Renal tubular acidosis pathophysiology: Difference between revisions
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*HCO3 reabsorption is facilitated by Na-H and proton pumps. | *HCO3 reabsorption is facilitated by Na-H and proton pumps. | ||
**Na-H reabsorbs about 80-90% of the filtered HCO3 at the proximal tubule. | **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. | *Collecting tubules serve the function of excretion of acid. | ||
**Hydrogen ions need a buffer to get excreted. | **Hydrogen ions need a buffer to get excreted. | ||
**The principal buffers in the urine are ammonia and phosphate. | **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. | ***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. | ***Ammonia diffuses freely across membranes, while ammonium does not. | ||
**The renal tubular production of ammonia is stimulated by intracellular acidosis. | ***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. | ***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. | ***Failure to excrete sufficient ammonium often leads to the net retention of hydrogen ions and the development of metabolic acidosis. | ||
[[Image:Renal_Diuretics.gif|thumb|center|400px|Source:By Haisook at English Wikipedia, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=2945979]] | [[Image:Renal_Diuretics.gif|thumb|center|400px|Source:By Haisook at English Wikipedia, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=2945979]] | ||
Revision as of 14:26, 16 May 2018
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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.
