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Background: WFS1-spectrum disorders are caused by a mutation in the WFS1 gene. The term includes a wide range of rare disorders, from the most severe Wolfram syndrome with autosomal recessive inheritance to milder clinical manifestations with a single causative variant in the WFS1 gene, such as Wolfram-like syndrome, low-frequency sensorineural hearing loss (LFSNHL), isolated diabetes mellitus (DM), nonsyndromic optic atrophy (OA), and isolated congenital cataracts. Methods: The aim of this study was to evaluate genotype–phenotype correlations in Polish patients with WFS1-spectrum disorders. The study group constituted 22 patients (10 F; 12 M), including 10 patients (3 F; 7 M) referred to the Outpatient Clinic for Rare Diseases in Children and Adolescents and Diabetogenetics between 2019 and 2024 with clinical symptoms suggestive of WFS1-spectrum disorders, and 12 of their first-degree relatives (7 F; 5 M) from 10 families in Poland. Molecular testing was performed using tNGS (Targeted Next Generation Sequencing; Illumina) and analyzed for variants in the WFS1 gene. Results: Thirteen different variants in the WFS1 gene were found in 22 individuals (10 patients and family members), including the identification of two new variants (c.1535T>C and c.2485C>G). All patients had hyperglycemia or DM, hearing impairment, OA, or a combination of these symptoms. Four patients in the study group were diagnosed with Wolfram syndrome and all were compound heterozygotes for variants in the WFS1 gene. Conclusions: The evaluation of molecular characteristics in combination with clinical symptoms broadens the understanding of WFS1-spectrum disorders and allows more accurate management and prognosis for patients with this diagnosis. [ABSTRACT FROM AUTHOR]

Background: Intense exercise leads to neutrophil extracellular traps (NETs) formation, which triggers cell disintegration. NET, as well as other processes of apoptosis, necrosis, and spontaneous secretion, result in increased levels of cell-free DNA (cf-DNA) in the circulation. An increment of cf-DNA is also observed in autoimmune diseases, such as type 1 diabetes mellitus (T1DM). Repeated exhaustive exercises are an impulse for physiological adaptation; therefore, in this case–control study, we compared the exercise-induced increase in cf-DNA in men with T1DM and healthy controls to determine the development of the tolerance to exercise. Methods: Volunteers performed a treadmill run to exhaustion at a speed matching 70% of their personal VO2 max at three consecutive visits, separated by a 72 h resting period. Blood was collected before and after exercise for the determination of plasma cell-free nuclear and mitochondrial DNA (cf n-DNA, cf mt-DNA) by real-time PCR, blood cell count and metabolic markers. Results: Each bout of exhaustive exercise induced a great elevation of cf n-DNA levels. An increase in cf mt-DNA was observed after each run. However, the significance of the increase was noted only after the second bout in T1DM participants (p < 0.02). Changes in cf-DNA concentration were transient and returned to baseline values during 72 h of resting. The exercise-induced increment in circulating cf n-DNA and cf mt-DNA was not significantly different between the studied groups (p > 0.05). Conclusions: Cf-DNA appears to be a sensitive marker of inflammation, with a lower post-exercise increase in individuals with T1DM than in healthy men. [ABSTRACT FROM AUTHOR]

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Background/Objectives: Patients referred for HNF1B testing present very heterogeneous phenotypes. Despite suggestive characteristics, many do not harbor mutations in HNF1B. Our objective was to evaluate the clinical characteristics of probands referred for HNF1B genetic testing through a nationwide monogenic diabetes screening program. Methods: Probands tested for HNF1B mutations in the 2005‐2018 period (N = 50) were identified in the Polish Monogenic Diabetes Registry, which prospectively recruits primarily pediatric patients and their families on a nationwide scale. Variants that had been reported pathogenic were reassessed using criteria of the American College of Medical Genetics and Genomics (ACMG). A structured medical interview was performed with all available individuals, their parents, and/or their physicians. For each patient, HNF1B score was calculated based on available clinical information. Results: The study group numbered 36 unrelated probands (28% lost to follow‐up): 14 with pathogenic or likely‐pathogenic variants in HNF1B, one with a variant of uncertain significance, and 21 negative for HNF1B mutations. Presence of cystic kidneys (OR = 9.17, 95% CI:1.87‐44.92), pancreatic abnormalities (OR = 15, 95% CI:1.55‐145.23), elevated liver enzymes (OR = 15, 95% CI:1.55‐145.23) best discriminated HNF1B‐positive cases from the negative ones. Presence of impaired glucose tolerance coupled with kidney disease in the proband and one parent was also highly predictive for HNF1B mutations (OR = 11.11, 95% CI:1.13‐109.36). HNF1B‐score with recommended cutoff distinguished patients with and without HNF1B findings with 100% sensitivity and 47.6% specificity. Addition of four clinical variables to select patients based on HNF1B score improved specificity to 71.4% (95% CI:47.8%‐88.7%) while retaining 100% sensitivity. Conclusions: Detailed medical interview may enable more accurate patient selection for targeted genetic testing. [ABSTRACT FROM AUTHOR]

Copyright of Pediatric Endocrinology, Diabetes & Metabolism is the property of Termedia Publishing House and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction. It remains unclear how HbA1c recommendations influence metabolic control of paediatric patients with type 1 diabetes mellitus. To evaluate this we compared reported HbA1c with guideline thresholds. Materials and Methods. We searched systematically MEDLINE and EMBASE for studies reporting on HbA1c in children with T1DM and grouped them according to targeted HbA1c obtained from regional guidelines. We assessed the discrepancies in the metabolic control between these groups by comparing mean HbA1c extracted from each study and the differences between actual and targeted HbA1c. Results. We included 105 from 1365 searched studies. The median (IQR) HbA1c for the study population was 8.30% (8.00%–8.70%) and was lower in “6.5%” than in “7.5%” as targeted HbA1c level (8.20% (7.85%–8.57%) versus 8.40% (8.20%–8.80%); p=0.028). Median difference between actual and targeted HbA1c was 1.20% (0.80%–1.70%) and was higher in “6.5%” than in “7.5%” (1.70% (1.30%–2.07%) versus 0.90% (0.70%–1.30%), resp.; p<0.001). Conclusions. Our study indicates that the 7.5% threshold results in HbA1c levels being closer to the therapeutic goal, but the actual values are still higher than those observed in the “6.5%” group. A meta-analysis of raw data from national registries or a prospective study comparing both approaches is warranted as the next step to examine this subject further. [ABSTRACT FROM AUTHOR]

Copyright of Pediatric Endocrinology, Diabetes & Metabolism is the property of Termedia Publishing House and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Pediatric Endocrinology, Diabetes & Metabolism is the property of Termedia Publishing House and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Monogenic diabetes are a heterogenic group of diseases with varied phenotypes. It is assumed that they may total up to 10% of all cases of diabetes. Diagnosis of these clinical conditions by an efficient selection of patients for genetic diagnostics may be problematic even for experienced diabetologists. Helpful information about selecting and directing patients for further examinations can be gained from guidelines created by diabetologic societies such as International Society of Pediatric and Adolescent Diabetes (ISPAD). This paper focuses on key aspects of these guidelines and elucidates crucial features of the clinical picture which can be used for differential diagnosis of diabetes. Among factors suggesting monogenic background of diabetes the most notable are: low daily insulin requirement (<0.5 U/kg), moderate hyperglycemia (5.5-8.5 mmol/l), positive familial history with a dominant pattern of inheritance, lack of immunologic markers typical for type I diabetes and presence of structural or functional abnormalities within other organs and systems. ISPAD guidelines however, are burdened by some inconsistencies, reflecting different screening and investigative approaches used by various authors. These incongruities have been resolved by the authors of this paper with added suggestions of how to implement relevant solutions in clinical practice. In this article current guidelines on the treatment of monogenic diabetes in children were also presented. Current therapeutic standards were taken into consideration as well as prospects for treatment of selected forms of monogenic diabetes. It will enable in the near future effective and causal treatment of genetic forms of diabetes in children. [ABSTRACT FROM AUTHOR]

Copyright of Pediatric Endocrinology, Diabetes & Metabolism is the property of Termedia Publishing House and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Pediatric Endocrinology, Diabetes & Metabolism is the property of Termedia Publishing House and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction: Recently the prevalence of overweight and obesity in pediatric population - also in type 1 diabetic adolescents - has increased. Aim of the study: Aim of the study was to evaluate prevalence of obesity and central obesity in type 1 diabetic youth. Material and methods: 192 patients (81 girls, 111 boys), aged 10-18 years, with diabetes duration 0.5-15 years were included into the study. The anthropometric parameters were examined. Obesity was recognized according to WHO definition: overweight - BMI 85-95 pc, obesity - BMI >95 pc and according to International Obesity Task Force (IOTF): overweight - BMI >IOTF 25 kg/m2, obesity - BMI >IOTF 30 kg/m2. Central obesity was defined as waist circumference above 90 percentile for sex and age and as waist/height rate (WHtR) >0.5. Local BMI and waist circumference percentiles charts were used. Results: According to WHO criteria overweight was found in 19 girls and 13 boys, obesity properly in 4 and 10, together in 28% and 20.9%. According to IOTF overweight was recognized in 21 girls and boys, obesity properly in 1 and 8, together in 29.3% and 26.4%. According to percentiles charts, central obesity was recognized in 21 girls (25.6%) and in 18 boys (16.4%), together in 20.3% patients. Using WHtR abdominal obesity was found in 7 girls (8.5%) and in 13 boys (11.8%), together in 10.3%. Conclusions: Irrespectively of adopted criteria, overweight/obesity was found in every fourth adolescent with type 1 diabetes. The prevalence of central obesity depends on the adopted criteria. According to local percentiles waist circumference charts, abdominal obesity was recognized twice more frequently than using WHtR. [ABSTRACT FROM AUTHOR]

The aims of the study were: 1. to evaluate the levels of insulin antibodies (IA) during the first 2 years of type 1 diabetes in children and adolescents, 2. to analyze relations between IA and several clinical and metabolic markers. Material and methods: Fifty seven patients (37 males and 20 females) aged 7.6-17.9 years (mean 13.2±2.4) participated in the study. Patients were treated with human insulins and/or with rapid acting human insulin analogs. During the 1st week after diabetes diagnosis, 6 months after diagnosis (N=57) and 24 months after diagnosis (N=42) the following parameters were studied: residual insulin secretion, daily insulin dose, HbA1c, BMI and insulin sensitivity. IA were measured by radioimmunoprecipitation (normal values <7%), C-peptide was measured by radioimmunoassay (the increase in C-peptide concentration 6 minutes after an intravenous injection of glucagon was measured, ΔC-pep). M index measured by euglycemic hyperinsulinemic clamp method by DeFronzo was the measure of insulin sensitivity (higher M index indicates higher insulin sensitivity). Results: Median values (and quartiles) of IA were: 6.7% (5.6-7.4), 16.6% (10.2-37.1) and 17.0% (9.4-38.9) respectively in the 1st week of diabetes and after 6 and 24 months of follow up. IA levels rose significantly during the first 6 months of diabetes (p<0.0001) and remained stable thereafter. After 6 months of diabetes duration the following statistically significant correlations were found: negative between IA and ΔC-pep (r=-0.36, p=0.007), positive between IA and M index (r=0.27, p=0.04) and negative between IA and BMI (ρ?=-0.4, p=0.02); a slight, statistically nonsignificant, correlation between IA and daily insulin dose was noted, too (r=0.19, p=0.16). After 24 months correlation coefficients were as follows: for IA and M index ρ?=0.16, p=0.32, for IA and ΔC-pep ?=-0.08, p=ns, for IA and BMI ρ?=-0.34, p=0.03. Conclusions: 1. Modern insulin preparations induce production of IA in young type 1 diabetic patients. 2. Patients with lower residual insulin secretion require higher daily insulin doses during the first months of diabetes, which may preclude higher IA production. 3. Negative correlation between IA and insulin resistance may be a) secondary to the well known correlation: lower BMI - higher insulin sensitivity or may be due to b) IA acting as a temporary "reservoir" of administered insulin or to c) hypoglycemic activity of IA-insulin complexes. [ABSTRACT FROM AUTHOR]

Introduction: Wolfram syndrome (WFS) is the most frequent syndromic form of monogenic diabetes coexisting with optic atrophy and many other disorders. The aim of this study was to estimate the prevalence of Wolfram syndrome among children with diabetes in Poland., Material and Methods: These calculations were performed among Polish diabetic children, aged 0-18 years, from three administrative regions between January 2005 and December 2011. Epidemiological data was obtained by matching the results from the EURO-WABBPoland Project and the PolPeDiab Registry., Results: Throughout the study period, we confirmed genetic diagnosis of Wolfram syndrome in 13 patients from Poland. Three patients originated from the studied regions with complete epidemiological data on paediatric diabetes. The total number of patients with diagnosed diabetes in the study equalled 2,568 cases. The prevalence of Wolfram syndrome among Polish children with diabetes is 0.12% (95% Confidence Interval 0.04-0.34%)., Conclusions: We estimate that Wolfram syndrome is: 26 to 35 times less frequent than monogenic diabetes (MODY and neonatal diabetes) in the Polish paediatric population.

Wolfram syndrome (WS), also known as DIDMOAD (Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness), is a rare autosomal recessive syndrome (1/770,000 in the United Kingdom), characterised by juvenile onset of diabetes mellitus, optic nerve atrophy, diabetes insipidus, sensorineural deafness, renal tract and neurological abnormalities, and primary gonadal atrophy. WS is caused mainly by biallelic mutations in the WFS1 gene, which encodes wolframin. Wide tissue distribution of wolframin and many mutations in the wolframin gene resulting in Wolfram syndrome may contribute to different phenotypes and the unusual combinations of clinical features. We describe a female patient with Wolfram syndrome diagnosed at the age of 25, with a previous false diagnosis of type 1 diabetes mellitus and misdiagnosed diabetic complications. The patient was found to be a compound heterozygote for two novel mutations in exon 8 of WFS1 gene: a 2-bp deletion AT at nt 1539 leading to a frameshift (Y513fs) and a single-base substitution 1174C > T resulting in a stop codon (Q392X). A detailed analysis of the patient's medical history and a review of the literature suggest that many cases of Wolfram syndrome may remain undiagnosed due to misdiagnosis as type 1 diabetes mellitus and incorrect interpretation of clinical symptoms of neurodegenerative abnormalities, especially in their early stages.

Introduction: Despite the progress in diagnosis and treatment of type 1 diabetes, diabetic ketoacidosis (DKA) is still a serious clinical problem. The aim of the study was too describe the epidemiology and clinical characteristic of DKA in children and adolescents with type 1 diabetes., Material and Methods: Medical records of 650 patients with type 1 diabetes who were under care of the Outpatient Clinic for Diabetic Children of the Medical University of Lodz from 1st January 2007 till 31 December 2009 were analysed., Results: 101 cases of DKA were reported; the incidence of DKA was 5.2/100 patients /year. Episodes of DKA occurred in 89 patients (39 girls and 50 boys). In 82 patients 1 episode of DKA was recorded, in 3 patients - 2 episodes, in 3 patients - 3 episodes and in 1 patient - 4 episodes. 58.4% (59/101) of DKA episodes occurred in patients with newly diagnosed diabetes (mean age: 8.04-4.78 years) and 41.6% (42/101) - in children with established type 1 diabetes (mean age: 13.3-3.37). DKA was diagnosed in 26,1% of children with new onset of the disease. The most frequent causes of DKA in patients with established type 1 diabetes were noncompliance (22/42) and acute infectious diseases (12/42). Severe DKA was diagnosed in 19/101 episodes, moderate - in 36/101 and mild - in 46/101. No lethal complication of DKA was recorded. The following complications of DKA were observed: dyselectrolitemia (68/101), acute pancreatitis (5/101), gastrorrhagia (1/101), insulin oedema (1/101). Mean duration of hospitalization was 12.03-5.58 days., Conclusions: Newly diagnosed type 1 diabetes is the main cause of DKA in children and adolescents.In established type 1 diabetes the most frequent cause of DKA is poor quality of self-management. Dyselectrolitemia is the most frequent complication of DKA in children. Acute pancreatitis should be considered in a young patient with DKA.

Introduction: Recent studies on the pathogenesis of type 1 diabetes (T1DM) show that autoimmune activity in human pancreatic 1-cells is accompanied by abnormalities of fatty tissue metabolism, which is the underlying process in type 2 diabetes.The aim of the study was to determine the correlation between C-peptide concentration, indicating residual insulin secretion, and free fatty acids (FFA) level in children with T1DM., Material and Methods: We recruited 178 diabetic patients (mean age 10.8 years; M/F 99/79). In all individuals the fasting C-peptide by a radioimmunological method and FFA serum levels using an enzymatic colorimetric method were measured at the onset and after 6 months of the diabetes duration., Results: Thirty four (19.1%) of the patients had the C-peptide level above the lower limit of normal range (>0.28 pmol/ml) at both time points. FFA level at onset was significantly higher as compared to the level after 6 months of follow-up (38.4+29.4 vs. 28.9 ± 23.1 mg/dl; p=0.0003). However, both values were positively correlated (r=0.31; p=0.0008). Interestingly, a negative correlation was found between FFA and C-peptide measurements at onset (r=-0.19; p=0.01) and at 6th month of the disease (r=-0.18; p=0.02). Moreover, when the C-peptide level was treated as a binominal variable(above and below 0.28 pmol/ml) higher levels of FFA were observed in children with C-peptide deficiency at onset of diabetes (41.1 vs. 29.9 mg/dl; p=0.03) and a similar trend was noticed at 6th month of the disease (31.0 vs. 23.7 mg/dl; p=0.1). No relation of FFA with age at onset, gender,insulin requirement and HbA1c were revealed., Conclusions: The obtained results, which link the FFA level with residual insulin secretion in T1DM,may serve as further evidence supporting the contribution of fatty tissue metabolism in the patho-genesis of T1DM.

Introduction: A clinical criterion of the Wolfram syndrome is the coexistence of diabetes and optic atrophy recognized before the age of 15. Diabetes present in Wolfram syndrome is a result of the selective β cell loss and failed insulin secretion which is probably associated with non-autoimmune pathogenesis., Aim of the Study: The aim of the study was an evaluation of HLA subtypes and presence of β-cell autoantibodies in patients with molecularly confirmed Wolfram syndrome., Material and Methods: 9 patients with Wolfram syndrome aged 10-24 years were examined. We also studied 218 patients with type 1 diabetes as a reference group. A control group of 176 healthy individuals was included in the study. Besides the clinical assessment the HLA typing by PCR-SSO was performed. Islet cell antibodies (ICA), antibodies to glutamic acid decarboxylase (GADA), thyrosine phosphatase antibodies (IA2A) and insulin antibodies (IAA) were also detected., Results: In all nine patients the coexistence of diabetes with optic atrophy was observed and in 8/9 individuals additional symptoms were recognized. In patients with Wolfram syndrome a significantly lower age of diagnosis of diabetes (Me=5.0 years) than in type 1 diabetic children (Me=10.4; p=0.002) was observed. Studies of HLA subtypes demonstrated an increased prevalence of HLA-DQw1, DRB1⋅03 and/or 04 and DR2. A comparison of the frequency of the HLA alleles in patients with Wolfram syndrome with type 1 diabetic children showed a more frequent presence of the DRB1⋅1501 (p=0.03; OR=13.28 (2.44-72.12)) and DQB1⋅06 (p=0.016; OR=10.15 (2.49-41.35)) alleles in patients with Wolfram syndrome., Conclusions: Polish patients with Wolfram syndrome have a different profile of the HLA antigens with the presence of DR2, DQw1 and DRB3/4 allele and are negative for diabetes-related autoantibodies, which may confirm non-autoimmune β-cell destruction in this syndrome.

Introduction: The pathogenesis of type 1 diabetes is connected with immune-mediated beta-cell destruction leading to insulin deficiency. The majority of patients will become completely incapable of insulin secretion within a few years, however, some individuals will have persistent beta-cell function years after the diagnosis of diabetes. Despite clinical symptoms of insulin deficiency, residual beta-cell secretion can modify the clinical course and can be an independent factor influencing the delay of development of chronic diabetic complications. The aim of the study was to compare a 10-year clinical course in children with type 1 diabetes with and without preserved beta-cell secretion., Material and Methods: 72 children and adolescents with diabetes lasting for minimum 10 years and available biological material to c-peptide evaluation (3-4 years and 10 years from the onset of diabetes) were chosen from 768 children with type 1 diabetes. We assessed fasting c-peptide and recruited 23 out of 72 patients whose concentration of c-peptide was below or over 0.23 ng/ml at all time points (this cut point derives from the definition of preserved beta-cell function according to DCCT). Afterwards we divided children into two subgroups: A (n=13) - without insulin secretion and B (n=10) - with preserved beta-cell function during 10 years of observation. We assessed markers of beta-cell autoimmunity (ICA, GADA, IA2, IAA) in the examined groups. Insulin requirement and concentration of glycated hemoglobin (assessed as the year mean from four measurements in each year) were compared between group A and B., Results: The age at onset of diabetes in children from both examined groups was similar. All children from group B and 12/13 from group A were positive for at least one type of the screened autoantibodies. There was no difference in insulin requirement between the groups (p=0.6). The level of glycated hemoglobin was significantly lower in group B during a 10-year observational period (p=0.04)., Conclusion: Repeated measures of c-peptide can enable us to define two groups of patients with immune-mediated diabetes with different levels of disease and metabolic control.

The most frequent form of diabetes in the childhood is type 1 diabetes. Moreover, the rare forms of diabetes have been also identified in children. Besides of neonatal diabetes caused by the mutations in KCNJ11, SUR1 and GCK genes, other forms of monogenic diabetes are associated with different chronic disorders. These rare forms of syndromic diabetes are related to mutations in genes which lead to Wolfram syndrome, Alström syndrome, Wolcott-Rallison syndrome or Roger's/TRMA syndrome. In this paper we discuss the clinical features of rare syndromic forms of monogenic diabetes, which gave suggestions on pathogenic mechanism of the diagnosed diabetes in childhood. This may be helpful for appropriate classification of the epidemiological, clinical and genetic data. It may be useful in the future to the form of the Polish National Survey of rare syndromic forms of monogenic diabetes in childhood.

The Aim: of this study was the evaluation of some factors having an influence on post-exercise albuminuria level in children with newly diagnosed type 1 diabetes as a prognostic factor of developing nephropathy., Material and Methods: 24 newly diagnosed type 1 diabetic children, aged 5.5-16.9 years, mean 10.2+/-3.2, were examined. In order to provoke albuminuria the patients underwent standardized exercise test using treadmill ramp according to the Bruce protocol. Pre- and post-exercise albuminuria and C-peptide levels by radioimmunoassay were evaluated. In urine of patients the albumin / creatinine ratio (ACR) was determined., Results: the tendency towards an increase in ACR ratio in children after exercise (10.5 mg/g (4-27.5) in comparison to the value in pre-exercise urine (7 mg/g (2.5-13), p=0.17) was observed. In 67% of patients (16/24) the ACR ratio was higher in post-exercise urine. In 25% of children (6/24) the ACR ratio was above 30 mg/g which was considered as post-exercise microalbuminuria. Next, parameters of metabolic control of type 1 diabetes were compared between patients with and without post-exercise microalbuminuria. No differences in the serum glucose, HbA1c, BMI, triglycerides, total cholesterol, insulin dose, frequency of ketoacidosis and C-peptide level between these groups of children were noted., Conclusions: we concluded that the post-exercise microalbuminuria as a marker of diabetic nephropathy risk may be observed in some patients already at the clinical onset of type 1 diabetes but further evaluation is needed to verify this hypothesis.