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.
Copyright 2002 by the National Kidney Foundation, Inc.