Renal failure · 2026
Differential serum dynamics of apelin, elabela, and angiotensinogen in CKD and haemodialysis: insights into peptide modulation across the dialysis procedure.
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Serwin Natalia Maria, Cecerska-Heryć Elżbieta, Grygorcewicz Bartłomiej, Cejko Mateusz, Jerzyk Adrianna, Ćwikła Kacper, Spajzer Emilia, Manelska Aleksandra, Woźniak Paulina, Gomółka Aleksandra, Cader-Ptak Aleksandra, Bąk Katarzyna, Lisak Marcin, Opara-Bajerowicz Martyna, Wojciuk Bartosz, Suwała Mariusz, Serwin Karol, Wiśniewska Magda, Dołęgowska Barbara
Аннотация
BACKGROUND: Emerging evidence suggests that apelinergic peptides and components of the renin-angiotensin system (RAS) are key regulators of cardiovascular homeostasis and fluid balance, both disrupted in chronic kidney disease (CKD). This study aimed to assess serum levels of apelin, elabela, and angiotensinogen across the CKD spectrum and evaluate their acute modulation during a single hemodialysis (HD) session. Serum samples from healthy controls (n = 21), non-dialysis CKD patients (n = 21), and HD patients (n = 44) were analyzed using high-sensitivity immunoassays. In HD patients, matched samples were collected before and after dialysis.
METHODS: Apelin levels were significantly lower in CKD compared to controls but elevated in HD patients prior to treatment. No significant change occurred post-dialysis, suggesting minimal dialytic clearance or rapid compensation. In contrast, elabela was markedly reduced pre-dialysis but increased post-dialysis in most patients, indicating dynamic regulation or partial removal. Angiotensinogen was elevated before HD and declined significantly after.
RESULTS: Correlations with estimated glomerular filtration rate (eGFR) were modest and not significant after adjusting for group membership, indicating that group stratification primarily drove associations. Linear regression showed that reductions in angiotensinogen correlated inversely with changes in apelin, while higher uric acid and urea predicted post-dialysis increases in elabela and suppression of angiotensinogen, respectively.
CONCLUSION: These findings highlight distinct, peptide-specific responses to HD and support a context-dependent interplay between uremic burden, peptide systems, and dialysis-induced shifts. Apelinergic and RAS peptides may represent promising biomarkers of intradialytic cardiovascular modulation. Further studies are warranted to explore their prognostic and therapeutic implications in CKD.
METHODS: Apelin levels were significantly lower in CKD compared to controls but elevated in HD patients prior to treatment. No significant change occurred post-dialysis, suggesting minimal dialytic clearance or rapid compensation. In contrast, elabela was markedly reduced pre-dialysis but increased post-dialysis in most patients, indicating dynamic regulation or partial removal. Angiotensinogen was elevated before HD and declined significantly after.
RESULTS: Correlations with estimated glomerular filtration rate (eGFR) were modest and not significant after adjusting for group membership, indicating that group stratification primarily drove associations. Linear regression showed that reductions in angiotensinogen correlated inversely with changes in apelin, while higher uric acid and urea predicted post-dialysis increases in elabela and suppression of angiotensinogen, respectively.
CONCLUSION: These findings highlight distinct, peptide-specific responses to HD and support a context-dependent interplay between uremic burden, peptide systems, and dialysis-induced shifts. Apelinergic and RAS peptides may represent promising biomarkers of intradialytic cardiovascular modulation. Further studies are warranted to explore their prognostic and therapeutic implications in CKD.