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Coronavirus disease 2019 (COVID-19)-associated acute kidney injury (AKI) was associated with a greater rate of estimated glomerular filtration rate (eGFR) decrease after hospital discharge compared with AKI in patients without COVID-19, independent of underlying comorbidities or AKI severity, according to a study published in JAMA Network Open. These findings suggest that patients recovering from COVID-19-associated AKI require monitoring of kidney function following hospital discharge.
“Although the acute effects of COVID-19 on kidney function have been studied, the intermediate- and long-term kidney outcomes after COVID-19-associated AKI remain unknown,” wrote James Nugent, MD, Yale University School of Medicine, New Haven, Connecticut, and colleagues. “In the absence of long-term follow-up data for patients with COVID-19-associated AKI, measuring the eGFR slope post hospitalisation may inform prediction of future kidney disease progression.”
“This eGFR trajectory may reinforce the importance of monitoring kidney function after AKI and studying interventions to limit kidney disease after COVID-19-associated AKI,” the authors noted.
The retrospective cohort study conducted at 5 hospitals in Connecticut and Rhode Island from March 10 to August 31, 2020 involved 182 patients with COVID-19-associated AKI and 1,430 patients with AKI not associated with COVID-19. The median age of the cohort was 69.7 years and half of the cohort were women.
Primary outcome was the rate of change in eGFR (eGFR slope) from the time of discharge among patients with and without COVID-19-associated AKI who had at least 1 serum creatinine level measurement as outpatients following their hospitalisation. The secondary outcome was the time to AKI recovery for the subgroup of patients whose kidney function had not returned to the baseline level by discharge.
In the unadjusted mixed-effects model, the mean rate of eGFR decline was –11.3 mL/min/1.73 m2/y (95% confidence interval [CI], –22.1 to –0.4 mL/min/1.73 m2/y; P = 0.04) faster for patients with COVID-19-associated AKI compared with patients with AKI not associated with COVID-19. The difference in eGFR slope persisted after adjusting for baseline demographic characteristics and comorbidities (–12.4; 95% CI, –23.7 to –1.2 mL/min/1.73 m2/y; P = 0.03).
In the fully adjusted model including both baseline patient characteristics and comorbidities as well as peak serum creatinine levels and dialysis requirements, patients with COVID-19-associated AKI continued to show an increased rate of eGFR decrease (–14.0; 95% CI, –25.1 to –2.9 mL/min/1.73 m2/y; P = 0.01).
Meanwhile, in the subgroup of patients who had not achieved AKI recovery by discharge (n = 319), COVID-19-associated AKI was associated with decreased kidney recovery during outpatient follow-up (adjusted hazard ratio, 0.57; 95% CI, 0.35-0.92; P = 0.02).
“Because patients with COVID-19 develop more severe AKI compared with those without COVID-19, patients with COVID-19-associated AKI may be expected to have a faster eGFR decrease after discharge, as we observed in our study population, independent of a patient’s underlying comorbidities,” the authors wrote. “The persistence of this outcome after adjusting for AKI severity, represented by peak creatinine levels and the need for dialysis, suggests that the accelerated eGFR decrease may be mediated by other markers of AKI severity, additional hospitalisation-related exposures associated with eGFR decrease, the hyperinflammatory state associated with COVID-19, or residual direct effects of SARS-CoV-2.”
“Identifying predictors of longitudinal eGFR decrease in patients with COVID-19-associated AKI may help prioritise which patients need close outpatient follow-up during the pandemic,” the authors added. “A better understanding of COVID-19–associated AKI should provide opportunities for clinical trials to improve outcomes and inform the guidelines of post-COVID-19–associated AKI outpatient management.”
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