ON THE CONCENTRATING DEFECT IN CIRRHOSIS OF THE LIVER.

The capacity of patients with cirrhosis of the liver to produce a dilute urine after a water load has been extensively investigated (1, 2). The concentrating ability of these patients has not been carefully studied, although the assumption has been made that a defect exists (1, 3). The present studies describe the characteristics-of the concentrating system in patients with cir-rhosis and attempt to clarify the mechanisms involved in any existing defect. Methods Twenty-seven patients with cirrhosis of the liver of varying severity associated with chronic alcoholism and 17 patients with other chronic diseases were studied. Each patient was receiving at least 75 g of dietary protein and at least 1 g of dietary sodium per day. None gave a history of renal disease, and all had normal uri-nalysis, nonprotein nitrogen, and serum creatinine. No patients above the age of 65 were included. Except for the absence of azotemia or intrinsic renal disease, the cirrhotics represented a wide range of patients with this disease. The mean age of cirrhotics was 50 and ranged from 35 to 62 years. The degree of ascites ranged from no apparent ascites (seven patients) to massive ascites (three patients) and included varying degrees of protein depletion as estimated by degree of muscle wasting. The mean age of the 17 chronically ill patients without cirrhosis was 49 and ranged from 38 to 58 years, and they represented the only noncirrhotic patients in the medical service (180 beds) at a given time who satisfied the above criteria for inclusion in the study. The degree of ascites and degree of muscle wasting were estimated in each cirrhotic by a scale of 0 to ++++. Age and sex were recorded. 1) Special studies were carried out in nine patients with cirrhosis to evaluate and characterize the maximal * t This investigation was carried out during tenure as a Clinical Pharmacology Trainee and was supported by grants from the U. measurement of urine osmolality (Ucam) starting at 14 hours after the last oral intake and 10 hours after 5 U of vasopressin in oil intramuscularly. Urine samples were obtained intermittently until a last sample was obtained after 21 to 25 hours of dehydration. 2) Volume and urea, ammonia, sodium, and potassium concentrations of Uma. urines were measured in 11 cir-rhotics. In other patients urine sodium excretion was recorded as 0 to ++++ based on the approximate percentage of the oral sodium …