{"id":"4896b1b4fd19","type":"article","url":"https://hartvaat.nl/2026/10/24/fosfaatadditieven-in-ultra-bewerkte-voeding-versnellen-nier-en-vaatziekte-bij-ck/","title":"Fosfaatadditieven in ultra-bewerkte voeding versnellen nier- en vaatziekte bij CKD","title_en":"Intestinal Phosphate Absorption and Phosphate Metabolism in Chronic Kidney Disease: Direct and Indirect Toxicity of Phosphate Additives in Ultra-processed Diets.","category":"chronische nierziekte","category_label":"Nierziekte","professions":["cardioloog","internist"],"tags":[],"journal":"Seminars in nephrology","doi":"10.1016/j.semnephrol.2026.151748","source_url":"https://doi.org/10.1016/j.semnephrol.2026.151748","authors":["Jaime Uribarri","Mona S Calvo"],"significance":5,"published":"2026-11-02","source_date":"2026-10-24","image":"","kennis":["https://hartvaat.nl/kennis/nierziekte/nierziekte-en-cardiovasculair-risico/","https://hartvaat.nl/kennis/cardiometabool/diabetes-en-cardiovasculair-risico/"],"congress":"","summary_en":"In chronic kidney disease (CKD), reduced renal phosphate excretion coincides with sustained intestinal absorption, disrupting phosphate homeostasis. A recent perspective highlights that phosphate additives in ultra-processed foods are absorbed more readily than natural dietary phosphate, driving harm through direct pathways (FGF23/PTH activation, vascular calcification) and indirect mechanisms (gut dysbiosis, systemic inflammation). Clinicians managing CKD and cardiorenal patients should emphasize whole-food diets and advocate for clearer phosphorus labeling to mitigate long-term cardiovascular and renal risk.","created":"2026-10-26T02:25:54Z","updated":"2026-10-26T02:25:54Z","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":"Bij chronische nierziekte (CKD) blijft de darmopname van fosfaat hoog ondanks een afnemende nierfunctie, wat de fosfaathuishouding verstoort. Een recente perspectiefstudie beschrijft hoe fosfaatadditieven in ultra-bewerkte voeding sneller worden opgenomen dan natuurlijk fosfaat en via directe (FGF23/PTH-activatie, vaatcalcificatie) en indirecte (dysbiose, ontsteking) mechanismen nierprogressie en cardiovasculaire schade versnellen. Voor de klinische praktijk benadrukt dit het belang van het aanmoedigen van onbewerkte voeding en het pleiten voor transparante fosfaatlabeling bij patiënten met CKD en cardiorenale aandoeningen.","abstract_original":"In chronic kidney disease (CKD), intestinal phosphate absorption stays largely constant even as the kidneys lose the ability to excrete phosphate, creating a tendency toward positive phosphate balance. Rising fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH) keep serum phosphate near normal until advanced CKD, but these same adaptations can cause systemic harm long before overt hyperphosphatemia develops. Ultra-processed foods worsen this burden through phosphate additives (Pi-additives) used as preservatives, emulsifiers, stabilizers, leavening agents, and moisture retainers. These additives are absorbed more readily than natural food phosphate and are poorly captured by nutrient databases. Therefore, true phosphorus exposure is easily underestimated. This perspective outlines 2 pathways of harm. The direct pathway involves PTH and FGF23 activation, vascular and soft-tissue calcification, endothelial dysfunction, disordered bone remodeling, faster CKD progression, and cellular senescence-effects documented in CKD and possibly relevant even with preserved kidney function. The indirect pathway reflects that Pi-additives rarely occur alone: they accompany added sugars, non-nutritive sweeteners, nitrites, emulsifiers, and preservatives in ultra-processed foods, combinations that may drive gut dysbiosis, intestinal barrier dysfunction, oxidative stress, inflammation, and the formation of advanced glycation endproducts and other gut-derived toxins. We synthesize current understanding of phosphate homeostasis with mechanistic and epidemiologic evidence linking Pi-additives-alone and combined with other additives-to cardiovascular, skeletal, renal, and metabolic disease. Future research should move beyond single-additive safety testing toward evaluating additive mixtures, cumulative exposure, and food-matrix interactions. Better exposure assessment and transparent phosphorus labeling are essential to clarify the long-term health effects of these ubiquitous additives."}