AN EXPLANATION FOR AND EXPERIMENTAL CORRECTION OF THE ABNORMAL WATER DIURESIS IN CIRRHOSIS *

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Abstract
Total and "free water" diuresis was studied in patients with cirrhosis and in normal subjects before and after Na depletion. "Acute" loading was done with 20 ml/kg of (a) water by mouth, (b) water by vein (containing metabolizable hexose) and (c) water containing mannitol by vein. Some studies were repeated with pitressin added to the infusates. Sustained loading was done with water by vein (containing metabolizable hexose) followed by water containing mannitol or saline. Patients with cirrhosis excreted less free water than normal subjects given identical loads by mouth or by vein. It is unlikely that the defect is primarily the result of excessive secretion or persistence of action of antidiuretic hormone, since (1) all excreted some free water with loading, (2) physiologic doses of pitressin prevented this, (3) the "escape" from this pitressin occurred at a normal rate, and (4) mannitol or saline infusion increased free water excretion in patients with cirrhosis and in Na depleted normal subjects, but decreased it in normal subjects receiving adequate Na. The increase, which was often accompanied by increased excretion of K, could be produced despite decreases in total solute and Na excretion. The defect in free water clearance probably represents relatively excessive reabsorption of Na in proximal renal tubular sites where reabsorption is isosmotic with filtrate, and (2) mannitol and saline in the infusates act by "delivering" proximal fluid to distal sites where free water is generated.