# Ontsteking als therapeutisch doelwit bij chronische nierziekte en cardiovasculaire complicaties

*geplaatst 2026-09-12 · Nierziekte · Nature reviews. Nephrology · doi 10.1038/s41581-026-01117-6 · https://hartvaat.nl/2026/09/04/ontsteking-als-therapeutisch-doelwit-bij-chronische-nierziekte-en-cardiovasculai/*

Chronische nierziekte gaat gepaard met een pro-inflammatoire toestand die zowel nierdeterioratie als cardiovasculaire complicaties aandrijft. Een overzicht in Nature Reviews Nephrology belicht de onderliggende ontstekingspaden en presenteert zowel onderzochte remmers (zoals ASK1-, JAK- en IL-1β/IL-6-antagonisten) als bewezen nier- en hartmedicatie met anti-inflammatoire eigenschappen, waaronder SGLT2-remmers, GLP-1-agonisten en niet-steroïde mineralocorticoïde-antagonisten. Het begrijpen van deze mechanismen biedt aanknopingspunten voor gerichte therapie om zowel de nierfunctie als het cardiovasculaire risico bij patiënten met CKD te verbeteren.

## English: Inflammation as a therapeutic target to improve kidney and cardiovascular outcomes.

Chronic kidney disease is driven by a pro-inflammatory state that accelerates both renal decline and major cardiovascular events. This review outlines key inflammatory pathways and highlights potential therapeutic targets, ranging from investigational agents (ASK1, JAK, and IL-1β/IL-6 inhibitors) to established cardiorenal medications with proven anti-inflammatory effects, including SGLT2 inhibitors, GLP-1 receptor agonists, and non-steroidal mineralocorticoid receptor antagonists. Integrating anti-inflammatory strategies into CKD management offers a promising avenue to mitigate cardiovascular risk and preserve kidney function.

## Abstract (original, from the publication)

Chronic kidney disease (CKD) is a leading cause of premature death due to the loss of kidney function and development of kidney failure, and because of attendant major adverse cardiovascular events. High-sensitivity C-reactive protein (hsCRP), a biomarker of systemic inflammation, is associated with increased risks of cardiovascular events and CKD progression. CKD is characterized by a pro-inflammatory state with upregulation of inflammatory pathways and disruption of anti-inflammatory mechanisms. The resulting systemic inflammation, along with local tissue-based inflammatory mechanisms, are key contributors to kidney damage, atherosclerosis and cardiac dysfunction. As a result, a series of inflammatory pathways and mediators have emerged as potential therapeutic targets for CKD and its major cardiovascular complications. Investigational treatments that have targeted inflammation include inhibition of apoptosis signal-regulating kinase-1 (ASK1) by selonsertib, Janus kinase (JAK) 1/2 inhibition with baricitinib, protein kinase C-β (PKCβ) inhibition with ruboxistaurin, nuclear factor erythroid 2-related factor 2 (Nrf2) activation with bardoxolone, phosphodiesterase inhibition with pentoxifylline and monoclonal antibodies against IL-1β and IL-6. Furthermore, proven therapies for CKD, including renin-angiotensin-aldosterone system inhibitors, sodium-glucose cotransporter-2 inhibitors, glucagon-like peptide-1 receptor agonists and non-steroidal mineralocorticoid antagonists, possess anti-inflammatory properties that might contribute to their previously established clinical benefits.

Auteurs: Katherine R Tuttle, Mehmet Kanbay, Radica Z Alicic, Juan Jesus Carrero, Sidar Copur, Ann Marie Navar, Brendon L Neuen, Vlado Perkovic, Peter Rossing, Nikolaus Marx, Paul M Ridker

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Bron: Nature reviews. Nephrology, https://doi.org/10.1038/s41581-026-01117-6. Bijgewerkt 2026-09-06T00:57:16Z. 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.