PROGRESION DE LA POLIQUISTOSIS RENAL AUTOSOMICA DOMINANTE Influencia de polimorfismos de genes de sintasa endotelial del óxido nítrico (ecNOS) y del sistema renina-angiotensina *

88 ADPKD patients, GFRd was assessed by 1/S Cr and compared with the association to AT1A1166C (AT1R), AGTM235T (angiotensinogen) and ecNOSGlu298Asp (NO endothelial synthase) polymorphisms. Age at S Cr values of 2 and 6 mg/dl were assumed as beginning of progressive phase (A2) and end-stage-renal disease (A6), respec- tively. 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 consid- ered, two populations were defined (≤ and > 55 years). In ≤ 55 (assumed as PKD1 phenotype) (n=42), A 2 and A 6 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). A 2 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 A 2 and A6 whereas AGT 235TT induce twofold increase in GFRd, suggesting that RAS and ecNOS are involved in ADPKD progression.