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The two major causes of hyperchloremic metabolic acidosis are HCO3– loss from the GI tract or defects in renal acidification (RTA) (Table 21–12 and Table 21–14). The compensatory increase in serum chloride (hyperchloremia) maintains electroneutrality and a normal anion gap. The urinary anion gap can help differentiate between these causes.
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The GI tract secretes bicarbonate at multiple sites. The most common cause of a non-anion gap metabolic acidosis from the GI tract is diarrhea (loss of bicarbonate rich stool fluid). An infrequent cause is a ureterosigmoidostomy, where ureters are implanted into the sigmoid colon for urinary diversion. Unlike the bladder, colonic mucosa secretes bicarbonate in exchange for chloride, resulting in metabolic acidosis. This procedure is rarely performed in the United States, though remains popular in other countries. More commonly, a neobladder is created using a loop of bowel (generally ileum or colon), which has significantly decreased the incidence of metabolic acidosis, though it can still occur when contact time between urine and mucosa is increased, typically as a result of an anastomotic stricture.
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B. Renal Tubular Acidosis
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Hyperchloremic acidosis with a normal anion gap and normal (or near normal) GFR, in the absence of diarrhea, defines RTA. The defect is either an inability to excrete H+ as ammonium (inadequate generation of new HCO3–) or inadequate reabsorption of filtered HCO3–. Three major types can be differentiated by the clinical setting, urinary pH, urinary anion gap, and serum K+ level.
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Understanding the various types of RTAs requires an understanding of normal bicarbonate regulation by the kidney. About 90% of the bicarbonate filtered by the kidney is reabsorbed in the proximal tubule. However, even if all filtered bicarbonate is reabsorbed, plasma bicarbonate would still decrease since it is consumed when buffering the daily acid load, a product of dietary protein intake and cellular metabolism. Therefore, generation of new bicarbonate ...