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New insights into COVID-19-associated kidney disease

01.09.2021: A recently published study by Vetmeduni Vienna deciphers the genetic programs of interferon activation and the regulation of the SARS-CoV-2 receptor ACE2 (angiotensin-converting enzyme 2) in the kidney. The study also demonstrates that the drug ruxolitinib can dampen the activation of interferon-activated transcriptomes and the SARS-CoV-2 receptor ACE2 in human renal proximal tubules. These findings allow for a new treatment approach for COVID-19-associated kidney disease.

SARS-CoV-2 infections can trigger cytokine storms and activate genetic programs that lead to progressive hyperinflammation in multiple organs of COVID-19 patients. While COVID-19 is known to impact kidney function, leading to increased mortality, the cytokine response of the renal epithelium has not been studied in detail.

New therapeutic option against kidney damage caused by COVID-19

In their recently published study, an international research team reports for the first time on the genetic programs activated by interferons in the proximal renal tubules. The researchers from Vetmeduni Vienna and the American National Institutes of Health (NIH) show robust cytokine response with 1,169 genes and efficient quenching of gene expression by the JAK inhibitor ruxolitinib that is used in COVID-19 treatment.

Research team for the first time identifies genetic processes in kidney cells

By integrating their data with those from other tissues, the researchers were able to identify kidney-specific interferon responses. According to Jakub Jankowski, the study’s first author, “The findings provide in-depth understanding of interferon-mediated immune responses in the kidney, especially in the context of the activation of the enzyme ACE2 observed in SARS-CoV-2 infection.”

Common COVID-19 complication: acute kidney injury 

A form of acute respiratory distress syndrome (ARDS) caused by SARS-CoV-2 is a major contributor to the death toll in COVID-19. ARDS is closely associated with cytokine storm, an unrestrained release of proinflammatory cytokines and chemokines. This in turn can lead to multiorgan failure and coagulopathies affecting the kidney and other organs. Acute kidney injury (AKI) is a known complication of COVID-19, and even before the SARS-CoV-2 pandemic, AKI was a significant medical and socioeconomic burden, with an estimated one-third of intensive care patients suffering from a decline in kidney function. In addition to other mechanisms, SARS-CoV-2 has been shown to infect kidney epithelium, directly contributing to kidney damage. It is also known that its infectivity depends on a receptor, angiotensin-converting enzyme 2 (ACE2).


The article “JAK inhibitors dampen activation of interferon-activated transcriptomes and the SARS-CoV-2 receptor ACE2 in human renal proximal tubules” by Jakub Jankowski, Hye Kyung Lee, Julia Wilflingseder and Lothar Hennighausen was published in iScience.

To the scientific article