Browse the corpus

©2013 UpToDate ® Print Email Chronic kidney disease factors that affect hemostasis Factors predisposing to bleeding Platelet abnormalities including subnormal dense granule content Reduction in intracellular ADP and serotonin Impaired release of the platelet α-granule protein and β-thromboglobulin Enhanced intracellular cAMP and abnormal mobilization of platelet Ca2+ Abnormal platelet arachidonic acid metabolism Defective cyclo-oxygenase activity Abnormality of the activation-dependent binding activity of GPIIb/IIIa Increased formation of vascular PGI2 Altered von Willebrand factor Indirectly Presence of uremic toxins, especially parathyroid hormone Anemia/altered blood rheology Erythropoietin deficiency Specific drug treatment (eg, nonsteroidal anti-inflammatory drugs) Procoagulant factors The high prevalence of systemic inflammation, atherosclerosis and diffuse endothelial damage may provide a substrate for hypercoagulability Dysfunctional activated protein C metabolism, possibly through multiple mechanisms The fibrinolytic system is also dysfunctional because of both elevated plasminogen activator inhibitor-1 to tissue-type plasminogen activator ratios and inhibition of plasmin by increased levels of lipoprotein(a) Defects in the expression of glycoprotein GPIb (the receptor for von Willebrand factor) ADP: adenosine di-phosphate; cAMP: cyclic adenosine di-phosphate; CKD: chronic kidney disease; GP: glycoprotein; PG: prostaglandin. Reproduced with permission from: Reinecke H, Brand E, Mesters R, et al. Dilemmas in the management of atrial fibrillation in chronic kidney disease. J Am Soc Nephrol 2009; 20:705. Copyright © 2009 American Society of Nephrology.