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Overview and pathophysiology of renal tubular acidosis and the effect on potassium balance

Michael Emmett, MD
Ellie Kelepouris, MD, FAHA
Section Editor
Richard H Sterns, MD
Deputy Editor
John P Forman, MD, MSc


The lungs and the kidneys are responsible for the maintenance of acid-base balance within the body. Alveolar ventilation removes carbon dioxide, while the kidneys reclaim filtered bicarbonate and excrete hydrogen ions produced by the metabolism of dietary protein (or bicarbonate when the diet generates more base than acid).

The term "renal tubular acidosis" (RTA) refers to a group of disorders in which, despite a relatively well-preserved glomerular filtration rate, metabolic acidosis develops because of defects in the ability of the renal tubules to perform the normal functions required to maintain acid-base balance [1]. All forms of RTA are characterized by a normal anion gap (hyperchloremic) metabolic acidosis. This form of metabolic acidosis usually results from either the net retention of hydrogen chloride or a salt that is metabolized to hydrogen chloride (such as ammonium chloride) or the net loss of sodium bicarbonate or its equivalent [2]. The major cause of a normal anion gap acidosis in patients without a significant impairment in renal function is diarrhea. (See "Approach to the adult with metabolic acidosis".)

This topic will review the classification and pathophysiology of the different forms of RTA and the impact these changes have on potassium balance. The major causes, diagnosis, and treatment of RTA are discussed separately. (See "Etiology and diagnosis of distal (type 1) and proximal (type 2) renal tubular acidosis" and "Treatment of distal (type 1) and proximal (type 2) renal tubular acidosis" and "Causes and evaluation of hyperkalemia in adults" and "Etiology, diagnosis, and treatment of hypoaldosteronism (type 4 RTA)".)


Prior to discussing renal tubular acidosis (RTA), it is helpful to briefly review the kidneys' role in the maintenance of acid-base balance and how disturbances in tubular function can result in metabolic acidosis. To maintain acid-base balance, the kidneys reclaim the filtered bicarbonate and excrete the daily acid load, which is primarily derived from the metabolism of sulfur-containing amino acids.

Reclaiming filtered bicarbonate — Most of the bicarbonate that is filtered by the glomerulus returns to the circulation, predominately as a result of Na-H exchange by the proximal tubules (figure 1). Approximately 85 to 90 percent of the filtered load is reclaimed at this site. By comparison, 10 percent is reclaimed in the distal nephron, primarily via hydrogen secretion by a proton pump (H-ATPase). Under normal conditions, there is virtually no bicarbonate in the final urine.


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Literature review current through: Sep 2016. | This topic last updated: Jun 30, 2015.
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