Platelet aggregation and prostaglandin metabolism in uremic patients

Citation
I. Pietrzak et al., Platelet aggregation and prostaglandin metabolism in uremic patients, AM J KIDNEY, 38(4), 2001, pp. S111-S114
Citations number
19
Categorie Soggetti
Urology & Nephrology
Journal title
AMERICAN JOURNAL OF KIDNEY DISEASES
ISSN journal
02726386 → ACNP
Volume
38
Issue
4
Year of publication
2001
Supplement
1
Pages
S111 - S114
Database
ISI
SICI code
0272-6386(200110)38:4<S111:PAAPMI>2.0.ZU;2-D
Abstract
The pathogenesis of depressed platelet activity in uremia is still unknown. The influence of some uremic toxins on platelet aggregation (PLA) and pros taglandin metabolism in 50 uremic patients treated by hemodialysis (HD) or continuous ambulatory peritonea[ dialysis (CAPD) was studied. Fifty-seven h ealthy volunteers (HVs) served for reference values. Adenosine diphosphate (ADP) and thrombin (Thr) were used as agonists of PLA. PLA was determined u sing the Born method. Malonyldialdehyde (MDA) levels in platelets as an ind icator of prostaglandin metabolism, after stimulation with arachidonic acid , were measured according to Stuart. The relationship of PLA and prostaglan din metabolism with plasma concentrations of methylguanidine (MG), guanidin osuccinic acid (GSA), and creatinine (Cr) was assessed. PLA-ADP values in r egular HD patients (42 +/- 5 mm) were significantly lower than in CAPD pati ents (65 +/- 8 mm) and HVs (73 +/- 3 mm). PLA-Thr values in HD patients (25 +/- 4 mm) were significantly lower than in CAPD patients (34.9 mm) and HVs (36 +/- 3 mm). MDA levels in HD patients (7 +/- 1 nmol/L/10(9)) were signi ficantly lower than in CAPD patients (12 +/- 2 nmol/L/10(9)) and HVs (15 +/ - 1 nmol/L/10(9)). In HD patients, inverse correlations of PLA-ADP with MG levels (r = -0.92), PLA-Thr with Cr levels (r = -89), and MDA levels with G SA levels (r = -0.86) were found. In CAPD patients, no relationship of PLA and MDA with uremic toxins was observed. Depressed activity of platelets an d prostaglandin metabolism was strongly expressed in HD patients. (C) 2001 by the National Kidney Foundation, Inc.