Metabolic Acidosis: Physiology, Presentation, and Diagnosis

Abstract

Uncomplicated metabolic acidosis (MA) is characterized by hypobicarbonatemia with low serum pH. The overproduction of ketoacids, lactic acid, or pyroglutamic acid, the ingestion of ethanol, methanol, ethylene glycol, paraldehyde, or salicylates, and the retention of fixed acid in renal failure cause MA with increased anion gap (AGMA). Diarrhea, ammonium or acid ingestion, and renal tubular acidosis (RTA) cause metabolic acidosis with normal anion gap (NAGMA). In proximal RTA the proximal tubule fails to reabsorb filtered bicarbonate normally and bicarbonate wasting develops. Proximal RTA is most often seen as part of the De Toni–Fanconi syndrome. Causes include hereditary conditions and drug toxicity. Distal RTA is marked by inability to lower urine pH normally or by diminished ammonium excretion. Distal RTA can be further characterized by the measurement of serum potassium, renin, and aldosterone levels. Causes of distal RTA include drugs, interstitial renal nephritis, hereditary diseases, low mineralocorticoid levels, and urinary tract obstruction. The diagnosis of MA in mixed acid–base disorders is more complicated. Diagnosis here involves the use of acid–base nomograms or equations to estimate the normally expected physiological compensation and also involves the comparison of changes in anion gap with changes in bicarbonate concentration.