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{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7283670","sourcedb":"PMC","sourceid":"7283670","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7283670","text":"2.4 Myocardial, gastrointestinal, and renal symptoms: homeostasis of electrolytes\nAn essential player in maintenance of electrolyte balance and blood pressure, ACE2 is regarded by many as the principal counter‐regulatory arm in the axis of renin–angiotensin‐aldosterone system (RAAS; Santos, Ferreira, \u0026 Simões e Silva, 2008). Upon infection, SARS‐CoV‐2 binds ACE2. This results in degradation of ACE2, which subsequently dampens the counter‐effect of ACE2 on RAAS. The final effect of ACE2 in an otherwise healthy adult is to increase reabsorption of sodium and the reciprocal excretion of potassium ions (K+). The concomitant re‐uptake of water with sodium reabsorption prompts an increase in blood pressure (Weir \u0026 Rolfe, 2010). Potassium is the predominant intracellular ion, that is majorly involved in regulation of cell membrane polarity. Too low levels of K+ in blood, known as hypokalemia, can result in cellular hyper‐polarity. A hyper‐polarized cell membrane tends to be depolarized faster than normal, causing aberrancy in the function of cardiac cells (Bielecka‐Dabrowa et al., 2012).\nIn a recent cohort study, patients diagnosed with COVID‐19 were categorized into three groups: severe hypokalemia, hypokalemia, and normokalemia. The study reported that 93% of patients with a severe clinical condition had hypokalemia. Scientists did not find a direct link between gastrointestinal symptoms and hypokalemia among 108 patients with both severe or moderate hypokalemia. Further investigations established an association between parameters such as body temperature, creatine kinase (CK), creatine kinase myocardial band (CK‐MB), lactate dehydrogenase (LDH), and C‐reactive protein (CRP) with the severity of hypokalemia. Reportedly, hypokalemia was most often observed with patients who had elevated levels of serum CK, CK‐MB, LDH, and CRP. Potassium (K+) loss in the urine was determined to be the primary cause of hypokalemia.\nHypokalemia requires strenuous efforts to be corrected. This is chiefly due to the incessant loss of K+ in the urine, as a result of ACE2 degradation. In the case of COVID‐19‐associated hypokalemia, however, the patients seemed to respond well to potassium supplements when the critical phase had passed [49]. Therefore, one should consider the impact of hypokalemia in COVID‐19 morbidity, and its effect on the outcomes of treatment. This is a condition that must be carefully addressed for, as patients with COVID‐19 are more inclined to develop dysfunctions in heart, lungs, and other vital organs (Li, Hu, Su, \u0026 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