Renal tubular acidosis induced by dietary chloride

Previous studies have demonstrated that dietary intake of anions with high renal reabsorbability (Cl^- > SO₄^2-) 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 mEg/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 < 0.01) and increase in [H⁺] from 38.5 ± 0.7 to 43.3 ± 0.8 nEq/liter (P < 0.001). Urine pH increased (P < 0.01), the cumulative change in net acid excretion decreased (-79 mEq, P < 0.05), and Cl^- retention (39 mEq, P < 0.05) occurred. No change in Na⁺, K⁺, or Pi excretion occurred. The renal acidosis was fully corrected when SO₄^2- 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.