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  • 1
    ISSN: 1432-0428
    Keywords: Keywords Renin-angiotensin system genes, glycaemic control, diabetic nephropathy, Type I diabetes.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Reports on a putative synergism between poor glycaemic control and carriage of the angiotensin II type 1 receptor (AGTR1) C1166-allele and risk of diabetic nephropathy have been conflicting. Therefore, we investigated the interaction between long-term glycaemic control and three polymorphisms in the genes coding for AGTR1 (A1166→C), angiotensin converting enzyme (ACE/ID) and angiotensinogen (M235T) on risk of developing diabetic nephropathy. Furthermore, we investigated the relation between a random measurement and long-term measurements of haemoglobin A1 c (HbA1 c).¶Methods. We studied Caucasian patients with Type I (insulin-dependent) diabetes mellitus and nephropathy (120 men 74 women, age 41.1 ± 9.6 years, diabetes duration 28 ± 8 years) and long-standing Type I diabetic patients with persistent normoalbuminuria (112 men 69 women, age 42.5 ± 10.0 years, diabetes duration 27 ± 9 years). Genotyping was PCR-based and metabolic control estimated from all measurements of HbA1 c done in each patient [average (range) n = 31 (6–74)]. The median observation time (range) was 13.5 (2–14) years.¶Results. Type I diabetic patients with a history of poor glycaemic control (HbA1 c above the median, 8.7 %) had an increased risk of diabetic nephropathy compared with patients with a better metabolic control, OR (95 % CI): 9.2 (5.8–14.7). The magnitude of this risk was similar in carriers and non-carriers of the mutations. The risk of nephropathy in patients with HbA1 c above compared with below the median in carriers of the mutant C1166-allele, D-allele, or T235-allele were 7.6 (95 % CI: 3.9–14.8), 10.4 (6.0–17.8) and 9.8 (5.4–17.9), respectively. A significant correlation (r = 0.74, p 〈 0.001) existed between a random and long-term measurements of HbA1 c with a small mean difference (limits of agreement) [0.2 (–1.8 to 2.1) %] between the two estimates.¶Conclusion/interpretation. Poor metabolic control is a major risk factor for diabetic nephropathy in Caucasian Type I diabetic patients. This risk was similar in carriers and non-carriers of the mutant alleles of the AGTR1(A1166→C), ACE/ID and angiotensinogen-M235T polymorphisms. The HbA1 c value measured at random reflects rather closely average long-term HbA1 c values. [Diabetologia (2000) 43: 794–799]
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Complement activation and inflammation have been suggested in the pathogenesis of diabetic vascular lesions. We investigated serum mannose-binding lectin (MBL) levels and polymorphisms in the MBL gene in type 1 diabetic (T1DM) patients with and without diabetic nephropathy and associated macrovascular complications. Polymorphisms in the MBL gene and serum MBL levels were determined in 199 T1DM patients with overt nephropathy and 192 T1DM patients with persistent normoalbuminuria matched for age, sex and duration of diabetes as well as in 100 healthy control subjects. The frequencies of high and low expression MBL genotypes were similar in patients with T1DM and healthy controls. High MBL genotypes were significantly more frequent in diabetic patients with nephropathy than in the normoalbuminuric group, and the risk of having nephropathy, given a high MBL genotype, assessed by odds ratio was 1.52 (1.02–2.27), P = 0.04. Median serum MBL concentrations were significantly higher in patients with nephropathy than in patients with normoalbuminuria [2306 µg/l (IQR 753–4867 µg/l) versus 1491 µg/l (IQR 577–2944), P = 0.0003], and even when comparing patients with identical genotypes, serum MBL levels were higher in the nephropathy group than in the normoalbuminuric group. Patients with a history of cardiovascular disease had significantly elevated MBL levels independently of nephropathy status [3178 µg/l (IQR 636–5231 µg/l) versus 1741 µg/l (IQR 656–3149 µg/l), P = 0.02]. The differences in MBL levels between patients with and without vascular complications were driven primarily by pronounced differences among carriers of high MBL genotypes (P 〈 0.0001). Our findings suggest that MBL may be involved in the pathogenesis of microvascular and macrovascular complications in type 1 diabetes and that determination of MBL status might be used to identify patients at increased risk of developing these complications.
    Type of Medium: Electronic Resource
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