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Diagnosis: Acute Tubulointerstitial Nephritis

Impaired renal function is a common complication affecting 5%–37% of hospitalized patients with COVID-19. SARS-CoV-2 is postulated to cause AKI by diverse mechanisms, including interaction with its cellular receptor angiotensin-converting enzyme 2 (ACE2), viral immune responses, cytokine storm, hypoxemia, reduced oral intake, circulatory collapse, prothrombotic effects, and multiorgan dysfunction. Specifically, SARS-CoV-2 may directly infect the kidney via ACE2 widely expressed in proximal tubular cells and podocytes. Viral-induced cytokine storm causes massive release of granulocyte colony–stimulating factor, various interleukins, and IFN, which can injure the kidney directly or indirectly via effects on other organs, such as heart and skeletal muscle. It has been described the potential for viral infection to influence innate or adaptive immune responses that in turn trigger new glomerular diseases (such as podocytopathies and anti-GBM nephritis) or exacerbate preexisting autoimmune or alloimmune conditions (such as lupus nephritis, membranous glomerulopathy, and allograft rejection). Acute tubular injury is common and likely multifactorial. The lack of definitive virus in kidney cells argues against direct viral infection as the major pathomechanism (Kudose S, et al. Kidney Biopsy Findings in Patients with COVID-19. J Am Soc Nephrol. 2020;31(9):1959-1968. [PubMed link]).

In our case, the clinical characteristics, time of evolution and temporal relationship of the acute kidney injury with the antibiotics received, lead us to think that the tubulointerstitial inflammation was more related to the drugs than to the virus.

The patient completely improved his kidney function a couple of weeks after the biopsy.

See the chapter: Tubulointerstitial diseases of our Tutorial.

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