{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T10:45:51Z","timestamp":1793097951715,"version":"4.5.0"},"reference-count":60,"publisher":"Oxford University Press (OUP)","license":[{"start":{"date-parts":[[2026,5,23]],"date-time":"2026-05-23T00:00:00Z","timestamp":1779494400000},"content-version":"am","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100018288","name":"AstraZeneca Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100018288","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Fondation Mont-Godinne"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Complement inhibitors are increasingly used in kidney diseases, ranging from complement-mediated thrombotic microangiopathies to glomerulonephritis. Because complement is central to host defence against encapsulated bacteria, therapeutic blockade creates a predictable infectious vulnerability requiring structured prevention strategies. This narrative review integrates complement biology with evidence from pivotal kidney trials, pharmacovigilance analyses, and national public health recommendations to propose a pragmatic framework for mitigating infection-risk in patients treated with complement inhibitors. Key complement functions (C3b-mediated opsonization, C3a\/C5a-driven inflammation, and membrane attack complex formation) underlie target-specific patterns of infectious risk. Terminal C5 inhibition (eculizumab, ravulizumab) confers a reproducible exposure-adjusted risk of invasive meningococcal disease, including rare but documented infection-related mortality, with breakthrough infections reported despite vaccination. In contrast, inhibition at the level of C3\/C3b or the alternative pathway amplification loop has not, to date, demonstrated a consistent encapsulated-pathogen signal in phase 3 kidney trials, although follow-up remains limited and rare events cannot be excluded. Effective prevention relies on target-adapted vaccination against encapsulated bacteria, consideration of antimicrobial prophylaxis when therapy must begin before vaccine protection is established\u2014and in selected higher-risk settings during sustained complement blockade\u2014and structured patient education with rapid-access pathways for febrile illness. Chronic kidney disease, dialysis exposure, transplantation, and concomitant immunosuppression may further amplify infectious risk and attenuate vaccine responsiveness. Infection risk under complement inhibition is target-dependent and not eliminated by vaccination alone, particularly with terminal C5 blockade. Mechanism-informed, kidney-specific prevention strategies are essential as complement therapies expand into routine clinical practice.<\/jats:p>","DOI":"10.1093\/ndt\/gfag113","type":"journal-article","created":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T11:50:14Z","timestamp":1779450614000},"source":"Crossref","is-referenced-by-count":2,"title":["Infection risk mitigation with complement inhibitors in kidney disease"],"prefix":"10.1093","author":[{"given":"Mathilde","family":"Berghmans","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, University Hospitals Namur (CHU UCL Namur) , Namur ,","place":["Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fran\u00e7ois","family":"Seghers","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University Hospitals Namur (CHU UCL Namur) , Namur 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