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July 1972

Defect in Urinary Acidification in Cirrhosis: The Role of Excessive Tubular Reabsorption of Sodium in Its Etiology

Author Affiliations

Haifa, Israel

From the Division of Nephrology, Susan Reba Isenberg Hemodialysis Unit, Cardio-Respiratory Laboratory, Rambam Government Hospital, Haifa, Israel. Dr. Better is presently visiting scientist, Renal Hypertension Service, Cedars-Sinai Medical Center, Los Angeles. Dr. Goldschmid is with the Department of Internal Medicine, Beilinson Hospital, Petah-Tiqvah, Israel.

Arch Intern Med. 1972;130(1):77-83. doi:10.1001/archinte.1972.03650010065012

Two of nine patients with cirrhosis of the liver could not lower their urinary pH during induced systemic acidosis. The defect in urinary acidification occurred when urinary excretion of sodium was low, presumably due to excessive tubular reabsorption of sodium. Administration of a mercurial diuretic or the infusion of sodium sulfate to each of the two patients resulted in at least tenfold increase in urinary sodium excretion and a simultaneous acidification of the urine. Spontaneous natriuresis due to diurnal rhythm, or natriuresis following mannitol infusion in one patient where it was followed, partially corrected the defect in urinary acidification. This suggests that in some cirrhotics the rate of delivery of sodium to the distal sodium-for-hydrogen exchange sites may be a factor in tubular ability to generate steep urine:plasma hydrogen ion gradients.

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