SYNONYMOUS with the development of COVID-19 is often kidney damage. Now, a study on kidney cells has been conducted to establish if this link is a direct result of viral infection, another condition, or the immune response of the body to infection. Conducted in Israel, the investigation was led by Benjamin Dekel, Sheba Medical Centre, Tel Aviv, Israel, and involved the cultivation of kidney cells before infection with coronavirus in lab dishes.
Dekel explained the purpose of the current research: “If we’re able to limit the common scenario of acute kidney injury in the first place, then there might be the possibility to minimise potential damage caused by the virus.”
Cells were cultured either as a 3D spheroid imitating the healthy kidney or as a 2D layer mimicking the cells of an acutely injured kidney. The researchers discovered that although the virus enters, infects, and replicates in human kidney cells, this did not always lead to cell death. Prior to infection, the cells contained high levels of interferon signalling molecules, with infection stimulating an inflammatory response that increased the presence of these signalling molecules. Contrastingly, kidney cells that were infected in the same way but deficient in such signalling molecules experienced cell death, suggesting a protective effect.
Dekel explained the data, which demonstrated that cells which mimicked an acutely injured kidney were more prone to infection and additional injury but not cell death: “The data indicate that it is unlikely that the virus is a primary cause of acute kidney injury seen in COVID-19 patients. It implies that if such injury takes place in the kidney by any cause, the virus might jump on the wagon to intensify it.”
Further study is needed in this area, building on the profound foundations the study lays. The current findings require expansion to carry greater weight in a field of literature spotlighted by the coronavirus pandemic.
