Laboratory Tests to Determine the Cause of Hypokalemia and Paralysis

TLDR

Hypokalemia and paralysis can arise from a short‑term shift of potassium into cells in hypokalemic periodic paralysis (HPP) or from a large potassium deficit in non‑HPP, and failing to distinguish between the two can lead to improper management. The study evaluated the diagnostic value of spot urine tests in patients with hypokalemia and paralysis over a 3‑year period. Before therapy, urine potassium concentration, potassium‑creatinine ratio, and transtubular potassium concentration gradient were measured in a second voided urine sample. Among 43 patients, 30 had HPP and 13 non‑HPP; urine potassium <20 mmol/L distinguished non‑HPP, while the transtubular potassium concentration gradient and potassium‑creatinine ratio reliably differentiated HPP from non‑HPP, and minimal potassium chloride supplementation was needed to prevent rebound hyperkalemia in HPP patients.

Abstract

<h3>Background</h3> Hypokalemia and paralysis may be due to a short-term shift of potassium into cells in hypokalemic periodic paralysis (HPP) or due to a large deficit of potassium in non-HPP. Failure to make a distinction between HPP and non-HPP may lead to improper management. Therefore, we evaluated the diagnostic value of spot urine tests in patients with hypokalemia and paralysis during 3 years. <h3>Methods</h3> Before therapy, the urine potassium concentration, potassium-creatinine ratio, and transtubular potassium concentration gradient were determined in a second voided urine sample. <h3>Results</h3> Forty-three patients with hypokalemia and paralysis were identified: 30 had HPP and 13 had non-HPP. There was no significant difference in the plasma potassium or bicarbonate concentrations and in the pH of arterial blood between the 2 groups. All but 2 patients in the non-HPP group had urine potassium concentration values less than 20 mmol/L. Although the potassium concentration was significantly lower in the HPP group, there was some overlap. In contrast, the transtubular potassium concentration gradient and potassium-creatinine ratio differentiated patients with HPP vs non-HPP. Although only a mean ± SD of 63 ± 36 mmol of potassium chloride was administered in the patients with HPP, rebound hyperkalemia (&gt;5 mmol/L) occurred in 19 (63%) of these 30 patients. <h3>Conclusions</h3> Calculating the transtubular potassium concentration gradient and potassium-creatinine ratio provided a simple and reliable test to distinguish HPP from non-HPP. Minimal potassium chloride supplementation should be given to avoid rebound hyperkalemia in patients with HPP.