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.