A 67-year-old Japanese woman with a history of contact with a COVID-19 patient presented with a one-day history of fever, malaise, and dyspnea, and was hospitalized with a positive nasopharyngeal swab test for SARS-CoV-2 LAMP. Chest CT revealed bilateral patchy infiltrates. The patient was treated with remdesivir and dexamethasone and supplemental oxygen supplied via a nasal cannula. The supplemental oxygen therapy was continued for 6 days, and the drug administration was completed on the 10th day of hospitalization. The patient was then scheduled to be discharged, when she developed severe hyponatremia with a serum Na level of 110 mEq/L, but no consciousness disorder.

The patient was diagnosed as having SIADH after several examinations suggesting higher levels of secretion of antidiuretic hormone, with a higher specific gravity of the urine than that of the serum, in addition to evidence of normal functioning of the thyroid, adrenal, and pituitary glands, and of the liver and kidneys. Whole-body CT showed no evidence of any tumors. The hospitalization was extended for correcting the serum sodium levels by restriction of water intake. It was assumed that the SIADH was caused by COVID-19, presumably by the elevated serum IL-6 levels inducing secretion of ADH, similar to the phenomenon reported in other inflammatory diseases associated with elevated serum IL-6 levels.

COVID-19 could lead to SIADH due of unresolved systemic inflammation even in the absence of worsening of the findings of chest imaging after the completion of antiviral treatments. Further studies are required to evaluate the correlation between the inflammatory state (e.g., serum concentration of IL-6) and serum ADH level causing hyponatremia during the clinical course of COVID-19.