Renal tubular acidosis induced by dietary chloride.

Previous studies have demonstrated that dietary intake of anions with high renal reabsorbability (Cl- greater than SO4=) can result in either exacerbation of chronic metabolic acidosis or correction of chronic metabolic alkalosis. These results, however, fail to predict the renal acid-base response to Cl- administration when systemic acid-base composition is initially normal, but accompanied by an extracellular fluid (ECF) volume-mediated renal avidity for Cl- reabsorption; that is, the renal options include HCl retention, KCl retention, and phosphaturia. Accordingly, the present metabolic balance studies evaluated the response to substitution of dietary Cl- (2.5 mEq/kg/day) for Pi in five dogs previously ECF-depleted with diuretics and maintained on a dietary K+ supplement, 5.0 mEq/kg daily as neutral Pi (electrolyte-free diet) during a steady-state control period. Dietary Cl- resulted in a decrease in arterial plasma [HCO3-] from 21.2 +/- 0.7 to 17.8 +/- 0.8 mEq/liter, (P less than 0.01) and increase in [H+] from 38.5 +/- 0.7 to 43.3 +/- 0.8 nEq/liter (P less than 0.001). Urine pH increased (P less than 0.01), the cumulative change in net acid excretion decreased (-79 mEq, P less than 0.05), and Cl- retention (39 mEq, P less than 0.05) occurred. No change in Na+, K+, or Pi excretion occurred. The renal acidosis was fully corrected when SO4= was substituted for dietary Cl- and redeveloped when Cl- was resubstituted . Superimposition of a large oral buffer load (creatinine) did not ameliorate Cl- -induced renal acidosis. The results indicate that dietary reabsorbable anions can result in renal acidosis when Cl- reabsorption is stimulated and suggest that anion reabsorbability characteristics and not anion buffer properties are responsible.