Platelets in uremia

Morgagni in 1764 in his Opera Omnia was the first to recognize the remarkable association between bleeding and renal dysfunction. Bleeding may be a serious complication of acute and chronic renal failure, and since the first review in 1907 on the association between uremia and abnormal bleeding, the clinical manifestations of uremic bleeding have been well described. Hemorrhagic complications varying from ecchymoses, epistaxis, bleeding from gums and venipuncture sites, and overt gastrointestinal bleeding have been observed in up to one-third of uremic patients, however, low-grade gastrointestinal bleeding may be even more common.

Bleeding became a clinical problem at the beginning of the dialysis era, when patients sometimes died from excessive bleeding from the gastrointestinal tract or abdominal organs.

With the advent of modern dialysis techniques and the use of erythropoietin to correct anemia the frequency of severe hemorrhage has decreased; however, this complication still limits surgery and invasive procedures in these patients.

The cause of uremic bleeding has been the subject of a major debate since the 1970s. The pathogenesis is considered multifactorial (Table 55.1); however, platelet–platelet and platelet–vessel wall interactions appear to be of crucial importance. Abnormalities of blood coagulation and fibrinolysis partially corrected by dialysis predispose the uremic patients to thrombosis rather than bleeding. Chronic renal failure also seems to be associated with an increased incidence of arterial and venous thromboembolic complications and this chapter will review the platelet and vascular defects in uremia.