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]

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.

Source:By Haisook at English Wikipedia, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=2945979

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:
    • Aldosterone increases the number of open sodium channels thereby increases sodium reabsorption.
    • The distal delivery of sodium and water , reabsorption of sodium is more rapid than that of chloride, resulting in a relatively electronegative lumen.
    • This relative negative charge provides a favorable gradient for passive potassium secretion from the tubular cell into the lumen through potassium channels in the luminal membrane.
• 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).