Key result
Pediatric predialysis CKD is linked to lower urinary angiotensin peptides that correlate positively with GFR.
Why the study?
Changes in local renin-angiotensin system independent of systemic renin-angiotensin system are suggested to play a role in CKD pathophysiology, but their relationship with echocardiographic parameters in children with predialysis CKD needed investigation.
Case-Control (n=85)
Circulating and local renin-angiotensin system molecules are altered in children with predialysis CKD and correlate with renal dysfunction, hypertension, and echocardiographic changes.
Should not yet guide therapy in pediatric predialysis CKD; leaves open angiotensin peptides as biomarkers of GFR and hypertension risk.
BACKGROUND: The changes in local renin-angiotensin system (RAS), independent of systemic RAS, are suggested to play a role in the pathophysiology of chronic kidney disease (CKD). This study aimed to investigate RAS molecules in children with predialysis 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, angiotensin-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 were lower in patients and were positively correlated with glomerular filtration rate (p < 0.001 for each). Urinary angiotensin peptides were 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 angiotensin-A were lower in CKD with hypertension compared to healthy children (p < 0.05). In logistic regression analysis, hypertension was negatively correlated with urinary angiotensin peptides. Serum angiotensin-A was negatively and angiotensin-2 was positively 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 lateral S 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 echocardiographic alteration in children with predialysis CKD.
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Pala et al. (2026) conducted a case-control in Predialysis chronic kidney disease (n=85). Angiotensin peptide levels vs. Healthy controls was evaluated on Serum and urinary angiotensin peptide levels and echocardiographic parameters. Urinary angiotensin peptides were lower in children with predialysis CKD compared to controls and positively correlated with glomerular filtration rate (p < 0.001).
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