title: Angiotensin-converting enzyme gene polymorphism and the progression rate of focal segmental glomerulosclerosis in Iranian children.
abstract: OBJECTIVE
  Focal segmental glomerulosclerosis (FSGS) is one of the most common forms of glomerulonephritis leading to end-stage renal disease (ESRD). A few clinical and paraclinical factors are considered as contributing factors in progression rate. However, there are controversial reports on the relationship between ACE gene polymorphism and rapidity of progression of FSGS to ESRD in different populations. To elucidate this issue, we investigated the relationship between the insertion (I) and deletion (D) ACE gene polymorphism and rapidity of progression of FSGS to ESRD in Iranian children.
  
  
  METHODS
  Forty-one children aged 1-18 years admitted to St AlZahra Hospital, Isfahan, and St Ali Asghar Hospital, Tehran, Iran, with idiopathic FSGS were enrolled. Renal death was defined as a glomerular filtration rate (GFR) of less than 50 mL/min per 1.73 m(2) or a decreased GFR to less than 50% compare to baseline. Reaching renal death in less or more than 2 years were labelled as rapid progressors (RP) or slow progressors (SP), respectively. Intron 16 of the ACE gene was amplified by the polymerase chain reaction technique.
  
  
  RESULTS
  Twenty-eight patients were male and 13 were female. In 15 RP patients, the genotype distribution was 26.6% DD, 6.7% II and 66.7% ID. In 26 SP patients, the genotype was similar (38.6% DD, 7.6% II and 53.8% ID, P > 0.05). There were no statistically significant differences for ACE I/D gene polymorphism between the two groups of patients (P > 0.05).
  
  
  CONCLUSIONS
  Our study revealed no correlation between ACE I/D gene polymorphism and rapidity of progression of FSGS to ESRD in Iranian children.
authors.affiliation: Departments of Paediatric Nephrology, Isfahan University of Medical Sciences, Tehran, Iran. gheisari@med.mui.ac.ir
authors.forename: Alaleh
authors.initials: A
authors.lastname: Gheissari
authors.forename: Mansour
authors.initials: M
authors.lastname: Salehi
authors.forename: Somayeh Bandi
authors.initials: SB
authors.lastname: Dastjerdi
authors.forename: Mansour
authors.initials: M
authors.lastname: Jahangiri
authors.forename: Nakisa
authors.initials: N
authors.lastname: Hooman
authors.forename: Hassan
authors.initials: H
authors.lastname: Otookesh
authors.forename: Alireza
authors.initials: A
authors.lastname: Merikhipour
authors.forename: Afshin
authors.initials: A
authors.lastname: Ajir
authors.forename: Alimohammad
authors.initials: A
authors.lastname: Foroughmand
authors.forename: Saeidreza
authors.initials: S
authors.lastname: Khatami
authors.forename: Shahrzad
authors.initials: S
authors.lastname: Shahidi
authors.forename: Abdolamir
authors.initials: A
authors.lastname: Atapour
authors.forename: Shiva
authors.initials: S
authors.lastname: Seirafian
authors.forename: Afsoon Emami
authors.initials: AE
authors.lastname: Naeini
mesh_terms: D000293:Adolescent; D002648:Child; D002675:Child, Preschool; D018450:Disease Progression; D005260:Female; D017353:Gene Deletion; D005838:Genotype; D005923:Glomerulosclerosis, Focal Segmental / Q000150:complications / Q000201:enzymology / Q000235:genetics* / Q000401:mortality / Q000473:pathology; D006801:Humans; D007223:Infant; D007438:Introns; D007492:Iran / Q000453:epidemiology; D007676:Kidney Failure, Chronic / Q000201:enzymology / Q000235:genetics* / Q000401:mortality / Q000473:pathology; D008297:Male; D016254:Mutagenesis, Insertional; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D010641:Phenotype; D011110:Polymorphism, Genetic; D013997:Time Factors
chemical_list: D007703:Peptidyl-Dipeptidase A