Renal Tubular Acidosis
Basic Information
Clinical Presentation
Etiology and Pathophysiology
• Etiology: Underlying cause is usually undetermined, but is generally acquired
Renal tubular toxins: Heavy metals, ethylene glycol, drugs (gentamicin, cephalosporins, tetracyclines, salicylate)
Type I (distal or classic RTA) is caused by an inability of the distal tubule cells to secrete H+ or to produce acidic urine. There is excessive K+ secretion and severe hypokalemia.
Type II (proximal RTA) is caused by a failure of HCO3− resorption in the proximal tubule with subsequent loss of HCO3− into urine. The proximal tubule is the site where the majority of filtered HCO3– is reabsorbed via Na+ and H+ exchange and the breakdown of carbonic acid to carbon dioxide and water under the influence of carbonic anhydrase. Hydrogen ions are usually secreted when HCO3− ion is reabsorbed. Failure to reabsorb HCO3− results in excessive urinary losses, basic urine pH, and systemic acidosis.
Hyperchloremia develops because of renal conservation of chloride to maintain electroneutrality consequent to HCO3− loss.
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