#898 Acceleration in kidney function decline after COVID-19 infection: the Stockholm CREAtinine Measurements (SCREAM) project

Background and Aims Severe COVID-19 infection, which usually presents as a viral pneumonia, has been observed to frequently be accompanied by acute kidney injury (AKI). However, possible effects of COVID-19 on long-term kidney function decline are not well quantified. We investigated whether kidney function decline is accelerated after COVID-19 infection, and whether the progression of decline differs from other respiratory tract infections. Method We undertook an observational study using the SCREAM project, including adults from Stockholm who survived COVID-19 infection (February 2020-December 2021), and adults who survived pneumonia caused by other pathogens (February 2018-December 2019, historical comparison cohort). We used generalized estimating equations to examine the age- and sex-adjusted slopes of estimated glomerular filtration rate (eGFR) decline in the 2 years before versus after each infection (i.e., intra-individual changes). We also compared to post-infection eGFR slopes of COVID-19 versus pneumonia (i.e., inter-individual changes) adjusting for a broad range of demographic, socioeconomic and clinical covariates (including pre-infection eGFR slope). We stratified analyses by whether the infection required hospitalization, hypothesizing more severe infection may lead to more rapid eGFR decline. Results We identified 59 267 COVID-19 survivors and 20 138 pneumonia survivors with repeated outpatient eGFR measurements. The pneumonia group was older, with lower income, and more comorbidities and healthcare utilization than the COVID-19 group. Both infections resulted in an accelerated decline of the observed eGFR slope, but with a greater magnitude of intraindividual slope changes after COVID-19 (Fig. 1): eGFR decline was 6.14 (95% confidence interval [95% CI] 5.88-6.41) ml/min/1.73 m2/year faster after COVID-19, and 2.52 (95% CI 2.17-2.88) ml/min/1.73 m2/year faster after pneumonia. When adjusting for pre-infection slope and other identified confounders (Fig. 2), COVID-19 survivors had an eGFR decline that was 0.47 (95% CI 0.29-0.66) ml/min/1.73 m2/year faster than that of pneumonia survivors. Observed intra- and inter-individual differences were larger in magnitude among participants whose infection required hospitalization. Conclusion COVID-19 infection is associated with a subsequent acceleration in eGFR decline, of a larger magnitude than other respiratory tract infections, and particularly among more severe cases that required hospitalization. We propose that survivors of severe COVID-19 receive monitoring of kidney function, and that policymakers consider implications for future healthcare planning and renal service provision.