title: ACE gene polymorphism in Egyptian children with idiopathic nephrotic syndrome.
abstract: BACKGROUND
  Idiopathic nephrotic syndrome is a common renal disease in children. ACE gene insertion/deletion (I/D) polymorphism has been studied as a predictor of clinical response to steroid therapy.
  
  
  OBJECTIVE
  To investigate the distribution of angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism in children with idiopathic nephrotic syndrome (INS), as well as its relation with patient's clinical response to steroid therapy.
  
  
  METHODS
  The studied subjects included 50 children with INS compared to 20 unrelated healthy children. Each individual genotype was determined using PCR amplification of extract genomic DNA and allele distribution based on size of the PCR fragments.
  
  
  RESULTS
  Patients with INS had a significantly higher percentage of DD genotype (p < 0.05) than the control group. D allele frequency was significantly higher in INS patients than healthy controls.
  
  
  CONCLUSIONS
  Our results showed that INS is associated with a higher incidence of DD genotype, especially in non-SS patients. This data suggested that DD genotype may play a role in the clinical response to steroid. Angiotensin II may be involved in part in the response to steroid treatment in children with INS (Tab. 4, Fig. 1, Ref. 20).
authors.affiliation: Pediatric Department, Research Institute of Ophthalmology, Cairo, Egypt. fahmymona80@hotmail.com
authors.forename: M E
authors.initials: ME
authors.lastname: Fahmy
authors.forename: A M
authors.initials: AM
authors.lastname: Fattouh
authors.forename: R A
authors.initials: RA
authors.lastname: Hegazy
authors.forename: M L
authors.initials: ML
authors.lastname: Essawi
mesh_terms: D002648:Child; D002675:Child, Preschool; D004534:Egypt; D005260:Female; D006801:Humans; D008297:Male; D009404:Nephrotic Syndrome / Q000235:genetics*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic
chemical_list: D007703:Peptidyl-Dipeptidase A