Acute kidney injury in patients with coronavirus disease 2019 – how much do we know?

Abstract

By the end of 2019, coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a new RNA virus belonging to the β-coronavirus cluster, started spreading in China. A few months later, it was declared a pandemic, and it is spreading all over the world causing millions of patients and hundreds of thousands of deaths. Despite respiratory manifestations being the most common symptoms with coronavirus disease 2019 (COVID-19), kidney affection was noted in many studies. There is noticeable heterogeneity in the available literature about the incidence of acute kidney injury (AKI) in COVID-19-infected patients. However, AKI was associated with higher rates of mortality. SARS-CoV-2 uses angiotensin-converting enzyme 2 receptor to enter target organs. Angiotensin-converting enzyme 2 is highly expressed in kidney tubules, which suggests that tubular injury is the main consequence of SARS-CoV-2. It remains unclear whether AKI in COVID-19-infected patients is a direct viral cytopathic effect or a part of a cytokine storm, hemodynamic instability, or hypercoagulability. It is more likely that the etiology of AKI is multifactorial. The available evidence for treatment of COVID-19 is either from observational studies or small limited controlled trials. Moreover, limited data are suggesting specific strategies for AKI management in COVID-19-infected patients. However, earlier detection and management of renal abnormalities, involving hemodynamic support, avoidance of nephrotoxic medications, and extracorporeal modalities, may help to mitigate the hazardous effect of AKI on COVID-19-infected patients. We tried to highlight the possible mechanism, management options, and magnitude of AKI in patients with COVID-19 infection.