Enhanced platelet function in glomerular renal disease.

Abstract

Abstract Platelet aggregation was assessed in 73 children suffering from a variety of acute and chronic glomerular disorders. Enhanced platelet aggregation in response to collagen and ADP was observed in 11 of 14 patients with nephrotic syndrome in relapse. Among patients with glomerulonephritis without nephrotic syndrome, 11 of 21 clinically characterized as active exhibited enhanced platelet aggregation. In contrast, platelet function was normal in all patients whose glomerular disease was characterized as inactive. The degree of platelet function abnormality was significantly correlated with the degree of proteinuria, the ratio of plasma fibrinogen to serum albumin, and with the serum albumin level. The correlations between the degree of platelet function abnormality and the hematocrit and the platelet count were not statistically significant. The abnormal platelet response was fully corrected by aspirin treatment. Placelet-poor plasma from children with abnormal platelet function significantly enhanced aggregation of normal washed platelets. This abnormal property of platelet-poor plasma from affected patients was not reversed by aspirin. Concentrated, dialyzed urinary protein in 6 of 20 patients showing abnormal platelet aggregation inhibited normal platelet function and normalized the platelet aggregation-enhancing effect of abnormal platelet-poor plasma. It is suggested that abnormal platelet aggregation in glomerular renal diseases may arise in part as a consequence of loss in the urine of plasma proteins normally responsible for inhibition of platelet aggregation.