Hypochloremic Metabolic Acidosis

The finding of hyperchloremia and hypocarbonatremia may be due to hyperchloremic metabolic acidosis or primary respiratory alkalosis. The pH on an arterial blood gas will differentiate between these two possibilities. The differential diagnosis for a hyperchloremic metabolic acidosis includes: urinary diversions such as an ileal conduit, Addison's disease, diarrhea and renal tubular acidosis (RTA). One can differentiate among these possibilities with the patients history, physical examination, and obtaining a spot urine sample and measuring sodium, potassium, and chloride. Ideally, direct measurement of urinary ammonium would help distinguish between renal and nonrenal metabolic acidosis. Urinary ammonium determinations, however, are technically difficult to perform. The urinary anion gap, defined as (Ung +UK)-Ucl is used to indirectly estimate the urinary ammonium excretion and normally ranges from -10 to +10. The urinary anion gap represents the amount of unmeasured anions in the urine. These unmeasured anions are accompanied by acid excreted in the form of ammonium. In patients with nonrenally induced metabolic acidosis (diarrhea), increased acid production is accompanied by increased renal acid excretion as the kidney compensates. As a result, the kidney excretes ammonium chloride (NH4CL) lending to a disproportionate increase in urine chloride in relation to urine sodium and potassium. Therefore, the urine anion gap is a large negative value (> -10). In contrast, when the kidney induces a metabolic acidosis by failing to excrete acid at a normal rate, urinary ammonium chloride is very low, leading to a positive urinary anion gap. For example, the urinary anion gap is positive (> +10) in RTA.

Renal tubular acidosis is most commonly due either to a defect in acid secretion by the distal tubule and/or aldosterone deficiency. Cyclosporine and tacrolimus commonly cause distal tubule damage to the sites where acid is secreted (into the urine) and may also render the distal tubule unresponsive to aldosterone. In the precyclosporine era, the development of RTA indicated immune-mediated impairment of hydrogen ion secretion as part of the rejection process. In addition, some patients are aldosterone deficient, primarily diabetics.

Treatment of metabolic acidosis attempts to correct the serum bicarbonate to near normal levels to improve growth in children and ameliorate the effects of acidosis on the bones. The distal tubule normally excretes 1 mEq of acid/kg body weight per day. Since we do not want to cause a metabolic alkalosis bicarbonate therapy may be initiated at 0.5 mEq per kg body weight and then adjusted by the serum bicarbonate level.

Selected Readings

1. Rao Uk ed Renal Transplantation Surgery Clinic North American 1998

2. Danovitch GM ed Handbook of Kidney Transplantation 2nd edition 1996, Little, Brown, and Co.

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