BICARBONATE REABSORPTION IN THE DOG WITH EXPERIMENTAL RENAL DISEASE*

Abstract

In the metabolic acidosis of chronic progressive renal disease the urine usually contains little or no bicarbonate, and during the infusion of bicarbonate, reabsorption has been found to be within the nor-mal range (1). A defect in base reabsorption con-sequently has not been emphasized as an im-portant factor in the genesis of the acidosis. How-ever, a recent study by Schwartz, Hall, Hays and Relman (2) indicated that such a defect could be demonstrated in some patients with chronic uremia if the lowered plasma bicarbonate concentrations were elevated to normal levels over a 2- to 3-day period by exogenous base administration. Prior to treatment these patients had chronic acidosis and excreted a bicarbonate-free urine. After therapy, significant bicarbonate excretion occurred and this continued until the arterial pH and plasma bicarbonate concentrations approached their pre-treatment levels. The present studies were de-signed to investigate the patterns of bicarbonate reabsorption by diseased kidneys over a wide range of plasma bicarbonate levels, using as an experimental model the dog with one normal and one diseased kidney. METHODS Fourteen experiments were performed on 11 young adult female dogs weighing from 9 to 22 kg. Ten ani-mals had unilateral pyelonephritis (3), and one had uni-lateral aminonucleoside nephritis (4). In all studies si-multaneous urine collections were made from both kid-neys. The majority of experiments was performed on trained unanesthetized animals which had previously been subjected to a bladder-splitting procedure (5); how-