• Gabor E Linthorst, Hans J Avis, and Marcel Levi.
• Department of Endocrinology and Metabolism, Academic Medical Center, Amsterdam, Netherlands. g.e.linthorst@amc.nl
• J. Am. Soc. Nephrol. 2010 May 1;21(5):753-5.

AbstractPlatelet dysfunction in renal failure is attributable to high levels of small, partly dialyzable molecules known as uremic toxins, hence the term "uremic thrombocytopathy." Although a variety of moieties contribute to platelet dysfunction or abnormal interactions between platelets and the vascular wall, urea remains a potential factor. Here, we studied three family members with familial azotemia, a rare autosomal dominant syndrome characterized by high plasma urea resulting from impaired urinary excretion but normal renal function otherwise. Platelet function, assessed in vitro and by traditional bleeding time, was normal in all individuals. Abnormal platelet function in patients with renal failure is not caused by high concentrations of urea.

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