This is the authors' abstract. We don't add key points for this paper.
Introduction Data on the incidence and risk factors for renal long COVID are scarce. We aimed to investigate two acute kidney injury (AKI) phenotypes – community (CA-AKI) and hospital-acquired (HA-AKI) – and the development of late kidney dysfunction in survivors of COVID-19 hospitalization. Methods This is a prospective cohort study of survivors of moderate to severe COVID-19 hospitalization in Brazil, from March to August 2020. Patients were assessed for up to 11 months after hospital discharge. Exposure was CA- and HA-AKI. Main outcome was kidney dysfunction defined as incident low estimated glomerular filtration rate (eGFR; <60 mL/min/1.73m 2 ) and/or eGFR decline ≥25% from discharge at follow-up. An adjusted binary logistic regression analysis was run. Results A total of 655 survivors were evaluated (6.5±1.9 follow-up months); 79% had AKI (35% CA and 43% HA); 14% used kidney replacement therapy. Late kidney dysfunction occurred in 28% of the patients (16% incident low eGFR and 27% eGFR decline ≥25%). CA-AKI, but not HA-AKI, was independently associated with late kidney dysfunction (adjusted odds ratio [aOR]=7.3, 95%CI: 3.6 to 15.8 and aOR=2.2, 95%CI: 0.9 to 4.8, respectively). Conclusion In conclusion, late kidney dysfunction affected one in four COVID-19 survivors. CA-AKI, but not HA-AKI, was an independent risk factor for late kidney dysfunction. These findings suggest that renal long COVID might be frequent and that a specific AKI phenotype (CA-AKI) may play a crucial role in its development. Our research highlights the need for CA-AKI prevention and for the long-term follow-up and care of patients affected by this AKI phenotype during COVID-19 infection.
No takes yet. Share an insight, caveat, or question.
Ribeiro et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: