The Role of Vasopressin and Urea in the Renal Concentrating Defect of Patients with Cirrhosis of the Liver

1. The maximal urine osmolality in response to vasopressin during water diuresis and during hydropenia was studied in twenty patients with cirrhosis and sixteen noncirrhotic subjects under controlled dietary conditions. 2. The cirrhotic patients exhibited a significantly lower maximal urine osmolality under both experimental conditions. 3. During water diuresis decompensated and compensated cirrhotics had comparable maximal urine osmolalities after vasopressin. A decreased response of the renal tubules to vasopressin does not appear to have a significant role in the concentrating defect. 4. The cirrhotic patients had a significantly lower excretion rate of urea at high (water diuresis) and low (vasopressin antidiuresis or hydropenia) urine flow rates. The lower urine urea concentration accounted for most of the decrease observed in maximal urinary concentration. After vasopressin administration the absolute tubular reabsorption of urea was also significantly lower in cirrhotic patients. The results suggest that a decrease in the medullary urea content decreases medullary osmolality resulting in the defect in urine concentration noted in these cirrhotic patients at low urine flow rates. 5. Protein depletion or decreased urea synthesis may in part be responsible for the decreased availability of urea for the concentrating process in cirrhosis. 6. Lack of correlation between concentrating and diluting capacity in these patients suggested that decreased delivery of sodium to the distal site might not be the limiting factor common to both renal functional abnormalities observed in cirrhosis of the liver.