Renal Tubular Acidosis

Renal tubular acidosis (RTA) encompasses disorders where the kidneys fail to properly acidify urine despite relatively preserved GFR, causing non-anion gap (hyperchloremic) metabolic acidosis. Type 1 (Distal RTA): the alpha-intercalated cells of the collecting duct cannot secrete hydrogen ions into the tubular lumen. Urine pH remains inappropriately > 5.5 despite systemic acidosis (the kidney cannot acidify urine). This causes hypokalemia (from compensatory increased potassium secretion and volume depletion), nephrolithiasis (calcium phosphate stones from alkaline urine and hypercalciuria), and nephrocalcinosis. Causes: autoimmune diseases (Sjögren syndrome, SLE), amphotericin B, lithium, sickle cell disease. Type 2 (Proximal RTA): the PCT has impaired bicarbonate reabsorption. Normally, the PCT reclaims ~85% of filtered bicarbonate; when this threshold is reduced, bicarbonate spills into urine until serum bicarb falls to the new (lower) reabsorptive threshold, at which point urine can acidify normally (pH < 5.5). Causes: Fanconi syndrome (generalized PCT dysfunction — glycosuria, aminoaciduria, phosphaturia, uricosuria), multiple myeloma (light chain toxicity to PCT), carbonic anhydrase inhibitors (acetazolamide). Also causes hypokalemia. Type 4 (Hyperkalemic RTA): hypoaldosteronism or aldosterone resistance reduces both potassium excretion and hydrogen secretion in the...