PEDIATRICS INTERNATIONAL, cilt.68, ss.1-9, 2026 (SCI-Expanded, Scopus)
Background: The changes in local renin-angiotensin system (RAS), independent of systemic RAS, are suggested to play a rolein the pathophysiology of chronic kidney disease (CKD). This study aimed to investigate RAS molecules in children with predi-alysis CKD and to evaluate their relationship with echocardiographic parameters.Methods: The patients with predialysis CKD (n = 37) and control group (n = 48) were included. Angiotensin-A, angioten-sin-2, angiotensin converting enzyme (ACE)-1, ACE-2, angiotensin 1–7 and alamandin levels were determined by ELISA.Echocardiography was performed with M-mode, pulsed wave Doppler, tissue Doppler, and speckle tracking strain.Results: Serum angiotensin peptide levels were similar between patients and controls. Urinary angiotensin peptides werelower in patients and were positively correlated with glomerular filtration rate (p < 0.001 for each). Urinary angiotensin peptideswere lower and serum angiotensin-2 and angiotensin 1–7 were higher in patients without hypertension compared to controls(p < 0.05). Serum ACE-2 was lower in patients with hypertension (p < 0.05). Urinary angiotensin peptides and serum angioten-sin-A were lower in CKD with hypertension compared to healthy children (p < 0.05). In logistic regression analysis, hyperten-sion was negatively correlated with urinary angiotensin peptides. Serum angiotensin-A was negatively and angiotensin-2 waspositively correlated with hypertension (p < 0.05). Mitral lateral E was positively correlated with serum alamandin and ACE-2(p < 0.05). Tricuspid E/A correlated with serum alamandin, angiotensin-A, ACE-1 and ACE-2 levels (p < 0.05). Tricuspid lateralS was negatively correlated with urinary alamandin and urinary angiotensin-A (p < 0.05).
Conclusion: Circulating and local RAS molecules may play a role in renal dysfunction, hypertension, and echocardiographicalteration in children with predialysis CKD.