Correlations between Plasminogen Activator Inhibitor-1 and Peritoneal Transport in Pediatric Ccpd Patients

Abstract

Plasminogen activator inhibitor-1 (PAI-1) is an important regulator of plasminogen activators and has been shown to be involved in the accumulation of extracellular matrix (ECM) in various tissues. Since peritoneal ECM is a resistance site for peritoneal transport, the production and release of PAI-1 in the peritoneum may affect the peritoneal transport of water and small solutes. The linear correlations between the dialysate PAI-1 levels and the variables of peritoneal transport during peritoneal equilibration tests (PET) were examined. A tertiary university hospital. Six stable pediatric patients (age 10.8 +/- 4 years) undergoing continuous cycler-assisted peritoneal dialysis were included. None. All data are mean +/- SD. There was a positive correlation between the infused volume and the net ultrafiltration (UF, 198 +/- 127 mL, r = 0.82, p < 0.05). The dialysate PAI-1 levels increased during the dwell time (2.44 +/- 2.23 ng/mL or 2.46 +/- 1.72 micrograms at 4 hours vs 0.04 +/- 0.1 ng/mL or 0.04 +/- 0.09 micrograms at 0 hour, p < 0.05). The saturation indices (dialysate/plasma ratio) of PAI-1 and albumin at 4 hours were 1.05 +/- 1.21 and 0.028 +/- 0.004, respectively. The changes from 0 hour dwell to 4 hour dwell in the dialysate PAI-1 concentration (PAI4-0, 2.4 +/- 2.2 ng/mL) or amount corrected to body surface area (APAI4-0/BSA, 2.61 +/- 2.11 micrograms/m2) negatively correlated with UF or UF/body surface area and positively correlated with the number of episodes of peritonitis. There was no correlation between PAI4-0,APAI4-0/BSA, or plasma PAI-1 concentration and the mass transfer coefficient and clearance of either urea or creatinine. The elevated PAI-1 level during the PET was likely from the local production and release of PAI-1. It had an inverse relationship with the amount of ultrafiltration. Repeated inflammation of the peritoneum was associated with an increased production and release of PAI-1 into the peritoneum.