Hypokalemia is highly prevalent among patients with coronavirus disease 2019 (COVID-19), according to investigators.

In a study of 175 patients with COVID-19 receiving care at hospitals in Wenzhou, Zhejiang Province, China, 64 (37%) had hypokalemia, 31 (18%) had severe hypokalemia, and 80 (46%) had normokalemia, Dong Chen, MD, of The Ding Li Clinical College of Wenzhou Medical University, and colleagues reported in JAMA Network Open.

The novel coronavirus that causes COVID-19 — severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) — binds to angiotensin-converting enzyme 2 (ACE2). The investigators concluded that the high prevalence of hypokalemia among patients with COVID-19 suggests the presence of disordered renin-angiotensin-system (RAS) activity, which increases as a result of decreased counteractivity of ACE2.

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Patients with severe hypokalemia (plasma potassium levels below 3 mmol/L) were treated with potassium chloride supplements at a dosage of 3 g/d, for a total mean of 34 g of potassium chloride during their hospital stay. Three severely ill patients with hypokalemia required potassium supplements for 10 to 14 days to have steady normokalemia, whereas 3 mildly ill patients with hypokalemia normokalemia after receiving potassium supplements for 5 to 8 days.

“Because of the possible effects on cardiovascular functions, neurohormonal activation, and other vital organs by hypokalemia, clinicians should pay attention to hypokalemia and the patients’ response to [potassium] supplements,” the authors advised.

Hypokalemia correction is challenging because of continuous renal loss of potassium resulting from the degradation of ACE2 by the binding of SARSCoV-2, according to the investigators.

The cessation of potassium loss may be a reliable, timely, and sensitive biomarker that reflects the end of disruption of the RAS by the coronavirus, they stated.

The present study also found that the degree of hypokalemia was associated with some clinical features that reflected the severity of the disease, including underlying conditions, high body temperature, and, notably, elevated laboratory indices reflecting myocardial injuries.

Although both gastrointestinal (GI) and urinary loss of potassium could cause hypokalemia, the study’s findings suggest that GI loss might not contribute much to hypokalemia, the investigators said. Only a small proportion of patients with hypokalemia had GI symptoms, they noted.

In addition, among patients with hypokalemia, there were no differences between those with and without diarrhea, and most patients had mild diarrhea. “Therefore, hypokalemia might primarily result from increased urine loss.”

The new report adds to growing evidence of COVID-19’s adverse effects on the kidneys. For example, investigators at the Feinstein Institutes for Medical Research in Manhasset, New York, found that acute kidney injury (AKI) developed in 1993 (36.6%) of 5449 patients hospitalized with COVID-19 at 13 Northwell Health hospitals in the New York metropolitan area from March 1 to April 5, 2020. According to the report, which was published in Kidney International, AKI was mainly observed in patients with respiratory failure, with AKI developing in 89.7% of patients on mechanical ventilation compared with 21.7% of patients not requiring ventilation.

This article originally appeared on Renal and Urology News