Radio-fibrinogen catabolism study is a sensitive way of assessing participation of fibrin in subjects with renal disease. In general accelerated fibrinogen catabolic rates are reflected by an increase of serum fibrin products (F-R antigen). Accelerated catabolism representing intravascular coagulation has been found with the onset of acute renal failure, in terminal uraemia, in malignant hypertension with vascular damage, in chronic nephritis with refractory hypertension, and in rapidly progressive glomerulonephritis and immune complex type nephritides. In chronic uraemia some lysis of fibrin appears to be an extravascular phenomenon. After the onset of acute renal failure accelerated catabolism persists until the recovery phase and may be a post-traumatic response, a reaction to acidosis, and to tissue damage and sub-clinical infection. Fibrin plays a part in the pathogenesis of acute renal failure due to septicaemia, trauma, malignant hypertension, obstetric accidents, and mismatched transfusion and may well be the cause of tubular necrosis. Increased extravascular passage of fibrinogen has been noted in acute nephritis, eclampsia, and rapidly progressive glomerulonephritis.
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