Role of the kidney in acid–base balance

Abstract 

Correction of disturbances in acid–base balance is achieved by: physicochemical buffering by extracellular and intracellular buffer systems (instantaneous), alveolar ventilation to control pCO₂ (rapid), and renal compensation (long term). Buffering and changes in ventilation limit changes in pH but cannot return acid–base status to normal. The kidney has a pivotal role: disturbances can be completely corrected through changes in H⁺ secretion and HCO₃⁻ reabsorption and production. HCO₃⁻ reabsorption is modified by changes in GFR (filtered load), changes in extracellular volume and by hormones which modify Na⁺ reabsorption via the Na⁺–H⁺ exchanger in renal tubular cells. Changing the activity of this exchanger influences H⁺ secretion and, hence, HCO₃⁻ reabsorption. Chronic (but not acute) changes in pCO₂ influence HCO₃⁻ reabsorption through changes in the filtered load and, in chronic acidosis, by the insertion of more H⁺ transport proteins in renal tubular cells. Renal HCO₃⁻ production is linked to H⁺ excretion: acid buffer salts (phosphate, creatinine), their availability and pK and tubular fluid pH. Formation and excretion of NH₄⁺ buffer salts are important – acidosis stimulates secretion of NH₄⁺ (proximal tubule) and NH₃ (collecting duct). There is a reciprocal relationship between extracellular K⁺ and NH₄⁺ excretion, hence HCO₃⁻ production.

Keywords: acid, ammonium, bicarbonate, production, reabsorption, renal