# GDF-15 correleert met eetlustverlies, spierafbraak en nierdeterioratie bij chronische nierziekte

*geplaatst 2026-09-22 · Nierziekte · Kidney international reports · doi 10.1016/j.ekir.2026.106995 · https://hartvaat.nl/2026/10/01/gdf-15-correleert-met-eetlustverlies-spierafbraak-en-nierdeterioratie-bij-chroni/*

In een prospectief cohort van bijna 3.000 patiënten met niet-dialyseafhankelijke chronische nierziekte (CKD) bleek een verhoogde GDF-15-spiegel onafhankelijk samen te hangen met eetlustverlies, verminderde spierkracht en spiermassa. Elke verdubbeling van GDF-15 ging gepaard met een 30% hoger risico op nierdeterioratie en een 72% hoger risico op overlijden na multivariabele correctie. Deze bevindingen onderstrepen de potentiële waarde van GDF-15 als prognostische biomarker voor cardiorenale en metabole complicaties bij CKD.

## English: Associations of Growth Differentiation Factor 15 in Chronic Kidney Disease.

In a prospective multicentre cohort of nearly 3,000 patients with non-dialysis-dependent chronic kidney disease, elevated circulating GDF-15 levels were independently associated with poor appetite, reduced handgrip strength, and lower estimated muscle mass. Each doubling of GDF-15 corresponded to a 30% higher risk of CKD progression and a 72% higher risk of all-cause mortality after multivariable adjustment. These findings highlight GDF-15 as a promising prognostic biomarker for cardiorenal and metabolic complications in CKD, potentially aiding risk stratification in clinical practice.

## Abstract (original, from the publication)

INTRODUCTION: Anorexia is common in chronic kidney disease (CKD), yet the underlying mechanisms remain poorly defined. Growth differentiation factor-15 (GDF-15) suppresses appetite in cancer, where anti-GDF-15 therapy improves appetite. METHODS: NURTuRE-CKD is a prospective, multicentre cohort study of 2996 individuals with non-dialysis-dependent CKD. At baseline, circulating GDF-15 was measured and appetite was assessed using a questionnaire. Muscle function and estimated muscle mass were evaluated using handgrip strength (kg) and creatinine muscle index (estimated glomerular filtration rate [eGFR] cystatinC × serum creatinine). CKD progression (≥ 40% decline in eGFR, incident eGFR < 15 ml/min per 1.73 m2, or dialysis initiation) and all-cause mortality were ascertained longitudinally. Multivariable logistic regression evaluated associations between GDF-15 and poor appetite, adjusting for eGFR, urea, nutritional and metabolic markers, CRP, comorbidities, and smoking. Cox models assessed associations with CKD progression (adjusted for Kidney Failure Risk Equation components) and all-cause mortality (additionally adjusted for CRP, comorbidities, and smoking). RESULTS: GDF-15 was measured in 2929 participants. The median concentration was 2503 pg/ml (interquartile range 1605-3851). Participants with poor appetite (n = 786, 27%) had higher GDF-15 (2965 vs. 2,350 pg/ml; P < 0.001). In adjusted analyses, each doubling of GDF-15 was associated with higher odds of poor appetite (odds ratio [OR] 1.44, 95% CI 1.28-1.62). GDF-15 correlated negatively with handgrip strength (ρ = -0.18; P < 0.001) and creatinine muscle index (ρ= -0.40; P < 0.001), but not with body mass index. Over a median follow-up of 50 (41-56) months, 893 (32%) experienced CKD progression and 527 (18%) died. Adjusted hazard ratios per doubling of GDF-15 were 1.30 (95% CI, 1.18-1.42) for CKD progression and 1.72 (95% CI, 1.58-1.89) for all-cause mortality. CONCLUSION: Among individuals with non-dialysis CKD, higher circulating GDF-15 concentrations were independently associated with poor appetite, sarcopenia markers, CKD progression, and all-cause mortality.

Auteurs: Thomas McDonnell, Samantha Hayward, Nicolas Vuilleumier, Moin A Saleem, Philip A Kalra, Maarten W Taal

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Bron: Kidney international reports, https://doi.org/10.1016/j.ekir.2026.106995. Bijgewerkt 2026-09-16T00:59:02Z. 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.