Renal tubular acidosis pathophysiology

	Renal tubular acidosis Microchapters
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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

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 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).

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.

Type of RTA	Primary defect	Plasma HCO₃ mEq/L	Urine pH	Plasma potassium	Urine anion gap	Urine calcium/creatinine ratio	Risk for nephrolithiasis
RTA type 1	Impaired distal acidification	< 10	>5.3	Hypokalemic	Positive	↑	↑
RTA Type 2	Reduced proximal HCO3 reabsorption.	12 to 20	<5.3	Hypokalemic	Negative	Normal	-
RTA type 4	Decreased aldosterone secretion Aldosterone resistance	>17	Variable	Hyperkalemia	Positive	Normal	-
Voltage-dependent RTA	Reduced sodium reabsorption	>17	Variable	Hyperkalemia	Positive	Normal	-