RENIN–ANGIOTENSIN–ALDOSTERONE SYSTEM INHIBITOR USE AFTER ACUTE KIDNEY INJURY: A SYSTEMATIC REVIEW AND META-ANALYSIS

 

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RENIN–ANGIOTENSIN–ALDOSTERONE SYSTEM INHIBITOR USE AFTER ACUTE KIDNEY INJURY: A SYSTEMATIC REVIEW AND META-ANALYSIS

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Omar
Elkoumi
Omar Elkoumi omarelkoumi@gmail.com Suez University Faculty of Medicine Suez Egypt *
Ahmed Elkoumi ahmedelkoumi@yahoo.com The Ministry of Health and Population Health Affairs Directorate of El Sharqeya El Sharqeya Egypt -
Mariam Khaled Elbairy mariam.ksah@med.suezuni.edu.eg Suez University Faculty of Medicine Suez Egypt -
Mostafa Adel T. Mahmoud mostafaadeltawfik12@gmail.com Beni Suef University Faculty of Medicine Beni Suef Egypt -
Ahmad Beddor Beddorahmad@gmail.com Yarmouk University Faculty of Medicine Irbid Jordan -
Mohamed Hamouda Elkasaby mohamedhamouda2182000@gmail.com Al-Azhar University Faculty of Medicine Cairo Egypt -
Elsayed S. Moubarak elsayed.said.moubarak@gmail.com Cairo University Faculty of Medicine Cairo Egypt -
Ayah Abdulgadir Abdulgadirayah@gmail.com University of Khartoum Faculty of Medicine Khartoum Sudan -
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The use of renin–angiotensin–aldosterone system inhibitors (RAASi) following an episode of acute kidney injury (AKI) remains controversial. While clinicians often avoid RAASi because of concerns about hyperkalemia and recurrent AKI, these agents confer well-established cardio-renal benefits in other settings. This systematic review and meta-analysis evaluated the association between post-AKI RAASi use and major clinical outcomes.

A comprehensive search of PubMed, Scopus, Web of Science, and Google Scholar was conducted from inception to October 2025. We identified studies assessing RAASi use versus non-use after AKI. The primary outcome was all-cause mortality; secondary outcomes included recurrent AKI, hyperkalemia, and intensive care unit (ICU) stay. Hazard ratios (HRs) or risk ratios (RRs) were pooled using a fixed-effects model when low heterogeneity was present (I² < 50%) and a random-effects model otherwise. Review Manager (RevMan) was used for statistical analysis.

Seventeen studies encompassing over 30,000 patients met the inclusion criteria. Post-AKI RAASi use was not associated with a statistically significant difference in all-cause mortality compared with non-use (HR: 0.88; 95% CI, 0.74–1.05; P = 0.15). Similarly, no significant differences were observed for recurrent AKI (HR: 0.96; 95% CI, 0.90–1.01; P = 0.13; I² = 0%), hyperkalemia (RR: 0.94; 95% CI, 0.68–1.29; P = 0.69), or intensive care unit stay (RR: 0.96; 95% CI, 0.87–1.05; P = 0.38).

Among patients who survived AKI, RAASi use was not associated with higher risks of mortality, recurrent AKI, or hyperkalemia compared with non-use. These findings indicate that concerns regarding the safety of post-AKI RAASi therapy may be overstated, supporting individualized clinical assessment. High-quality randomized controlled trials are needed to establish the optimal use of RAASi in the post-AKI setting.

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