Angiotensin Peptide Levels in Children With Predialysis Chronic Kidney Disease.
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.
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.
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).
Circulating and local RAS molecules may play a role in renal dysfunction, hypertension, and echocardiographic alteration in children with predialysis CKD.
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.
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).
Circulating and local RAS molecules may play a role in renal dysfunction, hypertension, and echocardiographic alteration in children with predialysis CKD.