Association of SARS-CoV-2 renal tropism with acute kidney injury

In their report on the association of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) renal tropism with acute kidney injury, Fabian Braun and colleagues¹ do not appear to have provided evidence for acute kidney injury as defined in the Kidney Disease: Improving Global Outcomes (KDIGO) clinical practice guidelines—that is, an increase in serum creatinine (SCr) by 26·5 μmol/L or more within 48 h; an increase in SCr to 1·5 times or more from baseline, which is known or presumed to have occurred within the previous 7 days; or a urine volume of less than 0·5 ml/kg per h for 6 h.² Using case 45 (a woman aged 87 years) as an example, SCr on admission was 103 μmol/L, with an estimated glomerular filtration rate (eGFR) of 43 mL/min per 1·73 m² using the Chronic Kidney Disease Epidemiology Collaboration equation.¹ Looking at the renal function dynamics in figure 1 of their appendix,¹ if the patient's eGFR had decreased to 35–40 mL/min per 1·73 m² (equivalent to an SCr of 107–121 μmol/L), then there is no clear evidence for acute kidney injury based on reported data.

It is surprising that two of the 12 patients (cases 17 and 48) with a reported history of chronic kidney disease had eGFR values of 60 mL/min per 1·73 m² or more, which is not consistent with the KDIGO definition of chronic kidney disease, unless there is persistent albuminuria.³ Acute kidney injury was reported in the other ten patients with chronic kidney disease.¹ In contrast, the seven patients who did not have acute kidney injury were not reported to have chronic kidney disease.¹ Underlying chronic kidney disease is a risk factor for acute kidney injury.⁴

In the absence of specific therapeutic options, application of the KDIGO supportive care guidelines (eg, regular monitoring of urinary output and SCr, and avoidance of nephrotoxins) could reduce the incidence and severity of acute kidney injury in COVID-19.⁵