Renal tubular acidosis pathophysiology: Difference between revisions
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* Almost all of the filtered potassium is reabsorbed passively in the proximal tubule and loop of Henle. | * Almost all of the filtered potassium is reabsorbed passively in the proximal tubule and loop of Henle. | ||
* The potassium excreted in the urine is derived from secretion into the tubular lumen by cells in the distal nephron. | * The potassium excreted in the urine is derived from secretion into the tubular lumen by cells in the distal nephron. | ||
* Distal potassium secretion is primarily influenced by two factors, both promote sodium reabsorption: | |||
* Depending upon the site of the defect and the mechanism responsible for the various forms of RTA, can result in hypokalemia or hyperkalemia: | * Depending upon the site of the defect and the mechanism responsible for the various forms of RTA, can result in hypokalemia or hyperkalemia: | ||
* Hypokalemia frequently develops in patients with distal RTA. | * Hypokalemia frequently develops in patients with distal RTA. | ||
** Usually improves with alkali therapy in contrast to to hypokalemia in proximal RTA which is exacerbated by alkali therapy. | ** Usually improves with alkali therapy in contrast to to hypokalemia in proximal RTA which is exacerbated by alkali therapy. | ||
* Hyperkalemia occurs frequently with hypoaldosteronism (type 4 RTA) and in patients with other defects in distal nephron sodium reabsorption (voltage-dependent RTA). | * Hyperkalemia occurs frequently with hypoaldosteronism (type 4 RTA) and in patients with other defects in distal nephron sodium reabsorption (voltage-dependent RTA). | ||
=== Distal (type 1) RTA === | |||
* It is characterized by impaired hydrogen ion secretion in the distal nephron. | |||
* If severe, this defect leads to an inability to excrete the daily acid load resulting in progressive hydrogen ion retention and a normal anion gap metabolic acidosis. | |||
* The plasma bicarbonate (HCO3 ion) concentration can fall below 10 mEq/L in the absence of treatment with exogenous alkali. | |||
* Patients with distal RTA almost always have hypocitraturia and frequently develop renal calcifications and calcium containing kidney stones. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Revision as of 18:30, 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) in the distal nephron reabsorbs remaining 10 percent of HCO3.
- There is no HCO3 in the final urine.
- 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.
- Acidosis stimulates ammonia production in renal tubules.
- While ammonia can freely diffuse across membranes, ammonium cannot.
- The secretion of hydrogen ions into the tubular lumen trap ammonia as ammonium which can easily flush out along with .
- Increased production of ammonium is required in cases of acidosis to maintain near-normal balance.
Potassium
- Potassium is the most common electrolyte abnormality that can be noticed with renal tubular acidosis.
- It can be either hypokalemic renal tubular acidosis or hyperkalemic renal tubular acidosis.
- Almost all of the filtered potassium is reabsorbed passively in the proximal tubule and loop of Henle.
- The potassium excreted in the urine is derived from secretion into the tubular lumen by cells in the distal nephron.
- Distal potassium secretion is primarily influenced by two factors, both promote sodium reabsorption:
- Depending upon the site of the defect and the mechanism responsible for the various forms of RTA, can result in hypokalemia or hyperkalemia:
- Hypokalemia frequently develops in patients with distal RTA.
- Usually improves with alkali therapy in contrast to to hypokalemia in proximal RTA which is exacerbated by alkali therapy.
- Hyperkalemia occurs frequently with hypoaldosteronism (type 4 RTA) and in patients with other defects in distal nephron sodium reabsorption (voltage-dependent RTA).
Distal (type 1) RTA
- It is characterized by impaired hydrogen ion secretion in the distal nephron.
- If severe, this defect leads to an inability to excrete the daily acid load resulting in progressive hydrogen ion retention and a normal anion gap metabolic acidosis.
- The plasma bicarbonate (HCO3 ion) concentration can fall below 10 mEq/L in the absence of treatment with exogenous alkali.
- Patients with distal RTA almost always have hypocitraturia and frequently develop renal calcifications and calcium containing kidney stones.