Renal failure in patients with cirrhosis of the liver: I. Clinical and pathologic characteristics

Abstract

A study was undertaken to determine the clinical course, complications and pathogenesis of renal failure in patients with cirrhosis of the liver. Azotemia was present in a high percentage of the patients who died of cirrhosis, particularly in those with hepatic coma. In patients who had cirrhosis without azotemia, impaired ability to excrete water strongly indicated that the development of renal failure was imminent and that the prognosis was grave. In some cases, elevations of blood creatinine and/or uric acid levels were apparent before elevations of blood urea nitrogen concentrations, and provided early indications that renal insufficiency existed. Serum sodium concentration was less than 125 mEq. per L. in 19 per cent of the patients who died of cirrhosis. Hyponatremia usually was due to overhydration. Despite oliguria and azotemia, serum potassium concentrations usually were normal or low rather than high. Renal function studies and fluid balances were followed serially in fifteen patients who eventually died of renal failure. Eight demonstrated clinical evidence of acute tubular necrosis and two had “prerenal” azotemia. In the remaining five patients azotemia developed following acute and apparently spontaneous reductions in glomerular filtration rate. Initially tubular functions were intact, but prior to death these also deteriorated. Decreases in the glomerular filtration rate often followed episodes of “spontaneous” hepatic precoma or coma. Hepatic coma or an associated metabolic abnormality may cause alterations in renal function, or aggravate pre-existing abnormalities in renal function associated with severe liver disease. In some patients with cirrhosis, impaired renal function is characterized by limited ability to excrete water, reductions in renal plasma flow and glomerular filtration rate, and intact tubular function. Although their exact cause and relation to hepatic disease are not established, these abnormalities are often demonstrable before renal insufficiency is overt. They may make patients with cirrhosis more susceptible to the development of progressive renal failure when intercurrent incidents known to affect renal function adversely are superimposed. In other cases the abnormalities may progress and cause renal failure that uniformly follows a clinical course ending with death.