[Evaluation of factors influencing platelet aggregation in patients with chronic glomerulonephritis (CGN)].

Platelets (PLT) play an important role in hemostasis, modulation of immunological and inflammatory processes. There is also evidence that PLT takes part in the development of atherosclerosis and glomerulosclerosis. The aim of presented study was to determine morphological and functional changes of platelets and their relation to the lipid, protein and coagulation factors disturbances in patients with chronic glomerulonephritis (CGN). The studies were carried out in 60 patients with CGN diagnosed by renal biopsy: 30 patients without nephrotic syndrome (NS)-CGN and 30 patients with NS-CGN+NS. Protein and lipid disturbances, coagulation factors were estimated using routine laboratory methods. Platelet count (PLT), mean platelet volume (MPV) and modal platelet volume (PLT-Mode) were measured using Technicon H1 hematological autoanalyser. Platelet function was assessed by aggregometry using turbidimetric method (inductors: ADP 1-3 microM, collagen 50g/ml, epinephrine 0.25-5 microM). Spontaneous platelet aggregation (SPA) was measured in platelet rich plasma (PRP) without inductors for 15 min, in 1-2 hours after venesection. SPA was observed in 9 of 30 patients with CGN and in 19 of 30 patients with CGN+NS. MPV and PLT Mode were significantly higher in patient showing SPA compared with those without. Significant correlations between SPA and the concentration of plasma albumin (r = -0,70; p < 0.02) TG and CH-LDL (r = 0,61; p < 0.05) were found in CGN+NS patients. APTT was significantly shorter in patients showing SPA compared with those without and negative significant correlation between SPA and APTT was found. Platelet aggregation to inductors in CGN and CGN+NS patients was diminished compared with control group. Lack of second phase aggregation in response to aggregation inducers was observed in patients with SPA. Conclusions. 1. Platelet hyperaggregation play an important role in hypercoagulation state in CGN patients. 2. SPA in vitro was observed in majority of CGN+NS patients and in some without NS. 3. Pathomechanism of SPA is probably multifactorial (hypoalbuminemia, dyslipidemia, changes in concentration of coagulation parameters).