Glycosuria induced hypernatremia secondary to COVID-19

ABSTRACT

Case Report The purpose of this study is to describe a case study of possible glycosuria-induced hypernatremia in a patient hospitalized with COVID-19 acute respiratory distress syndrome. Methods Used Case study and literature review Summary of Results A 55-year-old man with a past medical history of non-insulin-dependent type II diabetes and hypertension developed hypernatremia, glycosuria, and acute kidney injury in the setting of COVID-19 pneumonia after resolution of diabetic ketoacidosis. The patient was initially admitted with a positive SARS-COVID-19 screening, a creatinine of 1.1 mg/dL (0.5-1.2) with glycosuria, and sodium of 137 mmol/L (136-145). Seventeen days into his hospital admission for severe acute respiratory distress syndrome, he developed hypernatremia (147 mmol/L). Over the subsequent twenty-two days, the patient continued to have hypernatremia up to 153 mmol/L refractory to treatment. In addition, the patient had persistent glycosuria and an elevated creatinine of 2.3 mg/dL (greater than thirty percent above his baseline). His total fluid balance was +1444 mL during this phase of hospitalization. The patient's electrolyte derangements concomitant with his worsening renal function suggests possible Fanconi syndrome. We hypothesize this is secondary to COVID-19. Conclusion COVID-19 has been shown to be associated with renal dysfunction, including acute tubular injury, such as membranous nephropathy and Fanconi syndrome. Experimental data have suggested that COVID-19 can infect renal proximal tubular cells via the Angiotensin Converting Enzyme 2 with subsequent development of incomplete Fanconi syndrome preceding acute kidney injury. Studies have also shown that glycosuria, proteinuria, pyuria, and hematuria may occur with COVID-19 regardless of comorbidities. We concluded our patient developed refractory hypernatremia secondary to glycosuria induced incomplete Fanconi syndrome due to COVID- 19.