Abstract
Introduction
Pseudohyperkalemia is an artifactual elevation in serum potassium resulting from in vitro release of potassium during blood cell lysis. It should be suspected when hyperkalemia occurs in the absence of renal dysfunction, other electrolyte abnormalities, or relevant medications. Marked thrombocytosis, particularly in essential thrombocythemia (ET), can cause pseudohyperkalemia through platelet-mediated potassium release during clotting.
Distinguishing pseudohyperkalemia from true hyperkalemia is critical, as untreated hyperkalemia can cause life-threatening cardiac arrhythmias, while unnecessary treatment of pseudohyperkalemia may result in iatrogenic complications. Although hematologic causes of pseudohyperkalemia are well recognized, this condition remains underappreciated in clinical practice. We report a case of pseudohyperkalemia in a patient with marked thrombocytosis, later diagnosed with essential thrombocythemia.
Case Info
A 75-year-old man with a history of hypertension, ischemic stroke, adrenal incidentaloma, left peroneal deep vein thrombosis, and treated hepatitis C was found to have hyperkalemia on routine outpatient laboratory testing, prompting his primary care team to recommend evaluation in the emergency department (ED).
Laboratory testing revealed a serum potassium of 6.3 mmol/L in the setting of marked thrombocytosis (platelet count 807,000/µL). Renal function was at baseline (creatinine of 1.1 mg/dL), and there were no other electrolyte or acid-base abnormalities. The patient was asymptomatic and was not taking medications known to cause hyperkalemia. The critical result was relayed to the on-call resident, and the patient was instructed to seek immediate evaluation given the potential risk of cardiac arrhythmias. The patient declined evaluation in the ED and was subsequently contacted by the primary care office and instructed to return for repeat laboratory testing.
Repeat testing 10 days later demonstrated normalization of serum potassium to 4.3 mmol/L. No potassium-lowering therapy was administered. At the time of the hyperkalemia episode, the patient had persistent thrombocytosis. His platelet count had increased from 504,000/µL in 2023 to 807,000/µL at the time of the episode and ultimately peaked at 958,000/µL. Hematologic evaluation revealed a positive JAK2 V617F mutation, and bone marrow biopsy demonstrated findings consistent with ET. He was started on hydroxyurea and aspirin, with progressive improvement in his platelet count. Following treatment, his platelet count decreased to 385,000/µL, while serum potassium remained normal.
Disc Clinical
Pseudohyperkalemia may result from preanalytical factors, including improper blood collection, sample handling, transport, or storage, but can also occur despite appropriate specimen collection in the setting of marked leukocytosis or thrombocytosis. Among hematologic causes, pseudohyperkalemia is most frequently associated with ET but may also occur with reactive thrombocytosis. The mechanism involves potassium leakage into the serum from the numerous platelets trapped within the clot.
When unexplained hyperkalemia occurs in a patient with thrombocytosis, the potassium level should be reassessed using an anticoagulated plasma sample or venous whole blood. A normal potassium concentration in a simultaneously collected plasma or whole-blood sample supports pseudohyperkalemia.
Conclusion
In our patient, the temporal association between treatment of ET and normalization of serum potassium supported pseudohyperkalemia. Recognition of this association is important to prevent unnecessary diagnostic evaluation and potentially harmful treatment, including inappropriate administration of potassium-lowering therapies or dialysis.