scholarly journals An IGF-I gene polymorphism modifies the risk of developing persistent microalbuminuria in type 1 diabetes

2007 ◽  
Vol 156 (1) ◽  
pp. 83-90 ◽  
Author(s):  
Peter Hovind ◽  
Steven Lamberts ◽  
Wim Hop ◽  
Jaap Deinum ◽  
Lise Tarnow ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Gene Polymorphism ◽  
Urinary Albumin Excretion ◽  
Excretion Rate ◽  
Albumin Excretion Rate ◽  
Wild Type ◽  
Variant Type ◽  
Igf I

Objective: Derangements of the GH–IGF-I axis have been associated with microalbuminuria (MA) in type 1 diabetes. The aim of this study was to investigate whether an IGF-I gene promoter polymorphism influenced the development of persistent MA in type 1 diabetes. Design: A prospective follow-up study of a cohort of 277 patients with newly diagnosed type 1 diabetes consecutively enrolled between September 1979 and August 1984. Methods: Urinary albumin excretion rate over 24 h was measured in each patient at least once a year. Persistent MA was defined as a urinary albumin excretion rate between 30 and 300 mg/24 h. Results: During a median follow-up of 18.0 years (range 1.0–21.5), 79 of 277 patients developed persistent MA. IGF-I gene genotype was available for 216 subjects; in 73% of the subjects, the wild-type genotype of this IGF-I gene polymorphism was present, while 27% had the variant type. At baseline, there were no differences in IGF-I levels and HbA1c values between subjects with the wild type and subjects with variant type. By Kaplan–Meier analysis, subjects with the variant type of this polymorphism had during follow-up a higher risk of development of MA compared subjects with the wild type (P = 0.03). Conclusions: Subjects with the variant type of an IGF-I gene polymorphism had a significantly increased risk of developing MA. This risk was not mediated through changes in circulating IGF-I levels. Our study suggests that in type 1 diabetes, this IGF-I gene polymorphism is a risk factor of MA.

scholarly journals Angiotensin II type 1 receptor gene polymorphism could influence renoprotective response to losartan treatment in type 1 diabetic patients with high urinary albumin excretion rate

2010 ◽  
Vol 67 (4) ◽  
pp. 273-278 ◽  
Author(s):  
Tamara Dragovic ◽  
Boris Ajdinovic ◽  
Rajko Hrvacevic ◽  
Vesna Ilic ◽  
Zvonko Magic ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Gene Polymorphism ◽  
Urinary Albumin Excretion ◽  
Excretion Rate ◽  
Albumin Excretion Rate ◽  
Urinary Albumin Excretion Rate ◽  
Filtration Fraction ◽  
Investigation Period ◽  
Losartan Treatment

Background/Aim. Diabetic nephropathy (DN) is a clinical syndrome characterized by persistent albuminuria, increasing arterial blood pressure and progressive decline in glomerular filtration rate (GFR). When persistent albuminuria is established, antihypertensive treatment becomes most important factor in slowing the progression of diabetic glomerulopathy. The aim of this study was to examine if renoprotective response to a short-term losartan therapy depends on 1166 A/C gene polymorphism for its target receptor. Method. The study included 35 patients with diabetes mellitus type 1 and persistently high urinary albumin excretion rate (UAE: > 30 mg/24 h), genotyped for the 1166 A/C gene polymorphism for the angiotensin II type 1 receptor (AT1R). The participants were segregated into 3 genotype groups according to combinations of A or C allele: AA(16%), AC(15%) and CC(11%). The patients received losartan 50 mg daily for 4 weeks, following 100 mg daily for another 8 weeks. At baseline and after 12 weeks of the treatment period UAE, blood pressure, GFR and filtration fraction (FF) were determined. Results. After 12 weeks of the treatment with losartan, albuminuria was reduced from baseline by 9% [95% confidence interval (CI): 1-17, p = 0.039] in the AA genotype, and by 11% (95% CI: 6-17, p = 0.0001) in the AC genotype. Losartan treatment reduced albuminuria in the CC group by 5% (95%CI: -13-22, p = 0.47). Glomerular filtration rate remained unchanged in all genotype groups. Filtration fraction was significantly reduced from baseline by 0.018 ? 0.024 (p = 0.012) only in the AC genotype. In the AA genotype, FF was reduced from baseline by 0.017 ? 0.03 (p = 0.052), and in the CC genotype by 0.01 ? 0.008 (p = 0.092). In the AA group, systolic blood pressure declined from 136 ? 24 mmHg at baseline, to an average of 121 ? 18 mmHg at the end of the study (p = 0.001). The AC group achived reduction from 131 ? 10 mmHg at baseline to 115 ? 7 mmHg (p = 0.001) during the investigation period. In the AA genotype group losartan reduced diastolic blood pressure from 86 ? 13 mmHg at baseline to 78 ? 8 mmHg (p = 0.004), and in the AC genotype from 88 ? 5 mmHg at baseline to 11.7 ? 5.6 mmHg during the investigation period (p = 0.001). In the CC genotype diastolic blood pressure reduction remained nonsignificant (p = 0.066). Conclusion. The results of our small sample size study provide the evidence that 1166 A/C AT1R polymorphism could be associated with the renoprotective response to losartan therapy.

Genome-wide association study of urinary albumin excretion rate in patients with type 1 diabetes

Diabetologia ◽  
2014 ◽  
Vol 57 (6) ◽  
pp. 1143-1153 ◽  
Author(s):  
Niina Sandholm ◽  
◽  
Carol Forsblom ◽  
Ville-Petteri Mäkinen ◽  
Amy Jayne McKnight ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Genome Wide Association Study ◽  
Urinary Albumin Excretion ◽  
Excretion Rate ◽  
Albumin Excretion Rate ◽  
Urinary Albumin ◽  
Genome Wide Association ◽  
Urinary Albumin Excretion Rate ◽  
Genome Wide

scholarly journals Body Mass Index and Mortality in Individuals With Type 1 Diabetes

2019 ◽  
Vol 104 (11) ◽  
pp. 5195-5204 ◽  
Author(s):  
Emma H Dahlström ◽  
Niina Sandholm ◽  
Carol M Forsblom ◽  
Lena M Thorn ◽  
Fanny J Jansson ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Excretion Rate ◽  
Albumin Excretion Rate ◽  
Normal Weight ◽  
Onset Age ◽  
Diabetes Onset ◽  
Risk Of Mortality ◽  
The Relationship ◽  
Normal Albumin

Abstract Context The relationship between body mass index (BMI) and mortality may differ between patients with type 1 diabetes and the general population; it is not known which clinical characteristics modify the relationship. Objective Our aim was to assess the relationship between BMI and mortality and the interaction with clinically meaningful factors. Design, Setting, and Participants This prospective study included 5836 individuals with type 1 diabetes from the FinnDiane study. Main Outcome Measure and Methods We retrieved death data for all participants on 31 December 2015. We estimated the effect of BMI on the risk of mortality using a Cox proportional hazards model with BMI as a restricted cubic spline as well as effect modification by adding interaction terms to the spline. Results During a median of 13.7 years, 876 individuals died. The relationship between baseline BMI and all-cause mortality was reverse J-shaped. When analyses were restricted to those with normal albumin excretion rate, the relationship was U-shaped. The nadir BMI (BMI with the lowest mortality) was in the normal weight region (24.3 to 24.8 kg/m2); however, among individuals with diabetic nephropathy, the nadir BMI was in the overweight region (25.9 to 26.1 kg/m2). Diabetic nephropathy, diabetes-onset age, and sex modified the relationship between BMI and mortality (Pinteraction < 0.05). Conclusions Normal weight is optimal for individuals with type 1 diabetes to delay mortality, whereas underweight might be an indication of underlying complications. Maintaining normal weight may translate into reduced risk of mortality in type 1 diabetes, particularly for individuals of male sex, later diabetes-onset age, and normal albumin excretion rate.

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