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- Title
Potassium deficiency acidosis in the dog: Effect of sodium and potassium balance on renal response to a chronic acid load.
- Authors
Van Ypersele De Strihou, Charles; Dieu, Jean-Paul
- Abstract
Balance studies were carried out in 24 dogs in order to evaluate the effect of sodium and potassium depletion on the kidney's adaptation to a chronic acid load. In a first set of experiments, 12 dogs, adapted to an electrolyte-free diet supplemented with acid (either ammonium chloride, 1.7 mmoles, or calcium chloride, 1.25 mmoles/kg of body wt per day), were given repeated injections of furosemide, The resulting sodium and potassium deficit was associated with a sustained 2 mEq/liter fall in plasma bicarbonate, whereas urine pH remained at control levels, in order to dissociate the respective roles of sodium and potassium depletion in the maintenance of this increased metabolic acidosis, six dogs were given sodium chloride and the six others, potassium chloride. Correction of the sodium deficit failed to modify acid-base equilibrium. By contrast, repair of the potassium deficit resulted in a prompt 4.8 mEq/liter increase in plasma bicarbonate, a sustained fall in urine pH, and a transient rise in urine ammonia. Similar results were obtained when the six dogs, previously given sodium chloride, received a potassium chloride supplement. In a second set of experiments, 12 dogs in which potassium deficiency had been induced by a cation exchange resin were given an electrolyte-free diet supplemented with sodium chloride. Administration of a low (ammonium chloride, 1.7 mmoles/kg of body wt per day) or a high (ammonium chloride, 7 mmoles/kg of body wt per day) acid load resulted, respectively, in a 2 and 7 mEq/liter fall in plasma bicarbonate. Repair of the potassium deficit produced a sustained fall in urine pH, a rise in urine ammonia, and a 4.5 and 3 m Eq/liter rise in plasma bicarbonate, respectively. Urinary aldosterone excretion, measured prior to and during repair of the potassium deficit, remained stable. From these data we conclude that a) a moderate sodium deficit does not alter the steady state response to a chronic acid load, b) potassium depletion impairs the adaptation and the steady state renal response to a chronic acid intake, c) this disorder does not result from an inadequate delivery of sodium to distal exchange sites but from an apparent inability to lower urine pH, d) it is unlikely that changes in aldosterone secretion mediate this effect. It is suggested that potassium deficiency does not only enhance ammoniogenesis but also impairs the pH gradient achieved across the tubular cells. Our data indicate that the latter effect is predominant in the determination of the steady state response to a chronic acid load.
- Subjects
POTASSIUM deficiency diseases; ACIDOSIS; KIDNEYS; SALT in the body; POTASSIUM in the body; AMMONIA; URINALYSIS; NEPHROLOGY
- Publication
Kidney International, 1977, Vol 11, Issue 5, p335
- ISSN
0085-2538
- Publication type
Article
- DOI
10.1038/ki.1977.51