{"id":"68d5d6bcdd0d","type":"article","url":"https://hartvaat.nl/2025/12/30/overgang-van-aki-naar-ckd-rol-van-niermacrofagen-en-neutrofielen/","title":"Overgang van AKI naar CKD: rol van niermacrofagen en neutrofielen","title_en":"Key drivers and potential therapeutic targets in the AKI-to-CKD transition: roles of kidney-resident macrophages and neutrophils","category":"chronische nierziekte","category_label":"Nierziekte","professions":["internist"],"tags":["anemie-ckd","chronische-nierziekte","ijzertekort"],"journal":"Kidney International","doi":"https://www.kidney-international.org/article/S0085-2538(25)01028-2/fulltext","source_url":"https://doi.org/https://www.kidney-international.org/article/S0085-2538(25)01028-2/fulltext","authors":["Kensei Taguchi","Kei Fukami"],"significance":5,"published":"2025-12-30","source_date":"2025-12-30","image":"","kennis":["https://hartvaat.nl/kennis/nierziekte/anemie-bij-ckd/"],"congress":"","summary_en":"This review discusses the key drivers of the AKI-to-CKD transition, focusing on kidney-resident macrophages and neutrophils as potential therapeutic targets. Understanding innate immune mechanisms in maladaptive repair may identify new interventions to prevent CKD progression.","created":"2026-07-03T10:25:37Z","updated":"2026-07-03T13:25:01Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"CKD treft 15% van de volwassenen wereldwijd. De overgang van acuut nierletsel naar chronische nierziekte is een cruciaal proces. Dit overzicht bespreekt de rol van nierresidente macrofagen en neutrofielen als therapeutische doelwitten.","abstract_original":"Chronic kidney disease (CKD), characterized by irreversible kidney damage and a decline in kidney function for at least 3 months, affects 15% of adults worldwide and is tightly linked to kidney failure, cardiovascular disease, mental disorders, and heightened susceptibility to infections. Acute kidney injury (AKI) occurs in 23% of hospitalized patients, is associated with in-hospital mortality,1 and predisposes patients to CKD.2 After AKI, proximal tubular cells (PTCs) fail to repair through multifaceted mechanisms, including cell cycle arrest at the G2/M phase, maladaptive dedifferentiation (i.e., partial epithelial-mesenchymal transition or epithelial cell plasticity), mitochondrial dysfunction, and epigenetic alteration."}