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Chaolin Huang and colleagues1 have highlighted the putative renal consequences of COVID-19 at 6 months from discharge. A decreased estimated glomerular filtration rate (eGFR) was defined as less than 90 mL/min per 1·73 m2 and was observed in 35% of participants during follow-up. The term decreased eGFR is ambiguous. According to the mean age of the cohort, chronic kidney disease should be defined as an eGFR of less than 60 mL/min per 1·73 m2.2 The usual prevalence of eGFR less than 90 mL/min per 1·73 m2 in the Chinese general population of similar ages to those in Huang and colleagues' cohort ranges between 35% and 50%.3, 4 In other words, the prevalence of eGFR of less than 90 mL/min per 1·73 m2 in COVID-19 survivors might not differ from the general population. Furthermore, the majority of patients with eGFR less than 90 mL/min per 1·73 m2 during follow-up did not show acute kidney injury during the acute phase, which suggests that the eGFR of these patients was already less than 90 mL/min per 1·73 m2 before COVID-19. Therefore, the prevalence of patients with eGFR less than 60 mL/min per 1·73 m2 at 6 months from discharge is required to factually assess the long-term effect of COVID-19 on renal function. The pathological relevance of an eGFR between 60 and 90 mL/min per 1·73 m2 is questionable in the absence of proteinuria.2 Proteinuria has been frequently described in patients with COVID-19. Our follow-up observations suggest a spontaneous remission within a few weeks after discharge.5 The available data of Huang and colleagues do not support their alarming conclusions about the poor renal prognosis at 6 months after COVID-19.

We read with interest the long-term follow-up data from hospitalised patients with COVID-19 study by Chaolin Huang and colleagues.1 The investigators report that 107 (13%) of 822 study participants with an estimated glomerular filtration rate (eGFR; calculated with the Chronic Kidney Disease Epidemiology Collaboration equation2) of 90 mL/min per 1·73 m2 or more and no acute kidney injury during the acute phase had an eGFR of less than 90 mL/min per 1·73 m2 at follow-up. Huang and colleagues interpret this observation as persistent renal dysfunction. A persistent and potentially progressive reduction in eGFR in the absence of acute kidney injury at the time of acute infection would indeed have important implications for COVID-19 follow-up surveillance. However, we want to point out that an alternative explanation is possible. eGFR is calculated on the basis of serum creatinine values, which undergo small fluctuations over time as a result of shifts in hydration and other factors.3 Such fluctuations will stochastically place some individuals with normal GFR in the eGFR group of 90 mL/min per 1·73 m2 or more during acute disease and in the eGFR group of less than 90 mL/min per 1·73 m2 at follow-up, which is not necessarily a sign of worsening kidney function. Huang and colleagues show an opposite seeming improvement of kidney function with an eGFR of 90 mL/min per 1·73 m2 or more in 142 (29·7%) of 478 patients at follow-up with an eGFR of less than 90 mL/min per 1·73 m2 and no evidence of acute kidney injury during the acute disease. We encourage the investigators to show eGFR trajectories between acute phase and follow-up independent from cutoffs to substantiate the robustness of their findings.