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Medicina (Buenos Aires)

versión On-line ISSN 1669-9106

Resumen

AZURMENDI, Pablo et al. Glomerular filtration rate decline in autosomic dominant polycystic kidney disease. Influence of endothelial NO synthase (ecNOS) and renin angiotensin system gene polymorphisms. Medicina (B. Aires) [online]. 2004, vol.64, n.2, pp. 139-142. ISSN 1669-9106.

Glomerular filtration rate decline (GFRd) is variable in autosomic dominant polycystic kidney disease (ADPKD). In 88 ADPKD patients, GFRd was  assessed by 1/SCr  and compared with the association to AT1A1166C (AT1R), AGTM235T (angiotensinogen) and ecNOSGlu298Asp (NO endothelial synthase) polymorphisms. Age at SCr values of 2 and 6 mg/dl were assumed as beginning of  progressive phase (A2) and end-stage-renal disease (A6), respectively. Polymorphisms were studied by PCR-RFLP. The group as a whole showed GFRd (ml/min/year) of  6.9±0.5; A2 and A6 of 48.9±1.3 and 55.0±1.4 years and mean arterial pressure of 111.2±1.2 mmHg. When A6 was considered, two populations were defined (£ and > 55 years). In £ 55 (assumed as PKD1 phenotype) (n=42), A2 and A6 of the AT11166CC genotype were 36.0±1.2 and 41.4±0.9 years vs AA-AC (42.8±1.0 and 47.5±0.8, p<0.001). A2 and A6 of the ecNOS298Asp/Asp genotype were 34.8±1.5 and 41.1±0.6 years vs. Glu/Glu-Glu/Asp (42.4±0.9 and 47.1±0.8, p<0.02). In AGT235TT genotype, GFRd was 12.4±2.2 ml/min/year vs MM-MT (7.9±0.7, p<0.03). This difference was also observed when all ADPKD patients were considered (TT: 11.02±1.5 vs. MM-MT: 6.44±0.5 ml/min/year, p<0.003). AT1 1166CC and ecNOS 298Asp/Asp are associated with earlier A2 and A6 whereas AGT 235TT  induce twofold increase in GFRd, suggesting that RAS and ecNOS are involved in ADPKD progression.

Palabras llave : GFR decline; ADPKD; AT1A1166C; AGTM235T; ecNOSGlu298Asp.

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