Normal anion-gap acidosis. Caused by distal nephron acidification defect. Also lithium, amphotericin B, and toluene. Occasionally seen is a hyper kalemic form with SLE, obstructive uropathy, or sickle cell uropathy. Caused by a defect in the ability of proximal tubules to recover bicarbonate.
Treatment is to identify the primary cause and treat it.
Consider use of thiazide diuretics to cause ECF volume contraction to promote HCO 3 - reabsorption proximally. Similar presentation to hyporeninemic hypoaldosteronism. Interstitial renal disease. Ingestion of acetazolamide, ammonium chloride, chole-styramine, calcium chloride or magnesium chloride. Small bowel drainage or fistula, biliary drainage or fistula, or pancreatic drainage or fistulas.