Renal acidosis in mineralocorticoid deficiency is not dependent on NaCl depletion or hyperkalemia

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Abstract
Discontinuation of mineralocorticoid hormones in dexamethasone-sustained adrenalectomized (ADX) dogs results in renal NaCl wasting, K retention and hyperkalemia and metabolic acidosis of renal origin. Renal acidosis occurs despite prevention of hyperkalemia by restriction of K intake. In the present studies of ADX dogs, when mineralocorticoid hormones were discontinued, net acid excretion decreased and metabolic acidosis occured even though sufficient supplemental NaCl was administered in the diet or by continuous i.v. infusion to prevent the weight loss, hyperproteinemia and hyponatremia that ordinarily occur. Renal acidosis occurred despite the combination of continuous chronic i.v. NaCl infusion and restriction of K intake. The observed changes in urine acid-base and electrolyte composition permit the inference that mineralocorticoid deficiency results separately in a primary reduction in renal H+ secretion and a primary reduction in diffusion of NH3 into urine, neither of which is attributable to depletion of NaCl or hyperkalemia.