A role for coagulation in renal diseases is suggested by the presence of glomerular fibrin deposits in numerous experimental and human renal diseases, some of which are of toxic origin. Fibrin may exert detrimental effects by occluding glomerular capillaries, by attracting macrophages or by direct cytotoxicity to mesangial cells. Intraglomerular fibrin deposition or formation may result in part from changes in the normal multiple haemostatic properties of glomeruli. In glomerular clotting of systemic origin, e.g., glycerol-induced acute renal failure with intravascular coagulation, inhibition by drugs of glomerular fibrinolytic activity leads to persistent thrombi and permanent renal damage. In immune glomerulonephritis, fibrin formation may depend on activation of glomerular prothrombotic properties: for example, glomerular procoagulant (tissue factor-like) activity is enhanced at the peak of mercuric chloride-induced autoimmune glomerulonephritis, characterized by massive fibrin deposits. Finally, fibrin deposits probably contribute to the progressive renal lesions and chronic renal failure seen in rats with kidney damage, in which anticoagulant therapy has a beneficial effect.