Renal concentrating ability in cirrhosis III.Failure of hypertonic saline to increase reduced TcH2O formation

Renal concentrating ability in cirrhosis.III.Failure of hypertonic saline to increase reduced TcH2O formation.The present study examines the possibility that the solute-free water reabsorption (TcH2O) defect observed in some patients with cirrhosis of the liver may be due to decreased distal delivery of sodium.TcH2O was studied in cirrhotics with low TcH2O formation and in non-cirrhotic controls undergoing mannitol and saline diuresis on different days while receiving a low sodium intake.Despite a three-fold increase in urinary sodium excretion and an increase in serum sodium concentration with hypertonic saline, TcH2O formation was not improved or corrected in the cirrhotic patients and was always lower per unit of solute excretion than that observed in controls with comparable sodium excretion.The exact mechanism of the concentrating defect remains unknown but the data suggest that the TcH2O defect is not related to a decreased delivery of sodium to the distal nephron consequent to increased proximal reabsorption or to a lower tubular fluid concentration of sodium at the distal concentration site