Hypophosphatemia in Coronavirus Disease 2019 (COVID-19), Complications, and Considerations: A Systematic Review

Figure 2

Potential risk factors associated with hypophosphatemia in COVID-19. Green color: associated with low intake and malabsorption. Vitamin D deficiency decreases intestinal and renal phosphate absorption. Malnutrition could be mostly secondary to chronic diseases, including end-stage renal disease, pulmonary diseases, or malignancy. Red color: associated with increased renal excretion of phosphate. Carbonic anhydrase inhibitors, thiazides, and furosemide are among the most common effective factors in hypophosphatemia induction. Proximal tubular damage in COVID-19 infection might be attributed to renal phosphate loss. Blue color: associated with cellular shift mechanism. Volume overload is mainly seen in the setting of heart failure. Respiratory alkalosis results in cellular glycolysis and further phosphate shift into the cells. Glucocorticoids reduce the renal reabsorption of phosphate in addition to the effects on glucose synthesis. Catecholamine release through induction of glycogenolysis could cause hypophosphatemia. Insulin therapy increases cellular phosphate demand to produce high-energy phosphate bonds, ultimately resulting in hypophosphatemia.