Severe metabolic acidosis induced in a patient during fasting by KCl administration

Abstract

The purpose of this study was to determine the cause of an acute metabolic acidosis of the normal anion gap type which developed during a 3 day period when 64 mmol of KCl was administered daily to an obese but otherwise healthy subject fasted for 2 weeks (called the index case). She had typical ketoacidosis of fasting for the first 13 days of fasting; since the plasma [K] was 3.6 mmol/l, she was given 64 mmol of KCl daily for 3 days. On day 3 of KCl treatment, the plasma [HCO3] was 13 mmol/l with no change in the plasma anion gap or 3-hydroxybutyrate concentration; the plasma [K] had risen to 4.3 mmol/l. The cause of the acidosis was a reduction of urine ammonium excretion by 42 mmol/day without a parallel fall in the rate of 3-hydroxybutyrate excretion. Since renal ammonium production can be inhibited by K administration, 5 other obese subjects were studied in a similar fashion to gain insight into the problem. They had a similar reduction in the daily rate of ammonium excretion (41 mmol) after KCl; however, their daily 3-hydroxybutyrate excretions declined by a similar amount (47 mmol) and thus metabolic acidosis did not develop.