Peer-review started: June 25, 2020
First decision: August 22, 2020
Revised: October 3, 2020
Accepted: October 20, 2020
Article in press: October 20, 2020
Published online: November 29, 2020
Processing time: 152 Days and 16.3 Hours
Coronavirus disease 2019 (COVID-19) continues to affect millions of people around the globe. As data emerge, it is becoming more evident that extrapulmonary organ involvement, particularly the kidneys, highly influence mortality. The incidence of acute kidney injury has been estimated to be 30% in COVID-19 non-survivors. Current evidence suggests four broad mechanisms of renal injury: Hypovolaemia, acute respiratory distress syndrome related, cytokine storm and direct viral invasion as seen on renal autopsy findings. We look to critically assess the epidemiology, pathophysiology and management of kidney injury in COVID-19.
Core Tip: Kidney injury in coronavirus disease 2019 (COVID-19) is associated with increased mortality with hypovolaemia, acute respiratory distress syndrome (ARDS), cytokine storm and direct viral invasion having a prominent pathophysiological role. Haematuria and proteinuria are present in a high proportion of cases reflecting possible glomerular involvement, and collapsing glomerulopathy has also been reported in genetically predisposed patients. This is further supported by autopsy findings showing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in proximal tubules and podocytes. Evidence supports a conservative fluid management strategy in COVID-19 associated ARDS with standard indications for renal replacement therapy. Hypercoagulation is a prominent feature leading to filter clotting, thus regional citrate anticoagulation should be used. Kidney transplant recipients with COVID-19 should have immunosuppression reduced.