia and disease (19.6% vs 9.3%, P = .046 and 6.4% vs 17.9%, P = .015). No difference in biopsy-proven acute rejection, survival, or dnDSA development at 3 years was observed. Conclusions High tacrolimus variability was associated with significantly reduced graft function and increased cytomegalovirus viremia and disease but not biopsy-proven acute rejection, survival, or dnDSA development.

High-throughput DNA testing is becoming established as a standard diagnostic test in the renal clinic. Previously published studies on cohorts of patients with unexplained chronic kidney disease of a suspected genetic aetiology have suggested a diagnostic yield for genomic sequencing of up to 18%. Here we determine the yield of targeted gene panel in a clinically unscreened cohort of patients referred for percutaneous native renal biopsy. Patients who underwent renal biopsy for investigation of chronic kidney disease were sequenced using a genomic sequencing panel covering 227 genes in which variation is known to be associated with monogenic chronic kidney disease (CKD). Candidate disease-causing variants were assessed for pathogenicity using guidelines from the American College for Medical Genetics and Genomics. Fifty CKD patients were recruited and sequenced. A molecular diagnosis was obtained for two patients (4%). A molecular diagnosis is possible using genomic testing in ∼4% of clinically unscreened patients undergoing renal biopsy. Genetic screening may be useful for diagnosis in a subset of CKD patients but is most valuable when applied to patients with suspected heritable forms of kidney disease.

Background Highly trained athletes running 42 km or more demonstrate elevated cardiac biomarkers, ventricular dysfunction, and decreased glomerular filtration rate (GFR). Whether similar changes occur in the much larger population of recreational runners following half‐marathon distance running is unclear. Hypothesis Recreational runners exhibit changes in myocardial and renal biomarkers, including ventricular strain, after a half‐marathon treadmill run. Methods 10 recreational subjects (mean age 36.5 ± 6.5 years) ran 21 km on a treadmill (mean completion time 121.6 ± 16.1 minutes). Serum high‐sensitivity troponin T (hsTnT), amino‐terminal pro‐brain natriuretic peptide (NT‐proBNP), creatinine, and neutrophil gelatinase‐associated lipocalin (NGAL) were measured prior to, 1 hour post‐, and 24 hours post‐exercise. Pre‐ and post‐exercise echocardiograms were performed. Results All biomarkers increased 1 hour post‐exercise: hsTnT by 8.5 ± 8.5 pg/ml (P

Acute glomerulonephritis caused by Streptococcus pneumoniae is a low prevalence pathology. There are several reports communicating different nephritogenic serotypes, however, 6C has been scarcely indicated as such. It is presented the case of a 4-year-old patient who entered Intensive Therapy Unit with pleuropneumonia due to Streptococcus pneumoniae serotype 6C and concomitantly developed edemas, arterial hypertension, hematuria, proteinuria, decreased glomerular filtration rate and C3 complement level. Acute glomerulonephritis was diagnosed. His evolution was satisfactory in a short time. This pathology is usually of a transitory and benign course; however, sometimes it can potentially complicate the evolution of a critically ill patient, so it is necessary to have it among the differential diagnoses to consider.

Background Adiponectin secreted by adipocytes plays a key role in insulin sensitivity, anti-inflammation, and antiatherosclerosis. It is involved in several conditions including obesity, type 2 diabetes mellitus, cardiovascular disease, and chronic kidney disease (CKD). Glomerular filtration rate is monitored to indicate the kidney function and CKD progression. Objective To assess the serum adiponectin levels in individuals with normal and mildly decreased glomerular filtration rate, analyze the association of serum adiponectin with various physical and biological parameters, and test whether serum adiponectin is the risk factor of mildly decreased glomerular filtration rate. Methods This cross-sectional study was conducted in 172 individuals with 35–60 years of age. Serum samples were collected and divided into two groups, based on estimated glomerular filtration rate (eGFR): 90 with normal eGFR (G1, eGFR ≥90 mL/min/1.73 m2) and 82 with mildly decreased eGFR (G2, eGFR = 60–89 mL/min/1.73 m2). Anthropometric data were recorded. Serum adiponectin was measured by enzyme-linked immunosorbent assay. Results Serum adiponectin levels were significantly increased in individuals with mildly decreased eGFR (G2), compared to G1 (8.23 ± 3.26 µg/mL and 6.57 ± 3.24 µg/mL, respectively; P = 0.001). Serum adiponectin was positively associated with age and high-density lipoprotein cholesterol but negatively associated with weight, body mass index, triglyceride, and waist and hip circumferences. Univariate analysis showed that serum adiponectin was significantly correlated with mildly decreased eGFR; however, when adjusting for confounding factors, there were no correlations. Furthermore, multivariate regression analysis showed that individuals at the age of 46–55 years (4.0; 95% CI: 1.9–8.3) and > 55 years (11.4; 95% CI: 3.7–35.5) were significantly correlated with mildly decreased eGFR. Conclusions Serum adiponectin was significantly elevated in individuals with mildly decreased eGFR and may be a modulation factor, but was not an independent risk factor for mildly kidney damage. Further study is needed to clarify its potential benefits as monitoring biomarker for CKD progression.

Diabetic nephropathy is one of the fairly severe Diabetes Mellitus (DM) complications and the main cause of renal failure that can result in mortality. Hyperglycemia in DM induces kidney injury that may result in hemodynamic and metabolic alterations, endothelial dysfunction and inflammatory cells activation. A persistent and continuous inflammation is observed in diabetic nephropathy. One of the inflammation process progression indicators is Neutrophil-Lymphocyte Ratio (NLR). To find out the relationship between NLR and decreased Glomerular Filtration Rate (GFR) in diabetic nephropathy. This study was an observational study with a retrospective approach. This study was conducted in Clinical Pathology Laboratory Installation and Medical Record Installation of Dr. Wahidin Sudirohusodo Makassar Hospital by collecting the patient's data during February 2015 to February 2016. Patients that were diagnosed as type 2 DM without diabetic nephropathy complication were taken as control and those diagnosed as type 2 DM with diabetic nephropathy were treated as study subjects. One hundred and thirteen (113) samples met the inclusion criteria, consisting of 73 diabetic nephropathy patients with Chronic Kidney Disease (CKD) 13 diabetic nephropathy patients without CKD and 27 type 2 DM patients without diabetic nephropathy complication. Patients consisted of 57 males (50.4%) and 56 females (49,6%). Neutrophil-lymphocyte ratio and GFR values in the group of diabetic nephropathy without CKD were 2.03±0.68 and 85.38±24.63, respectively. Whereas, the NLR and GFR values in control group were 1.74±0.54 and 90.03±28.60, respectively. In the group of diabetic nephropathy with CKD, NLR value increased by 3.19±1.83 and GFR decrease by 30.54±16.45. Spearman test indicated a significant relationship between NLR increase and decreased GFR (r = -0.635, p=0.00). There is a significant relationship between NLR increase and decreased GFR in patients with diabetic nephropathy.

The glomerular filtration barrier (GFB) plays a critical role in ensuing protein free urine. The integrity of the GFB is compromised during hypoxia that prevails during extreme physiological conditions. However, the mechanism by which glomerular permselectivity is compromised during hypoxia remains enigmatic. Rats exposed to hypoxia showed a decreased glomerular filtration rate, podocyte foot-processes effacement, and proteinuria. Accumulation of hypoxia-inducible factor-1α (HIF1α) in podocytes resulted in elevated expression of zinc finger E-box binding homeobox 2 (ZEB2) and decreased expression of E- and P-cadherin. We also demonstrated that HIF1α binds to hypoxia response element localized in the ZEB2 promoter. Furthermore, HIF1α also induced the expression of ZEB2-natural antisense transcript, which is known to increase the efficiency of ZEB2 translation. Ectopic expression of ZEB2 induced loss of E- and P-cadherin and is associated with enhanced motility of podocytes during hypoxic conditions. ZEB2 knockdown abrogated hypoxia-induced decrease in podocyte permselectivity. This study suggests that hypoxia leads to activation of HIF1α–ZEB2 axis, resulting in podocyte injury and poor renal outcome.

Objective The aim of the study was to observe the influence of 11-days complete water fasting (WF) and regeneration diet (RD) on renal function, body weight, blood pressure and oxidative stress. Background Therapeutic WF is considered a healing method. Methods Ten volunteers drank only water for 11 days, followed by RD for the next 11 days. Data on body weight, blood pressure, kidney functions, antioxidants, lipid peroxidation, cholesterols, triacylglycerols and selected biochemical parameters were obtained. Results WF increased uric acid and creatinine and decreased glomerular filtration rate. After RD, the parameters were comparable to baseline values. Urea was not affected. Lipid peroxidation (TBARS) decreased and maintained stable after RD. Fasting decreased α-tocopherol and increased γ-tocopherol, no significant changes were found after RD. Coenzyme Q10 decreased after RD. HDL-cholesterol decreased in WF. Total- and LDL-cholesterol decreased after RD. Other biochemical parameters were within the range of reference values. Conclusions The effect of the complete fasting on kidney function was manifested by hyperuricemia. Renal function was slightly decreased, however maintained within the reference values. After RD, it returned to baseline values. The positive effect of the complete water fasting was in the reduction of oxidative stress, body weight and blood pressure (Tab. 3, Ref. 25).

Fabry disease (FD) is an X-linked lysosomal storage disorder resulting from the deficiency or absence of the alpha galactosidase A enzyme. Organic involvement in men is well known, but in women it is controversial, partly due to the random X-chromosomes inactivation (Lyon hypothesis). The aim of this study was to describe the organic involvement in women at the time of FD diagnosis. A descriptive, cross-sectional and multicenter study was carried out. Thirty-five women with FD from three reference centers in Argentina were evaluated. The mean age of the whole group (n=35) was 26.6±16.9 years; 22 were adult (over 18) and 13 were paediatric patients. Enzymatic activity was performed in 29/35 patients, which was normal in 24/29 (82.8%). Seven different mutations of the GLA gene were found. The results showed urinary protein loss (45.7%) and decreased glomerular filtration rate (31.4%), mainly in adults. And also, cornea verticillata (56.5%), peripheral neuropathy (51.4%), cardiovascular manifestations (31.4%), hearing loss (20%), angiokeratomas (20%), central nervous system (17.1%), and gastrointestinal involvement (14.3%). Organic compromise in females with FD may be as severe as in men. This analysis has demonstrated a significant proportion of women with signs, symptoms, and major organic involvement at FD diagnosis.

Calcitriol has important effects on cellular differentiation and proliferation, as well as on the regulation of the renin gene. Disturbances in renal development can be observed in rats exposed to angiotensin II (AngII) antagonists during lactation period. The lack of tubular differentiation in losartan-treated rats can affect calcitriol uptake. This study evaluated the effect of calcitriol administration in renal development disturbances in rats provoked by losartan (AngII type 1 receptor antagonist) administration during lactation. Animals exposed to losartan presented higher albuminuria, systolic blood pressure, increased sodium and potassium fractional excretion, and decreased glomerular filtration rate compared to controls. These animals also showed a decreased glomerular area and a higher interstitial relative area from the renal cortex, with increased expression of fibronectin, alpha-SM-actin, vimentin, and p-JNK; and an increased number of macrophages, p-p38, PCNA and decreased cubilin expression. Increased urinary excretion of MCP-1 and TGF-β was also observed. All these alterations were less intense in the losartan + calcitriol group.The animals treated with calcitriol showed an improvement in cellular differentiation, and in renal function and structure. This effect was associated with reduction of cell proliferation and inflammation.

Decreased glomerular filtration rate (GFR) has been suspected as a risk factor for arterial stiffness. Whether high GFR is the risk factor of arterial stiffness and cardiovascular disease remains uncertain. We aim to evaluate the association between high estimated GFR (eGFR) and arterial stiffness in Chinese adults.We performed a cross-sectional study involving 9136 Chinese adults without chronic kidney disease. Arterial stiffness was measured by brachial-ankle pulse wave velocity (baPWV) and pulse pressure (PP). We divided participants into four groups according to age-specific quartiles of eGFR. Renal hyperfiltration (RHF) was defined with the highest age-specific quartile of eGFR. The odds ratios (ORs) of elevated baPWV and PP were estimated using multivariate logistic regression models and were further tested using propensity score matching analysis between participants with or without RHF.RHF was associated with 11 and 32% higher risk of elevated baPWV and PP in age-adjusted models, P = 0.35 and 0.005, respectively. After adjusting for covariates, RHF was significantly associated with 23 and 39% increased risk of elevated baPWV and PP, P = 0.01 and 0.001, respectively. These associations were further confirmed in propensity score matching analysis. The adjusted ORs (95% confidence interval) were 1.17 (1.03-1.30) for elevated baPWV and 1.28 (1.13-1.46) for elevated PP, P = 0.02 and P value less than 0.001, respectively.RHF was associated with elevated baPWV and PP, suggesting that RHF might be an early indicator for the detection of arterial stiffness.

Chronic kidney disease (CKD) is associated with mineral and bone disorder (MBD), which is the main cause of the extensively increased cardiovascular mortality in the CKD population. We now aimed to establish a new murine experimental CKD-MBD model. Dilute brown non-Agouti (DBA/2) mice were fed with high-phosphate diet for 4 (HPD4) or 7 (HPD7) days, then with standard chow diet (SCD) and subsequently followed until day 84. They were compared to DBA/2 mice maintained on SCD during the whole study period. Both 4 and 7 days HPD-fed mice developed phosphate nephropathy with tubular atrophy, interstitial fibrosis, decreased glomerular filtration rate, and increased serum urea levels. The abdominal aorta of HPD-treated mice showed signs of media calcification. Histomorphometric analysis of HPD-treated mice showed decreased bone volume/tissue volume, low mineral apposition rate, and low bone formation rate as compared to SCD-fed mice, despite increased parathyroid hormone levels. Overall, the observed phenotype was more pronounced in the HPD7 group. In summary, we established a new, noninvasive, and therefore easy to perform reproducible CKD-MBD model, which showed media calcification, secondary hyperparathyroidism, and low-turnover bone disease.

Objectives: To describe the effect of low-dose (111MBq) radioiodine therapy (RAI) on thyroid and renal function in hyperthyroid cats over a 12 month follow-up period.Materials and Methods: Client-owned hyperthyroid cats underwent treatment with low-dose RAI and were followed for 12 months post-RAI treatment. Immediately prior to RAI treatment, and subsequently at one, six and 12 months post-RAI treatment, thyroid function was evaluated using total thyroxine (TT4) and thyroid stimulating hormone (TSH) and renal function was evaluated using serum creatinine concentration and glomerular filtration rate (GFR).Results: Fifteen of the 24 (63%) cats achieved euthyroidism following low-dose RAI treatment. The incidence of development of overt hypothyroidism was 25% (6/24 cats). Of the cats developing overt hypothyroidism, 3/6 (50%) had decreased renal function, with decreased GFR preceding development of azotaemia in 2 out of 3 of these cats. Transient overt or subclinical hypothyroidism prior to restoration of euthyroidism was not observed in any cats.Clinical Significance: Low-dose RAI is effective for most cats with hyperthyroidism, however, overt hypothyroidism may develop in some. Concurrent early decline in renal function may only be detected by measuring GFR rather than serum creatinine in some patients. Monitoring of patients post-RAI treatment should include TT4 and TSH with consideration of GFR measurement in non-azotaemic cats.

International audience; Rationale & objective: Chronic kidney disease (CKD) characterized by decreased glomerular filtration rate (GFR) is often accompanied by various degrees of impaired tubular function in the cortex and medulla. Assessment of tubular function may therefore be useful in establishing the severity of kidney disease and identifying those at greater risk for CKD progression. We explored reductions in urinary concentrating ability, a well-known feature of CKD, as a risk factor for GFR decline and end-stage renal disease (ESRD).Study design: Prospective longitudinal cohort study.Setting & participants: 2,084 adult patients with CKD stages 1 to 4 from the French NephroTest Cohort Study.Predictor: Fasting urinary osmolality measured using delta cryoscopy.Outcomes: ESRD, mortality before ESRD, and measured GFR (mGFR) assessed using 51Cr-EDTA renal clearance.Analytical approach: Cause-specific hazards models were fit to estimate crude and adjusted associations of urinary osmolality with ESRD and death before ESRD. Linear mixed models with random intercepts were fit to evaluate the association of urinary osmolality with slope of decline in mGFR.Results: At baseline, mean age was 58.7±15.2 (SD) years with a median mGFR of 40.2 (IQR, 29.1-54.5) mL/min/1.73m2 and a median fasting urinary osmolality of 502.7±151.7mOsm/kg H2O. Baseline fasting urinary osmolality was strongly associated with mGFR (R=0.54; P < 0.001). 380 ESRD events and 225 deaths before ESRD occurred during a median follow-up of 5.9 (IQR, 3.8-8.2) years. Patients with lower baseline fasting urinary osmolality had higher adjusted risk for ESRD but not for mortality (HRs of 1.97 [95% CI, 1.26-3.08] and 0.99 [95% CI, 0.68-1.44], respectively, for the lowest vs highest tertile). Based on a mixed linear model adjusted for baseline mGFR and clinical characteristics, patients in the lowest tertile of baseline urinary osmolality had a steeper decline in kidney function (-4.9% ± 0.9% per year; P < 0.001) compared with patients in the highest tertile.Limitations: Fasting was self-reported.Conclusions: Fasting urinary osmolality may be a useful tool, in addition to GFR and albuminuria, for assessing nonglomerular damage in patients with CKD who are at higher risk for CKD progression.

CKD is characterized by chronic (>3 months), often irreversible, evidence of kidney injury or dysfunction with consequences for health (1). A diagnosis is made in the presence of decreased glomerular filtration rate (GFR) or if there is analytical (most commonly pathological albuminuria), histological or imaging evidence of kidney injury. The criterion “with consequences for health” implies that CKD is associated with an increased risk of progression to end-stage renal disease (ESRD) requiring renal replacement therapy, which is the best-known consequence of CKD.

The aim of this study was to estimate prevalence and severity of renal insufficiency in systemic sclerosis (SSc) and to assess risk factors associated with reduced glomerular filtration rate (GFR) in SSc patients. Seventy-three consecutive patients with SSc (67 women and 6 men), mean age 56.2 years, mean disease duration 6.7 years, were included in this cross-sectional study. GFR was measured by creatinine clearance (CCr) in all patients, as well as 24-h proteinuria. We assessed frequency and severity of renal insufficiency in our patients with SSc and estimated the association of renal insufficiency with age, disease duration, subtype of the disease, earlier diagnosed arterial hypertension, and medications for which we assumed to affect renal function—cytostatics, nonsteroidal anti-inflammatory drugs, glucocorticoids, ACE inhibitors, diuretics, and calcium channel blockers (CCB). Fifty-six out of 73 patients with SSc (76.7%) had reduced GFR (CCr lower than 90 ml/min), compared to 17/73 (23.3%) of patients with normal renal function. Mild renal insufficiency was noticed in 28/73 (38.4%), moderate in 21/73 (28.8%) and severe renal insufficiency in 5/73 (6.8%). End-stage renal disease (CCr < 15 ml/min) was found in 2/73 (2.7%) of patients. Using the univariate general linear statistical model, we have found that previously diagnosed arterial hypertension and treatment with glucocorticoids are independent risk factors for reduced GFR. On the other hand, age, disease duration, disease form, as well as antibodies (anticentromere antibodies—ACA and anti-topoisomerase I antibodies—ATA) were excluded as independent risk factors. Patients with SSc and arterial hypertension treated with CCB had significantly higher mean CCr than patients treated with diuretics (90.4 vs 53.5 ml/min, p = 0.03), or patients treated with ACE inhibitors (90.4 vs 41.7 ml/min, p = 0.001). Decreased GFR is common in SSc. Most of patients have mild or moderate renal insufficiency. Previously diagnosed arterial hypertension, especially when treated with ACE inhibitors or diuretics, and glucocorticoids are independent risk factors associated with reduced GFR in SSc. These medications should be therefore used with caution in SSc patients.

Few studies have investigated the association between metabolic syndrome (MS) and chronic kidney disease in the elderly. Accordingly, the aim of this study was to examine the sex-specific association between MS and decreased glomerular filtration rate (GFR) in a Chinese elderly population. We performed cross-sectional analyses of older (age ≥60 years) males (n = 19,015) and females (n = 23,310) classified as 0, 1, 2, 3, 4, and 5 component(s) or MS group based on the presenting MS component(s). Sex-specific relationship of decreased GFR with MS component(s) was analyzed by logistic regression models. Compared with participants with 0 component of MS, males with 1, 2, 3, 4, and 5 component(s) had 1.40-, 1.79-, 2.41-, 3.29-, and 4.09-fold risks for decreased GFR; females with 1, 2, 3, 4, and 5 component(s) had 1.65-, 1.71-, 1.88-, 2.32-, and 1.96-fold risks for decreased GFR, respectively. The multivariate-adjusted odds ratios for decreased GFR in males and females with MS compared with those without MS were 1.79 and 1.25, respectively. For participants without hypertension and diabetes, the association of MS with decreased GFR was still significant. In this study of 42,325 Chinese participants aged ≥60 years, MS was significantly associated with decreased GFR, and the association was more profound for males than females.

Advanced chronic kidney disease is associated with high rates of cardiovascular disease. Considering the crucial role of capillaries in renal function, our study aimed to evaluate microparticles related to vascular physiology examining the link between stages of chronic kidney disease with circulating endothelial (EMP), platelet (PMP) and monocytic (MMP) microparticles. Cross-sectional study with blinded endpoints included subjects of both sexes, aged 40-75 years (n = 247), with established cardiovascular disease (coronary heart disease, ischemic stroke, or peripheral artery disease). They were stratified 1:1 by the presence or absence of decreased glomerular filtration rate (GFR 60 mL/min/1.73 m

BackgroundThere is limited information on the role of low socioeconomic status (SES) in the development of new chronic kidney disease (CKD) in the general population, especially from developing countries. This study will test the hypothesis that low SES increases the risk of incidence of decreased glomerular filtration rate (GFR, used as an estimate for CKD) in a Thai worker cohort.MethodIn this prospective, longitudinal observational study, we evaluated the association of income and educational attainment on incident decreased GFR (iGFR2) over a 27-year period in employees of Electricity Generating Authority of Thailand. In 1985, subjects participated in a health survey and were re-examined in 1997, 2002, 2007 and 2012. Education was classified into three categories: low, 0–8th grade; medium, 9–12th grade; and high, >12th grade. Income was categorised as follows: low 20 000 THB/month. HRs ofiGFR2were estimated using Cox interval-censored models with high income or education as the reference groups after adjustments for clinical risk factors.ResultsParticipants (n=3334) were followed for 23 (15, 27) years. When evaluated separately, both education and income were risk factors foriGFR2(adjusted HR education: medium—1.26 (95% CI 1.13 to1.42) and low—1.57 (95% CI 1.36 to 1.81) and adjusted HR income: medium—1.21 (95% CI 0.97 to 1.50) and low—1.47 (95% CI 1.18 to 1.82)). When both income and education were included together, low and medium education remained independently associated withiGFR2.ConclusionsLow education was independently associated with increased risk of decreased GFR in a Thai worker population. Strategies to identify risk factors among low SES may be useful to prevent early CKD.

To identify correlations between parameters of vascular stiffness and characteristics of the clinical course of acute cerebrovascular accident (stroke).Two hundred and seven patients with stroke (mean age 64.6±10.9 years; 115 men) treated in a neurological department of «Municipal Clinical Hospital Br. Bakhrushins of the Health Care Department of Moscow» were studied. All patients underwent a standard neurological and clinical-instrumental examination, including assessment of arterial stiffness by sphygmography. Analysis of the data was carried out depending on the severity of stroke and the pathogenetic subtype of stroke.The pathological value of the CAVI was detected in all patients with cerebral infarction. The highest values were noted in patients with an atherothrombotic subtype of stroke. A positive correlation was revealed between CAVI and the age of patients (The factors determining the severity of stroke are age, arterial hypertension, type 2 diabetes, carotid atherosclerosis, left ventricular remodeling, and decreased glomerular filtration rate. The CAV and the toe-brachial index, rather than the ankle-brachial index, significantly distinguished patients with ischemic stroke from patients with transient ischemic attack.Выявление связей между параметрами жесткости артериальной стенки и особенностями клинического течения острого нарушения мозгового кровообращения (ОНМК).Обследованы 207 больных (115 мужчин, 92 женщины) с ишемическим инсультом (ИИ) и транзиторной ишемической атакой (ТИА), средний возраст 64,6±10,9 года, пролеченных в неврологическом отделении ГБУЗ «ГКБ им. братьев Бахрушиных ДЗМ». Всем больным были проведены стандартное неврологическое и клинико-инструментальное обследования, а также оценка показателей жесткости артериальной стенки методом объемной сфигмографии. Анализ полученных данных проводился в зависимости от тяжести ОНМК и патогенетического подтипа инсульта.Патологическое значение сердечно-лодыжечного сосудистого индекса (CAVI) определялось у всех больных ИИ. При этом наиболее высокие его значения отмечены у больных атеротромботическим подтипом инсульта. Выявлена положительная корреляционная связь индекса CAVI с возрастом пациентов (Факторами, определяющими тяжесть течения инсульта, явились возраст, наличие артериальной гипертензии, сахарного диабета 2-го типа, стенозирующего атеросклероза брахиоцефальных артерий, ремоделирования левого желудочка сердца, снижения скорости клубочковой фильтрации. Индекс CAVI и пальце-плечевой индекс, а не лодыжечно-плечевой индекс достоверно отличали больных ИИ от больных с ТИА.

Patients with chronic kidney disease and severely decreased glomerular filtration rate (GFR) are at high risk for kidney failure, cardiovascular disease (CVD) and death. Accurate estimates of risk and timing of these clinical outcomes could guide patient counseling and therapy. Therefore, we developed models using data of 264,296 individuals in 30 countries participating in the international Chronic Kidney Disease Prognosis Consortium with estimated GFR (eGFR)s under 30 ml/min/1.73m(2). Median participant eGFR and urine albumin-to-creatinine ratio were 24 ml/min/1.73m(2) and 168 mg/g, respectively. Using competing-risk regression, random-effect meta-analysis, and Markov processes with Monte Carlo simulations, we developed two- and four-year models of the probability and timing of kidney failure requiring kidney replacement therapy (KRT), a non-fatal CVD event, and death according to age, sex, race, eGFR, albumin-to-creatinine ratio, systolic blood pressure, smoking status, diabetes mellitus, and history of CVD. Hypothetically applied to a 60-year-old white male with a history of CVD, a systolic blood pressure of 140 mmHg, an eGFR of 25 ml/min/1.73m(2) and a urine albumin-to-creatinine ratio of 1000 mg/g, the four-year model predicted a 17% chance of survival after KRT, a 17% chance of survival after a CVD event, a 4% chance of survival after both, and a 28% chance of death (9% as a first event, and 19% after another CVD event or KRT). Risk predictions for KRT showed good overall agreement with the published kidney failure risk equation, and both models were well calibrated with observed risk. Thus, commonly-measured clinical characteristics can predict the timing and occurrence of clinical outcomes in patients with severely decreased GFR.

Thromboxane (Tx) A2has been suggested to be involved in the development of sepsis-induced acute kidney injury (AKI). Therefore, we investigated the impact of cyclooxygenase (COX)-1 and COX-2 activity on lipopolysaccharide (LPS)-induced renal TxA2formation, and on endotoxemia-induced AKI in mice. Injection of LPS (3 mg/kg ip) decreased glomerular filtration rate (GFR) and the amount of thrombocytes to ∼50% of basal values after 4 h. Plasma and renocortical tissue levels of TxB2were increased ∼10- and 1.7-fold in response to LPS, respectively. The COX-1 inhibitor SC-560 attenuated the LPS-induced fall in GFR and in platelet count to ∼75% of basal levels. Furthermore, SC-560 abolished the increase in plasma and renocortical tissue levels of TxB2in response to LPS. The COX-2 inhibitor SC-236 further enhanced the LPS-induced decrease in GFR to ∼40% of basal values. SC-236 did not alter thrombocyte levels nor the LPS-induced increase in plasma and renocortical tissue levels of TxB2. Pretreatment with clopidogrel inhibited the LPS-induced drop in thrombocyte count, but did not attenuate the LPS-induced decrease in GFR and the increase in plasma TxB2levels. This study demonstrates that endotoxemia-induced TxA2formation depends on the activity of COX-1. Our study further indicates that the COX-1 inhibitor SC-560 has a protective effect on the decrease in renal function in response to endotoxin. Therefore, our data support a role for TxA2in the development of AKI in response to LPS.

Diabetes is associated with increased risk for development of kidney disease, and an increased glomerular filtration rate is an early indication of altered kidney function. Here we determine whether reduced adenosine A 2a receptor–mediated vasodilation of the efferent arteriole contributes to the increased glomerular filtration rate in diabetes. The glomerular filtration rate, renal blood flow, and proximal tubular stop flow pressure were investigated in control and streptozotocin-diabetic rats during baseline and after administration of the adenosine A 2a receptor antagonist ZM241385 or the adenosine A 2a receptor agonist CGS21680. The diabetes-induced glomerular hyperfiltration was reduced by 24% following A 2a receptor stimulation but was unaffected by A 2a receptor inhibition. Contrarily, glomerular filtration rate in controls increased by 22% after A 2a receptor inhibition and was unaffected by A 2a stimulation. The increased glomerular filtration rate after A 2a receptor inhibition in controls and decreased glomerular filtration rate after A 2a receptor activation in diabetics were caused by increased and decreased stop flow pressure, respectively. None of the interventions affected renal blood flow. Thus, the normal adenosine A 2a receptor–mediated tonic vasodilation of efferent arterioles is abolished in the diabetic kidney. This causes increased efferent arteriolar resistance resulting in increased filtration fraction and hyperfiltration.

BACKGROUND Renal transplant dysfunction has been shown to be an independent risk factor for cardiac, non-cardiovascular, and all-cause mortality in post-transplantation follow-up. MATERIAL AND METHODS We enrolled 73 renal transplant recipients who were more than 12 months post-renal transplant surgery, had stable graft function, and were on standard immunosuppression. The purpose of the study was to observe the relation between renal dysfunction and endothelial dysfunction parameters (nitrates, asymmetric and symmetric dimethylarginine, and endothelial nitric oxide synthase), and renalase, and to hypothesize the best predictor of early renal dysfunction by multivariate modeling. The other aim was to observe differences with regard to immunosuppression. RESULTS Non-adjusted odds ratio showed a significant risk of reduced glomerular filtration rate in transplant recipients with increased renalase concentration (p=0.026); age-adjusted odds ratio showed a significant risk of reduced glomerular filtration rate with increased renalase concentration (p=0.042), also after multivariable adjustment (p=0.032). Increased plasma endothelial nitric oxide synthase concentration was a protective factor for glomerular filtration rate (p=0.011). After adjustment for age (p=0.045), and after multivariate modeling, endothelial nitric oxide synthase was shown to be a protective factor for glomerular filtration rate (p=0.014). Significant differences in immunosuppression were found in plasma renalase in patients maintained on cyclosporine (p=0.027). CONCLUSIONS Renalase was shown to be strong predictor of decreased glomerular filtration rate and was significantly higher in the group of patients on cyclosporine. Endothelial nitric oxide synthase was identified as a strong protective factor for kidney function.