A Varied Presentation of Fanconi Syndrome Following AKI in COVID-19 Infection
- Fluid, Electrolyte, Acid-Base Disorders: Clinical - I
November 02, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
- Sivaprakasam, Thabuna, University of South Dakota, Sioux Falls, South Dakota, United States
- Panneerselvam, Deepan, University of South Dakota, Sioux Falls, South Dakota, United States
Renal pathology in COVID-19 may manifest as glomerulopathies, tubular injuries, acute kidney injury (AKI), and CKD. One such pathology is generalized proximal convoluted tubular (PCT) dysfunction, referred to as Fanconi’s syndrome. We present a case of COVID-19 infection associated with AKI followed by Fanconi syndrome, characterized by persistent electrolyte abnormalities and metabolic acidosis. Incomplete Fanconi's syndrome in COVID has occurred before the onset of AKI, but here our patient develops it after the resolution of the AKI.
A 60-year-old female was admitted for severe COVID-19 infection and intubated due to respiratory failure. She eventually developed AKI which resolved quickly with fluids. Labs showed persistent normal anion gap metabolic acidosis (NAGMA) even after AKI resolution, along with hyponatremia, hypokalemia, hypophosphatemia, hypocalcemia, and hypomagnesemia. Nephrology was consulted for the persistent electrolyte disturbances despite adequate replacement and hyperchloremic NAGMA. Urine studies showed mild renal tubular acidosis but negative for proteinuria and glycosuria. Post-COVID Fanconi syndrome was suspected, and electrolyte monitoring with replacement was continued. Eventually, she was extubated and with the recovery of her respiratory status - electrolyte disturbances, and metabolic acidosis also slowly normalized. The patient was discharged on electrolyte supplements and had stable renal function and electrolytes at the follow-up.
Tubulopathies can be explained by the direct toxic effect of the virus via the ACE2 ligand, expressed on proximal and distal tubular cells. Incomplete Fanconi’s in COVID-19 infection has been described based on 4 specific PCT abnormalities (proteinuria, renal phosphate wasting, hyperuricosuria, and glycosuria). But this case presented differently with varied electrolyte disturbances and acidosis. Fanconi’s in COVID usually precedes AKI, possibly acting as a predictor of AKI or can occur alone. But here, it evolved after the resolution of AKI, questioning its utility as such a predictor. It is important to acknowledge this significant association between COVID-19 and tubulopathies to explain some persistent electrolyte and acid-base abnormalities in such patients. This case also emphasizes that there might be more unique ramifications of COVID-19 to be expected in every organ system.