Hemostasis in chronic renal failure.

Hemostasis is a process of blood clot formation at the site of vessel injury. When a blood vessel wall breaks, the hemostatic response must be quick, localized, and carefully regulated. Bleeding or a thrombosis may occur due to missing or dysfunctional moieties of the coagulation or fibrinolytic factors. The pathways of thrombin-stimulated fibrin clot formation and plasmin-induced clot lysis are linked and commonly regulated. When they work in coordinated harmony, a clot is laid down to stop bleeding, followed by eventual clot lysis and tissue repairing. Abnormal bleeding can result from diminished thrombin generation (e.g., due to factor VIII deficiency) or enhanced plasmin formation (e.g., due to alpha-2-antiplasmin deficiency). Conversely, excessive production of thrombin (e.g., due to an inherited thrombophilia) can lead to thrombosis. Clot formation and its subsequent lysis may be decided in the four steps: initiation and formation of the platelet plug, propagation by the coagulation cascade, termination of the clotting by antithrombotic control mechanisms and removal of the clot by fibrinolysis. In a variety of slowly progressive renal diseases such as chronic glomerulonephritis, diabetic nephropathy, and polycystic kidney disease, it is at present, not possible or very difficult to correct the underlying disease. Eventual progression to renal failure is common in patients with various kidney diseases once the serum creatinine exceeds 1.5 to 2.0 mg/dL. This may occur even if the underlying disorder is “cured”. After a certain point, a reduction in the number of functioning nephrons eventually leads to loss of the more normal remaining nephrons. Renal failure may be associated with a variety of signs and symptoms that are collectively referred to as the uremic state. However, the is no predictable correlation between the development of these problems and the severity of renal disease. Loss of renal function results in the accumulation of metabolic waste products and alters the normal homeostatic mechanisms. Potential consequences of these abnormalities are the signs and symptoms of uremia. Using renal replacement therapy in a form dialyses or kidney transplantation, the physician can treat these disturbances and improve the quality of life in many patients with chronic, end-stage renal disease.