Socio-economic factors influencing the development of end-stage renal disease in people with Type 1 diabetes - a longitudinal population study.

AIMS: The development of end-stage renal disease (ESRD) in Type 1 diabetes is multifactorial. Familial socio-economic factors may influence adherence to and understanding of diabetes treatment, and also general health behaviour. We investigate how parental and personal education level and exposure to low economic status, indicated by the need for income support, influence the development of ERSD caused by Type 1 diabetes. METHODS: Participants were retrieved from the nationwide Swedish Childhood Diabetes Registry, which was linked to the Swedish Renal Registry, to find people with ESRD caused by Type 1 diabetes, and to Statistic Sweden to retrieve longitudinal socio-economic data on participants and their parents. Data were analysed using Cox regression modelling. RESULTS: Of 9287 people with diabetes of duration longer than 14 years, 154 had developed ESRD due to diabetes. Median diabetes duration (range) for all participants was 24.2 years (14.0-36.7 years). Low maternal education (≤ 12 years) more than doubled the risk of developing ESRD, hazard ration (HR) = 2.9 [95% confidence interval (95% CI): 1.7-4.8]. For people with a low personal level of education HR was 5.7 (3.4-9.5). In an adjusted model, the person's own education level had the highest impact on the risk of ESRD. If at least one of the parents had ever received income support the HR was 2.6 (1.9-3.6). CONCLUSIONS: Socio-economic factors, both for the parents and the person with diabetes, have a strong influence on the development of ESRD in Type 1 diabetes. It is important for caregivers to give enough support to more vulnerable people and their families.

The V16A polymorphism in SOD2 is associated with increased risk of diabetic nephropathy and cardiovascular disease in type 1 diabetes.

AIMS/HYPOTHESIS: Hyperglycaemia increases oxidative stress and may thereby increase the risk of diabetic complications, including diabetic nephropathy. Cells are protected from oxidative damage by, for example, the manganese superoxide dismutase enzyme (MnSOD), but the functional polymorphism V16A affects the localisation of MnSOD and therefore its ability to scavenge superoxide radicals. In a Danish cohort of type 1 diabetes patients, we sought to confirm previous findings of association between the V allele and the risk of diabetic nephropathy and to investigate the influence of this polymorphism on the development of cardiovascular disease. METHODS: Type 1 diabetes patients attending the Steno Diabetes Center, Gentofte, Denmark, between 1993 and 2001 were enrolled in this study. A total of 441 cases with diabetic nephropathy (albumin excretion > or =300 mg/24 h) and 314 controls with persistent normoalbuminuria (<30 mg/24 h), despite diabetes of duration > or =20 years, were identified. The median duration of diabetes was 35 years (range 12-73 years). RESULTS: We confirmed the significant association between carrier status of the V allele and diabetic nephropathy. The association was independent of age at diabetes onset, HbA(1c), sex, smoking and diabetes duration (OR 1.7, 95% CI 1.2-2.4). The VV and AV genotypes considered together also predicted the risk of cardiovascular disease, independently of age at follow-up, HbA(1c), sex, smoking, systolic blood pressure, cholesterol and nephropathy status. The hazard ratio was 1.6 (95% CI 1.0-2.5). CONCLUSIONS/INTERPRETATION: The MnSOD V16A polymorphism is involved in the development of nephropathy caused by type 1 diabetes and seems to predict cardiovascular disease during follow-up.

Hospitalization for vascular complications in childhood onset type 1 diabetes--effects of gender and age at onset.

AIMS: To study the cumulative incidence of hospitalization for severe diabetic vascular complications in childhood onset type 1 diabetes patients with special regards to age at onset and gender. METHODS: The Swedish Childhood Diabetes Register (SCDR) was linked to the Swedish Hospital Discharge Register up to 31 December 2004. The following diagnoses were traced: diabetic kidney disease, myocardial infarction, stroke, lower limb arterial disease and diabetes with multiple complications. Cox proportional hazards survival method was applied with the following covariates: maternal age, birthweight deviation from gestational week standard, age at onset and gender. RESULTS: Until 31 December 9974 children had been followed for at least 10 years corresponding to 141 839 person years at risk and 103 (7.3 per 1000 person years) had been hospitalized at least once at the maximum duration of follow-up of 26 years. Diabetic kidney disease was the most common cause of hospitalization and 63 patients had more than one diabetic complication. Female gender (RR=2.02, 95% CI=1.05-3.89) and age at onset of diabetes (RR=1.37, 95% CI=1.20-1.56) were significant risk factors for severe complication. CONCLUSIONS: Hospitalization for severe diabetic complications at a maximum follow-up of 26 years is rather low in Sweden. There is a higher hospitalization rate among females than among males, and also among patients diagnosed with diabetes after 10 years of age than among patients diagnosed before the age of 10 years.

Genetic influences of the intercellular adhesion molecule 1 (ICAM-1) gene polymorphisms in development of Type 1 diabetes and diabetic nephropathy.

AIM: The intercellular adhesion molecule-1 (ICAM-1) gene is located on chromosome 19p13, which is linked to Type 1 diabetes (T1D). ICAM-1 expression is related to development of T1D and diabetic nephropathy. The present study aims to evaluate the genetic influence of ICAM-1 gene polymorphisms on the development of T1D and diabetic nephropathy. METHODS: Five valid single nucleotide polymorphisms (SNPs) were genotyped in 432 T1D patients (196 patients had diabetic nephropathy) and 187 non-diabetic control subjects by using dynamic allele-specific hybridization (DASH) and pyrosequencing. RESULTS: SNPs rs281432(C/G) and rs5498 E469K(A/G) had high heterozygous indexes. They were significantly associated with T1D [P = 0.026, OR = 1.644 (95% CI 1.138-2.376) and P < 0.001, OR = 2.456 (1.588-3.8)]. Frequencies of the C allele in SNP rs281432(C/G) and the A allele in SNP rs5498 E469K(A/G) increased stepwise from non-diabetic control subjects to T1D patients without diabetic nephropathy and T1D patients with diabetic nephropathy. Further analysis for these two SNPs indicated that T1D patients had increased frequency of the common haplotype C-A, in comparison with non-diabetic control subjects (38.1 vs. 32.1%, P = 0.035). CONCLUSION: The present study provided evidence that SNPs rs281432(C/G) and rs5498 E469K(A/G) in the ICAM-1 gene confer susceptibility to the development of T1D and might also be associated with diabetic nephropathy in Swedish Caucasians.

Higher intakes of fish protein are related to a lower risk of microalbuminuria in young Swedish type 1 diabetic patients.

OBJECTIVE: To examine the influence of dietary intake from various protein and fat sources on the occurrence of microalbuminuria in type 1 diabetic patients. RESEARCH DESIGN AND METHODS: In this nested case control study, 1,150 patients with diabetes duration >5 years reported dietary habits for the previous 12 months and submitted urinary samples for the analysis of albumin excretion rate (AER). A total of 75 cases of albuminuria (overnight AER > or = 15 microg/min) were identified and compared with 225 duration-matched control subjects. RESULTS: Neither mean protein, fat intake, average fish protein intake (control subjects 4.56 +/- 3.83 g/day and cases 3.82 +/- 2.87 g/day; P = 0.12), nor intake of meat and vegetable protein differed between the cases of albuminuria and the control subjects. High consumers of fish protein (greater than the 75th percentile) (12 cases and 63 control subjects, mean intake 9.35 g fish protein/day, i.e., approximately 53 g fish/day) had lower odds ratios (ORs) for microalbuminuria than individuals consuming less fish protein (mean 2.72 g/day) (crude OR 0.49 and 95% CI 0.25-0.97). When adjusted for known confounding factors, such as HbA1c, mean arterial pressure, diabetes duration, age, sex, smoking, BMI, country region, and total energy, individuals with a high intake of fish protein and fish fat showed a reduction in the risk for microalbuminuria (OR 0.22 and 0.31, respectively; 95% CI 0.09-0.56 and 0.13-0.76, respectively). When fish protein and fat were adjusted for each other, a high intake of fish protein but not of fish fat was still significantly associated with a decrease in the risk for microalbuminuria. CONCLUSIONS: Total protein and fat intake were not associated with the presence of microalbuminuria, but a diet including a high amount of fish protein seemed to lessen the risk.