Abstract: PO1125
Transient Hyperkalemia Following Treatment of Chronic Hypokalemia: A Case Report and Review of Distal Tubule Physiology
Session Information
- Salt, Potassium, and Water Balance: Clinical
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolyte, and Acid-Base Disorders
- 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Breeggemann, Matthew Clarence, University of California San Francisco, San Francisco, California, United States
- Gluck, Stephen L., University of California San Francisco, San Francisco, California, United States
Introduction
Hypokalemia is a frequently encountered electrolyte disorder usually resulting from decreased dietary intake, gastrointestinal, and/or renal wasting. In distal tubule cells, with no lysine (WNK) kinases bind with Ste20-related proline-alanine-rich kinase (SPAK) and oxidative stress-responsive kinase-1 (OSR1) to form WNK bodies. WNK bodies are thought to increase the activity of the sodium-chloride cotransporter (NCC) leading to decreased sodium delivery to the epithelial sodium channel (ENaC) found in principal cells. This process is critical in hypokalemic states as it results in decreased urinary potassium wasting through the renal outer medullary potassium channel (ROMK). Here we report a case of a young man with alcohol use disorder and chronic hypokalemia who was hospitalized for muscle weakness, abdominal pain, and intractable emesis. During treatment of his hypokalemia, he unexpectedly developed transient hyperkalemia.
Case Description
The clinical intrigue of this case was the unexpected finding of acute transient hyperkalemia during treatment for hypokalemia. His potassium was 2.5 mEq/L on the day of admission. Four days later, with a creatinine at baseline (0.9 mg/dL), potassium abruptly increased to 6.7 mEq/L. Repeat measurement one hour later was 6.4 mEq/L. Over the course of his hospitalization prior to the critical hyperkalemia lab result, he had received approximately 340 mEq of potassium supplementation. 24 hour urine potassium was 35 mEq/L. Aldosterone was 5.8 ng/dL and renin was 0.3 ng/mL/hr (ratio 19). Potassium levels returned to normal following administration of furosemide and sodium polystyrene sulfonate.
Discussion
We propose that the adaptive mechanisms of the distal tubule during hypokalemia require time to revert back to a nonactive state. Transient hyperkalemia may be observed during these "refractory" periods. The time required for disassembly of WNK bodies following resolution of hypokalemia is unknown. Our postulation could explain a similar observation of transient hyperkalemia seen in a case published in 1953 of a young woman treated for chronic hypokalemia (Schwartz, 1953). Critical hyperkalemia is an important consideration when treating patients with chronic hypokalemia.