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Renin-angiotensin system polymorphisms and renal scarring
Rafael Pardo1, Serafín Málaga, Eliecer Coto
1Department of Pediatric Nephrology, Hospital Central de Asturias, Oviedo, Asturias, Spain. rpardo@hcas.insalud.es
Pediatric Nephrology (Berlin, Germany)
|February 13, 2003
Summary
Genetic variations in renin-angiotensin-aldosterone genes do not predict renal scarring in children with vesicoureteral reflux. The ACE D allele was linked to higher ACE serum levels but not to adverse renal outcomes.
Area of Science:
- Nephrology
- Genetics
- Pediatrics
Background:
- Vesicoureteral reflux (VUR) can lead to reflux nephropathy (RN) and renal scarring.
- The renin-angiotensin-aldosterone system (RAS) plays a role in renal function and disease.
- Polymorphisms in RAS genes have been investigated as potential risk factors for RN.
Purpose of the Study:
- To investigate the association between DNA polymorphisms in RAS genes and the development of renal scarring in patients with VUR.
- To determine if specific genotypes, such as the ACE DD genotype, are linked to adverse renal prognosis in RN.
Main Methods:
- Genotyping of ACE I/D, AT1 A1166C, AT2 A3123C, and AGT M235T polymorphisms using polymerase chain reaction.
- Measurement of serum ACE levels.
- Recruitment of 246 patients with VUR, RN, chronic renal failure due to RN, and a control group.
Main Results:
- No statistically significant differences in RAS polymorphism distribution were found between patient groups.
- The ACE D allele was associated with higher serum ACE levels.
- No association was observed between ACE I/D polymorphism and hypertension, proteinuria, VUR grade, or laterality.
- Patients with the ACE DD genotype showed a lower incidence of febrile urinary tract infection as the initial symptom.
Conclusions:
- Genetic polymorphisms of RAS components are not independent prognostic indicators of renal scarring in patients with VUR.
- The ACE DD genotype may be associated with a milder presentation of VUR/RN.
- Further research is needed to elucidate the role of RAS in VUR and RN pathogenesis.