Chronic hypokalaemia and nephrocalcinosis.

Abstract

Unravelling chronic hypokalaemia can be a clinical challenge in some patients. History and physical examination can be misleading or inaccurate. Diagnostic steps usually involve assessing urinary potassium excretion, transtubular potassium gradient (TTKG) and concomitant acid–base disturbances. In those patients with low urinary potassium excretion, a gastrointestinal cause for the hypokalaemia would come to mind. In patients with a high urinary potassium excretion, the kidneys themselves are implicated. In any event, acid–base status is extremely helpful and generally indicates which end of the gastrointestinal tract or which level of the nephron is responsible. In patients with high urinary potassium with metabolic alkalosis, the urinary chloride concentration can be particularly helpful in separating surreptitious vomiting from Bartter's syndrome or Gitelman's syndrome. Diuretic abuse may be a confounder; however, metabolic breakdown products and the temporal course of chloride excretion generally solve the mystery. We recently encountered a patient who taxed our diagnostic skills.