The association between renal dysfunction and bleeding was recognized more than 200 years ago . However, there remains an incomplete understanding of the underlying pathophysiology. Impaired platelet function is one of the main determinants of uremic bleeding. This impairment is multifactorial and includes defects intrinsic to the platelet as well as abnormal platelet-endothelial interaction. Uremic toxins and anemia also play a role.
This topic reviews platelet dysfunction in uremia. Platelet dysfunction in the general population is discussed elsewhere. (See "Congenital and acquired disorders of platelet function".)
CLINICAL AND LABORATORY MANIFESTATIONS
Clinical bleeding in uremia may involve the skin, resulting in easy bruising, or the oral and nasal mucosa, gingiva, gastrointestinal and urinary tracts, and respiratory system. Excessive bleeding may also occur in response to injury or invasive procedures [2-4].
Uremic patients may display increased bleeding sensitivity to aspirin as there is a transient, cyclooxygenase-independent prolongation of the bleeding time following the use of aspirin in uremic patients that is greater than that seen in normal subjects taking aspirin .
Although an association between bleeding time prolongation and uremia has long been suggested , there are no good studies that unequivocally demonstrate an increased risk of either spontaneous bleeding or bleeding with a procedure that is associated with a prolonged bleeding time among patients with chronic kidney disease (CKD).