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) 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.
- Distal RTA is commonly associated with hypokalemia due to renal potassium wasting.
| 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 | - |