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John C Lieske, Commentary, Clinical Chemistry, Volume 62, Issue 3, 1 March 2016, Page 440, https://doi.org/10.1373/clinchem.2015.248690
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Hypokalemia is commonly encountered in clinical medicine. In the vast majority of cases, it is a result of losses in the gastrointestinal tract or urine. Thus, the key diagnostic test is urine potassium measurement. If low, gastrointestinal losses are likely; if, as in this case, urine potassium is high, then the kidney is implicated (i.e., renal potassium wasting), and serum aldosterone, the key hormone that stimulates renal potassium excretion, is likely to be high. The question then becomes whether the patient clinically appears volume expanded (suggestive of primary hyperaldosteronism or perhaps licorice ingestion) or volume depleted (in which case aldosterone is still high but “appropriate” and secondary). In this case, the patient apparently did not appear volume expanded, and indeed there was evidence for metabolic alkalosis, which is consistent with volume contraction. Overall, this common scenario results when a patient is taking diuretics. But what if, as in this case, none are being taken? Think Bartter or Gitelman syndrome.
