Almost a quarter of patients hospitalized with coronavirus disease 2019 also develop acute kidney injury. The pathophysiology is thought to involve local and systemic inflammatory and immune responses, endothelial injury, and stimulation of coagulation pathways and the renin-angiotensin system. 

Even though doubtful, direct viral infection with renal tropism of the virus has also been suggested. 

Some other factors commonly seen in critically ill patients include mechanical ventilation, hypoxia, hypotension, low cardiac output, and nephrotoxic agents, leading to kidney injury or functional decline in the patients who have developed severe disease.

The most common assessment in patients with COVID 19 acute kidney injury is acute tubular injury. Proteinuria, collapsing glomerulopathy, endothelial injury, or thrombotic microangiopathy have also been reported. Viral RNA and protein were detected in the kidney in some studies. Besides, SARS_CoV-2 samples have also been reported in urine samples, suggestive of the release of viral particles from infected, damaged tubule epithelial cells or the filtration of viral fragments. Hence, it has been confirmed that SARS-CoV-2 can infect kidney tissue; however, a direct role of the virus in developing acute kidney injury is still not established. 

One of the key mechanisms working towards damaging renal kidney tissues is the increased release of inflammatory mediators by immune and resident kidney cells. Inflammatory mediators such as TNF and FAS might bind to their receptors in the endothelial and tubular epithelial cells leading to a direct injury. Therefore, it has been suggested that anti-inflammatory drugs such as steroids and IL-6 blockers may play an important role in restricting the progression of severe acute kidney injury in COVID 19 patients. 

Reference: Legrand M, Bell S, Forni L, Jonnidis M, Koyner JL. Pathophysiology of COVID 19 associated acute kidney injury. Nature Reviews Nephrology. 2021; DOI;10.1038/s41581-021-00452-0