Authors: Fontana F, Cazzato S, Giovanella S, Ballestri M, Leonelli M, Mori G

PMID: 32838081 PMCID: PMC7363608 DOI: 10.1016/j.ekir.2020.07.008


Kidney dysfunction is frequently reported in patients with coronavirus disease 2019 (COVID-19). A recent large cohort study described an incidence of acute kidney injury (AKI) of 36% in patients who were hospitalized with COVID-19; AKI (often mild) was temporally linked with respiratory failure and associated with a poor prognosis.1 Many factors may be at play in determining kidney dysfunction in patients with COVID-19 who are critically ill; moreover, human kidneys have been reported as potential targets for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Most pathologic descriptions of kidney involvement in COVID-19 are derived from autopsy studies,S1–S5 with the main abnormality reportedly being acute tubular injury (ATI) claimed as being caused by viral infection. Few reports of kidney biopsy specimens obtained on clinical indications in patients with COVID-19 are currently available; interestingly, most of them describe a picture of collapsing glomerulopathy considered secondary to viral infection.2,3 Only Rossi et al.4 recently reported a case of ATI and focal acute tubular necrosis with no evidence of kidney viral localization in a critically ill patient with COVID-19. AKI in critically ill patients with COVID-19 can be multifactorial, and the toxicity of drugs used to treat septic status could contribute to kidney damage. We describe ATI and oxalate nephropathy likely caused by excessive vitamin C administration in 2 patients who underwent kidney biopsy procedures for slowly resolving AKI after acute respiratory distress syndrome (ARDS) due to COVID-19.

Keywords: Vitamin C, COVID-19, Oxalate Nephropathy