Renal tubular acidosis induced by dietary chloride

R. D. Toto, H. N. Hulter, S. Mackie, A. Sebastian

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)26-32
Number of pages7
JournalKidney International
Volume25
Issue number1
StatePublished - 1984

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Renal Tubular Acidosis
Chlorides
Kidney
Acidosis
Anions
Extracellular Fluid
Acids
Buffers
Familial Hypophosphatemia
Alkalosis
Base Composition
Dietary Supplements
Diuretics
Electrolytes
Creatinine
Urine
Dogs
Diet

ASJC Scopus subject areas

  • Nephrology

Cite this

Toto, R. D., Hulter, H. N., Mackie, S., & Sebastian, A. (1984). Renal tubular acidosis induced by dietary chloride. Kidney International, 25(1), 26-32.

Renal tubular acidosis induced by dietary chloride. / Toto, R. D.; Hulter, H. N.; Mackie, S.; Sebastian, A.

In: Kidney International, Vol. 25, No. 1, 1984, p. 26-32.

Research output: Contribution to journalArticle

Toto, RD, Hulter, HN, Mackie, S & Sebastian, A 1984, 'Renal tubular acidosis induced by dietary chloride', Kidney International, vol. 25, no. 1, pp. 26-32.
Toto RD, Hulter HN, Mackie S, Sebastian A. Renal tubular acidosis induced by dietary chloride. Kidney International. 1984;25(1):26-32.
Toto, R. D. ; Hulter, H. N. ; Mackie, S. ; Sebastian, A. / Renal tubular acidosis induced by dietary chloride. In: Kidney International. 1984 ; Vol. 25, No. 1. pp. 26-32.
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