There is evidence that type 1 plasminogen activator inhibitor (PAI-1) may have an important role in peritoneal function. We studied the effect of physiologically relevant PAI-1 promotor polymorphisms on peritoneal permeability. We performed a standard peritoneal equilibration test (PET) in 100 new continuous ambulatory peritoneal dialysis (CAPD) patients. We studied another 48 prevalent CAPD patients who had a baseline PET performed 2 years before; a standard PET was repeated on enrollment. The PAI-1 promotor polymorphism was examined. All patients then were followed up for 16.7 +/- 15.0 months. Prevalences of 4G/4G, 4G/5G, and 5G/5G genotypes were 31.8%, 46.6%, and 21.6%, respectively. Of the 100 new CAPD patients, there was no difference in net ultrafiltration (UF), dialysate-plasma (D/P) creatinine ratio at 4 hours, or mass transfer area coefficient (MTAC) of creatinine among the three genotype groups. D/P creatinine ratios at 4 hours were 0.595 +/- 0.133, 0.607 +/- 0.137, and 0.627 +/- 0.142 for the 4G/4G, 4G/5G, and 5G/5G groups, respectively (one way analysis of variance, P = 0.715). Of the 48 prevalent patients, PAI-1 genotype did not affect the longitudinal change in net UF, D/P creatinine ratio at 4 hours, or MTAC of creatinine. During follow-up, 16 patients developed peritonitis episodes that required Tenckhoff catheter removal. One patient died, 8 patients returned to long-term CAPD therapy after peritonitis resolved, and the other 7 patients developed peritoneal failure and were switched to long-term hemodialysis therapy. PAI-1 promotor genotype did not predict peritoneal failure after an episode of severe peritonitis (chi-square test, P = 0.328). We conclude that PAI-1 promotor polymorphism is not associated with peritoneal transport characteristics in stable peritoneal dialysis patients, longitudinal change in peritoneal transport, or development of peritoneal failure after an episode of severe peritonitis.

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