title: Genetic polymorphisms and the risk of progressive renal failure in elderly Hungarian patients.
abstract: The relationship between renal disease progression and genetic polymorphism of enzymes influencing endothelial function remains incompletely understood. We genotyped three cohorts of elderly Hungarian patients: 245 patients with end-stage renal disease (ESRD) on chronic hemodialysis (HD), 88 patients with mild chronic kidney disease (CKD), and 200 healthy controls. The underlying diagnoses of renal diseases were primary glomerulonephritis, interstitial nephritis, hypertension, diabetic nephropathy, and hereditary diseases. We examined genetic polymorphisms of eight candidate genes associated with endothelial function: endothelial constitutive nitric oxide synthase (ecNOS) T-786C, endothelin-1 G5727T, methylenetetrahydrofolate reductase (MTHFR) C677T, paraoxonase-1 Q192R and M55L, angiotensinogen M235T, angiotensin-converting enzyme (ACE) I/D and angiotensin II type 1 receptor A1166C gene. Six gene polymorphisms were detected by real-time polymerase chain reaction with melting-point analysis, and two via allele-specific amplification and gel electrophoresis. Control group patients were in Hardy-Weinberg equilibrium for all tested genotypes. In ESRD patients attributed to hypertension, the endothelin gene G5727T GG genotype occurred significantly less but GT genotype more frequently (P < 0.01 for both). In ESRD patients attributed to primary glomerulonephritis, more ACE DD and less ID genotypes were found (P < 0.02 for both) than in the controls. The underlying diagnosis may modify the association of genetic polymorphism and dialysis-dependent ESRD.
authors: Szent Rókus Kórház Nephrológia Ambulancia, Baja, Hungary.
authors: Marianna
authors: M
authors: Zsom
authors: Tibor
authors: T
authors: Fülöp
authors: Lajos
authors: L
authors: Zsom
authors: Akos
authors: A
authors: Baráth
authors: Zoltán
authors: Z
authors: Maróti
authors: Emoke
authors: E
authors: Endreffy
mesh_terms: D000328:Adult; D043303:Aryldialkylphosphatase / Q000235:genetics; D019332:Endothelin-1 / Q000235:genetics; D005260:Female; D006801:Humans; D006814:Hungary / Q000453:epidemiology; D007676:Kidney Failure, Chronic / Q000235:genetics* / Q000401:mortality / Q000628:therapy*; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000235:genetics; D008875:Middle Aged; D052250:Nitric Oxide Synthase Type III / Q000235:genetics; D007703:Peptidyl-Dipeptidase A / Q000235:genetics; D011110:Polymorphism, Genetic; D006435:Renal Dialysis; D012307:Risk Factors
chemical_list: D019332:Endothelin-1; C496314:NOS3 protein, human; D052250:Nitric Oxide Synthase Type III; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D043303:Aryldialkylphosphatase; C468406:PON1 protein, human; C488034:ACE protein, human; D007703:Peptidyl-Dipeptidase A