Renal tubular acidosis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
Pathophysiology
Normal Physiology of Acid-Base balance
- Normally kidneys reabsorb the filtered bicarbonate and excrete acid to maintain acid-base balance.
- HCO3 reabsorption is facilitated by Na-H and proton pumps.
- Na-H reabsorbs about 80-90% of the filtered HCO3 at the proximal tubule.
- Proton pumps (H-ATPase and H-K ATPase) the distal nephron via hydrogen reabsorbs remaining 10 percent.
- There is no bicarbonate in the final urine in normal situations.
- Collecting tubules serve the function of excretion of acid.
- Hydrogen ions need a buffer to get excreted.
- The principal buffers in the urine are ammonia and phosphate.
- Ammonium excretion requires the renal synthesis of ammonia and the secretion of hydrogen ions into the tubular lumen where they are trapped as ammonium.
- Ammonia diffuses freely across membranes, while ammonium does not.
- The renal tubular production of ammonia is stimulated by intracellular acidosis.
- When the systemic acid load is modestly increased, near-normal balance is maintained by increases in ammonium production and excretion.
- Failure to excrete sufficient ammonium often leads to the net retention of hydrogen ions and the development of metabolic acidosis.
