CORRELATIONS BETWEEN PLASMINOGEN-ACTIVATOR INHIBITOR-1 AND PERITONEALTRANSPORT IN PEDIATRIC CCPD PATIENTS

Citation
Jj. Lin et al., CORRELATIONS BETWEEN PLASMINOGEN-ACTIVATOR INHIBITOR-1 AND PERITONEALTRANSPORT IN PEDIATRIC CCPD PATIENTS, Peritoneal dialysis international, 15(6), 1995, pp. 246-251
Citations number
31
Categorie Soggetti
Urology & Nephrology
ISSN journal
08968608
Volume
15
Issue
6
Year of publication
1995
Pages
246 - 251
Database
ISI
SICI code
0896-8608(1995)15:6<246:CBPIAP>2.0.ZU;2-E
Abstract
Objective: Plasminogen activator inhibitor-1 (PAI-1) is an important r egulator of plasminogen activators and has been shown to be involved i n the accumulation of extracellular matrix (ECM) in various tissues. S ince peritoneal ECM is a resistance site for peritoneal transport, the production and release of PAI-1 in the peritoneum may affect the peri toneal transport of water and small solutes. Design: The linear correl ations between the dialysate PAI-1 levels and the variables of periton eal transport during peritoneal equilibration tests (PET) were examine d. Setting: A tertiary university hospital. Patients: Six stable pedia tric patients (age 10.8+/-4 years) undergoing continuous cycler-assist ed peritoneal dialysis were included. Interventions: None. Results: Al l data are mean+/-SD. There was a positive correlation between the inf used volume and the net ultrafiltration (UF, 198+/-127 mL, r = 0.82, p < 0.05). The dialysate PAI-1 leveIs increased during the dwell time ( 2.44+/-2.23 ng/mL or 2.46+/-1.72 mu g at 4 hours vs 0.04+/-0.1 ng/mL o r 0.04+/-0.09 mu g at 0 hour, p < 0.05). The saturation indices (dialy sate/plasma ratio) of PAI-1 and albumin at 4 hours were 1.05+/-1.21 an d 0.028+/-0.004, respectively The changes from 0-hour dwell to 4-hour dwell in the dialysate PAI-1 concentration (PAI(4-0), 2.4+/-2.2 ng/mL) or amount corrected to body surface area ((A)PAI(4-0)/BSA, 2.61+/-2.1 1 mu g/m(2)) negatively correlated with UF or UF/body surface area and positively correlated with the number of episodes of peritonitis. The re was no correlation between PAI(4-0), (A)PAI(4-0)/BSA, or plasma PAI -1 concentration and the mass transfer coefficient and clearance of ei ther urea or creatinine. Conclusions: 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. Repeat ed inflammation of the peritoneum was associated with an increased pro duction and release of PAI-1 into the peritoneum.