Treatment with oral sodium bicarbonate, 0.5 mEq/kg/d, is appropriate. This patient with chronic kidney disease (CKD) has a normal anion gap metabolic acidosis. Normal anion gap metabolic acidosis may be due to failure of the kidneys to excrete the daily fixed acid load, gastrointestinal loss of bicarbonate, diversion of urine through a gastrointestinal conduit, or retention of hydrogen ions derived from organic anions that are excreted in the urine as sodium salts. The cause is often apparent from the history. This patient's history of analgesic nephropathy, normal anion gap metabolic acidosis, and hyperkalemia suggests the presence of distal (type 4) renal tubular acidosis. Studies have demonstrated that administration of oral alkali to maintain serum bicarbonate levels between 23 and 29 mEq/L (23-29 mmol/L) reduces the risk of progression of CKD. Typical starting doses of alkali for metabolic acidosis due to CKD are 0.5 to 1.0 mEq/kg/d.

The patient has a relatively mild and asymptomatic decrease in serum bicarbonate, and there is no indication for acute administration of intravenous sodium bicarbonate.

Although citrate becomes metabolized to bicarbonate and is therefore considered to be a “bicarbonate equivalent,” this patient has hyperkalemia, which is likely due to the decreased ability of the kidneys to excrete potassium in the setting of CKD. Potassium citrate could therefore exacerbate the existing hyperkalemia and should be avoided. Bicarbonate treatment will help correct this patient's hyperkalemia.

Current guidelines suggest treatment with alkali to keep serum bicarbonate levels between 23 and 29 mEq/L (23-29 mmol/L). Therefore, providing no alkali therapy to this patient with a serum bicarbonate level of 18 mEq/L (18 mmol/L) would be inappropriate.