Urinary loss of acid

Most diuretics generate metabolic alkalosis by directly causing losses of chloride, sodium, potassium, and fluid to the urine. Volume contraction, aldosterone secretion, chloride depletion, and potassium depletion all contribute in some way to enhancement of proximal bicarbonate reabsorption and/or distal proton excretion.

Post-hypercapnic alkalosis is a two-step process commonly observed in critical care units. First, sustained respiratory acidosis determines a compensatory retention of bicarbonate and a concomitant excretion of chloride by the kidney. If chloride is not available when the hypercapnia is reversed, the bicarbonate excess cannot be eliminated. Such a post-hypercapnic alkalosis commonly occurs when patients with congestive heart failure due to respiratory disease are submitted to sodium chloride restriction or diuretic therapy.

Mineralocorticoid excess alone causes mild metabolic alkalosis, but the alkalosis is much more serious when potassium depletion is also present. The mechanisms by which the two factors combine to generate the alkalosis remain to be fully clarified. Mineralocorticoid excess, potassium depletion, and chloride depletion all contribute to the alkalosis in Bartter's syndrome.

It has been reported that severe isolated potassium depletion generates metabolic alkalosis by causing renal chloride wasting. Penicillin and related dugs can generate mild metabolic alkalosis, possibly as non-reabsorbable anions. Hypercalcemia may be associated with metabolic alkalosis or acidosis.

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