Abstract: SA-PO994

Unusual Case of Severe Hypokalemia, Metabolic Alkalosis, and Starvation Ketosis

Session Information

Category: Nephrology Education

  • 1302 Fellows and Residents Case Reports


  • Jani, Nihar, Temple University School of Medicine, Philadelphia, Pennsylvania, United States
  • Lee, Iris J., Temple University School of Medicine, Philadelphia, Pennsylvania, United States
  • Johnstone, Duncan B., Temple University School of Medicine, Philadelphia, Pennsylvania, United States
  • Rao, Swati, Temple University School of Medicine, Philadelphia, Pennsylvania, United States

Severe hypokalemia is a life threating emergency and requires prompt therapeutic and diagnostic intervention. Causes of inappropriate renal potassium (K) loss are traditionally divided into conditions based on concomitant acidosis or alkalosis. We present a case of severe hypokalemia with combined metabolic alkalosis and acidosis.


A 59 y/o African American male presented with 2 weeks of decreased oral intake due to severe food paranoia. He appeared malnourished and hypovolemic with BP 107/56mmHg. Laboratory data revealed K of 1.3 mEq/L, glucose of 134mg/dl, bicarbonate of 40 mEq/L, anion gap (AG) of 23, lactate 3.6mmol/l, arterial pH 7.56 and ketonuria. With aggressive K repletion (920 mEq oral and IV), K improved from 1.3 to 2.2mg/dl. Urine studies were consistent with renal K wasting: high urine K (27mEq/L), high TTKG (9.9) and high FeK (21%). Over the next few days, the patient increased his oral intake and starvation resolved along with normalization of patient’s electrolyte derangements. Renal K handling normalized and the patient remained normokalemic with acid-base equilibrium.


In our case, identifying a unifying diagnosis of hypovolemia, renal K wasting with combined severe metabolic alkalosis and acidosis was challenging. Genetic (Bartter, Gittleman) and pathological (diuretic abuse) causes were considered given low blood pressure, K wasting and alkalosis. The AG acidosis however, remained unexplained and unaccounted for by the level of lactate. In our patient, a prolonged duration of starvation ketoacidosis addressed all metabolic findings. Starvation resulted in renal excretion of non-absorbable anions (ketones) along with increased obligatory loss of cations (such as K). Ensuing hypokalemia and hypovolemia caused and sustained a metabolic alkalosis, due to distal tubular exchange of K with hydrogen (H) via H-K ATPase and activation of H-ATPase. Normalization of severe electrolyte and acid-base disturbances as well as renal K handling after adequate nutrition, confirmed a transient reversible defect in renal K handling.
Although ketone body production from starvation is commonly associated with metabolic acidosis, our case instead presented with alkalosis and alkalemia. We believe this is a rare presentation of severe hypokalemia and metabolic alkalosis due to starvation ketosis overwhelming renal tubular handling capacity.