Abstract

Increased platelet aggregability on stimulation with sodium arachidonate (NaAA), collagen and ADP was found in a group of 14 patients with nephrotic syndrome when compared with age and sex matched controls. Five of the group also exhibited spontaneous platelet aggregation (SPA), associated with synthesis of thromboxane B2 (TxB2), and which appeared to correlate with a markedly increased serum triglyceride concentration. Thromboxane B2 generation in response to NaAA was increased and reflected both the low serum albumin concentration and the platelet aggregation response to this agent. Addition of albumin in vitro decreased the amount of TxB2 generated for a given dose of NaAA and increased NaAA and collagen-induced platelet aggregation thresholds. However, albumin had no significant effect on collagen-induced TxB2 production. The results suggest that the hypoalbuminaemia and associated reduced binding of arachidonic acid and increased synthesis of TxA2 account in part for the increased platelet aggregability seen in the nephrotic syndrome but that other mechanisms are also involved.

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