Circulating amyloid beta 1-40 peptide as an associate of renal function decline

• Verfasst von: Mavraganis, Georgios [VerfasserIn]
• Verfasst von: Georgiopoulos, Georgios [VerfasserIn]
• Verfasst von: Zervas, Georgios [VerfasserIn]
• Verfasst von: Aivalioti, Evmorfia [VerfasserIn]
• Verfasst von: Delialis, Dimitrios [VerfasserIn]
• Verfasst von: Petropoulos, Ioannis [VerfasserIn]
• Verfasst von: Rachiotis, Nikolaos [VerfasserIn]
• Verfasst von: Konstantaki, Christina [VerfasserIn]
• Verfasst von: Moustou, Chrysoula [VerfasserIn]
• Verfasst von: Dimopoulou, Maria-Aggeliki [VerfasserIn]
• Verfasst von: Sachse, Marco [VerfasserIn]
• Verfasst von: Tual-Chalot, Simon [VerfasserIn]
• Verfasst von: Sopova, Kateryna [VerfasserIn]
• Verfasst von: Psimmenou, Erasmia [VerfasserIn]
• Verfasst von: Stellos, Konstantinos [VerfasserIn]
• Verfasst von: Stamatelopoulos, Kimon [VerfasserIn]
• Titel: Circulating amyloid beta 1-40 peptide as an associate of renal function decline
• Verf.angabe: Georgios Mavraganis, Georgios Georgiopoulos, Georgios Zervas, Evmorfia Aivalioti, Dimitrios Delialis, Ioannis Petropoulos, Nikolaos Rachiotis, Christina Konstantaki, Chrysoula Moustou, Maria-Aggeliki Dimopoulou, Marco Sachse, Simon Tual-Chalot, Kateryna Sopova, Erasmia Psimmenou, Konstantinos Stellos, Kimon Stamatelopoulos
• E-Jahr: 2025
• Jahr: May 2025
• Umfang: 13 S.
• Fussnoten: Online veröffentlicht: 24. Februar 2025 ; Gesehen am 02.06.2025
• Titel Quelle: Enthalten in: European journal of clinical investigation
• Ort Quelle: Oxford [u.a.] : Wiley-Blackwell, 1970
• Jahr Quelle: 2025
• Band/Heft Quelle: 55(2025), 5, Artikel-ID e70006, Seite 1-13
• ISSN Quelle: 1365-2362
• DOI: doi:10.1111/eci.70006
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: all-cause mortality
• Sach-SW: amyloid Αβ1-40
• Sach-SW: glomerular filtration rate
• Sach-SW: kidney function
• Sach-SW: mediation analysis
• K10plus-PPN: 1927250757

Abstract

Background Recent evidence suggests that Alzheimer's amyloid-beta (1-40) (Αβ1-40), an emerging biomarker of cardiovascular disease, may be involved in the heart-brain-renal axis. We aimed to comprehensively explore the association between circulating Aβ1-40 levels and renal function and its clinical relevance. Methods Consecutively recruited subjects in the Athens Angiometabolic Registry with measured Aβ1-40 plasma levels (n = 811) were analysed. Αβ1-40 was measured by enzyme-linked immunosorbent assay and glomerular filtration rate (GFR) was calculated using the abbreviated four-variable Modification of Diet in Renal Disease (MDRD) formula. All-cause mortality was the main clinical endpoint across a median follow-up of 47 months. Results Cross-sectionally, a bidirectional association between Αβ1-40 [adjusted odds ratio (adjOR) = 3.67 for highest tertile of Αβ1-40 and chronic kidney disease (CKD) stage ≥3, p < .001] and CKD stage ≥3 (adjOR = 3.52 for association with highest Aβ1-40 tertile, p < .001) was observed. Longitudinally, increased Αβ1-40 at baseline was associated with decline in renal function at follow-up (adjOR for CKD stage ≥3 = 2.26, p = .033). Similarly, longitudinal changes in Aβ1-40 were inversely associated with changes in GFR (OR = .77 per 1 SD increase in Aβ1-40, p = .006). Aβ1-40 was associated with all-cause mortality, independently of traditional risk factors (hazard ratio = 1.20 per 1 SD increase in Aβ1-40, p = .016). An indirect effect of GFR on the association between Aβ1-40 and mortality (p < .05) with an estimated indirect-to-total effect ratio of .334, but not of Αβ1-40 on GFR with mortality, was observed. Conclusions In a population with a wide range of GFR, we found a bidirectional association between Αβ1-40 levels and renal function. The association of Αβ1-40 with all-cause mortality was partly mediated by lower GFR.