COVID-19 is a major worldwide health concern that is linked to severe morbidity and mortality. In contrast to the majority of COVID-19 patients who experience moderate symptoms, about 5% of the patients experience serious manifestations such as acute respiratory distress syndrome, septic shock, and fatal organ failure. Although pneumonia is the main symptom of COVID-19, other organs, such as the kidneys, might also be affected by the condition. Acute kidney injury is one of the most frequent extrapulmonary symptoms of severe COVID-19. Indeed, it has been suggested that COVID-19 affects the kidney as the second most common organ after the lungs. This is due to the fact that the virus attaches to angiotensin-converting enzyme 2 (ACE2) receptors, which have significant expression in the kidney, before entering the host cells. It is important to follow up and monitor patients with COVID-19 for the occurrence of kidney damage, as timely treatment measures will lead to better clinical results and lower patient mortality. Even minor renal function impairment is a distinct risk factor for COVID-19 infection, hospitalization, and death. Furthermore, SARS-CoV-2 infections can raise mortality for those with underlying renal disorders as well as make it more difficult to treat and care for them. It can also produce new kidney damage. Kidney tubular damage is the predominant symptom of SARS-CoV-2 infection's impact on the kidney, with proteinuria as the primary clinical symptom. The pathogenesis of kidney and damage in COVID-19 patients is varied and complicated. In COVID-19 patients, the virus has the ability to infect renal tubular epithelium and podocytes directly, which is linked to Bowman's capsule protein leakage, acute tubular necrosis, mitochondrial dysfunction, and collapsing glomerulopathy. Other causes of acute kidney injury (AKI) in COVID-19 patients, including cytokine storm, lymphopenia, and macrophage activation syndrome, have been caused by SARS-CoV-2-induced immune response dysregulation. Interactions between organs, endothelial dysfunction, hypercoagulability, sepsis, and rhabdomyolysis are considered other major AKI mechanisms. In the present review, we focus on the role of each of these factors involved in AKI in COVID-19 patients.
