In a study conducted by the Feinstein Institutes for Medical Research and Northwell Health’s Nephrology Division and Department of Pathology, it was reported that biopsies performed in patients who developed acute kidney injury (AKI) after being diagnosed with coronavirus disease 2019 (COVID-19)did not detect any presence of severe acute respiratory syndrome-coronavirus2 (SARS-CoV-2) virus in the kidneys.

The reverse transcriptase-polymerase chain reaction (RT-PCR) test had confirmed the presence of SARS-CoV-2 infection; however, immunohistochemical staining of kidney biopsy samples for SARS-CoV-2 was negative in all the 10 patients included in the study. In this study published in the Journal of the American Society of Nephrology, it was seen that all patients had proteinuria, and eight required dialysis. Biopsy samples showed different grades of acute tubular necrosis in all patients with one patient even experiencing associated myoglobin cast nephropathy.

However, the pathologic analysis of biopsied kidneys did not depict any immunohistochemical evidence of SARS-CoV-2 and ultrastructural examination found no viral particles.

Another similar study was conducted in a group of 17 patients with COVID-19. Out of these, 16 patients had comorbidities, including hypertension, obesity, diabetes, malignancy, or a kidney or heart allograft. In these patients no definitive evidence of SARS-CoV-2 in the kidney cells was reported, diagnosis via biopsy formed the basis of treatment and prognosis in these patients. The authors suggested that even though patients with COVID-19 develop a wide-spectrum of glomerular and tubular diseases, there is no evidence against direct viral infection of the kidneys as the major pathomechanism for COVID-19–related kidney injury. It was concluded that cytokine-mediated effects and increased adaptive immune responses could be the causative factor behind various kidney related disorders in COVID-19 patients.

These studies clearly indicate that acute tubular necrosis is the most common finding in patients with COVID-19 and AKI. However, there has been no evidence of detecting viral presence in the kidney. There has been some evidence that the onset of COVID 19-associated AKI is temporally linked to systemic collapse and mechanical ventilation with vasopressor support was temporally related to the development of AKI. The possible mechanisms working here may be renal tropism of SARS-CoV-2. The role of cytokine-induced epithelial injury in this case is also interested, especially in patients with a carrier state of the kidney disease high-risk variants of APOL1 gene. Findings have elucidated that COVID-19 affects the kidneys in the tubular, vascular and glomerular compartments.

Resources:

1. Sharma P, Uppal NN, Wanchoo R, et al. COVID-19-associated kidney injury: A case series of kidney biopsy findings. J Am Soc Nephrol. 2020;31(9):1948-58.
2. Kudose S, Batal I, Santoriello D, et al. Kidney biopsy findings in patients with COVID-19. J Am Soc Nephrol. 2020;31(9):1959-68.