This is a topical review of the effects of coronaviruses on the kidney and includes a description of the mechanisms of kidney damage by SARS, MERS and COVID-19. The authors quote two previous reports which estimate the incidence of acute kidney injury (AKI) of 29% in those who recovered from COVID-19 and 37.55% in those who did not. Baseline serum creatinine level was increased at admission in 15.5%, proteinuria in 44%, and haematuria in 26.9%. Twenty-nine percent had AKI and eventually 17% received renal replacement therapy. SARS-CoV-2 has been confirmed to enter the body via binding to ACE2; ACE2 and members of the serine protease family are highly expressed on renal podocytes and tubular epithelium. Electron microscopy and other detection modalities have confirmed the presence of SARS-CoV-2 in proximal tubular epithelium and podocytes. The specific mechanism of renal injury remains unconfirmed. This review raises several pertinent issues. Attention should be paid to the early monitoring of renal function, with balanced fluid resuscitation and avoidance of known nephrotoxic agents to reduce the impact of SARS-CoV-2 on the kidney. Although currently viral transmission is thought to occur through respiratory droplets, viral nucleic acid has been detected in urine in 4 out of 58 cases (6.9%) in one study and in none in another, which makes urine-mediated transmission a possibility, albeit less frequent. The authors postulate splashing of urine, which may generate aerosol, and direct urine-oral transmission from contact with urine during urological procedures may be potential modes of viral transmission; this is as yet unconfirmed. They recommend avoidance of direct contact with urine, wearing of respiratory shields and other barrier systems when performing cystoscopies and other urological procedures, and flushing toilets with the lid down as general measures.