title: Insertion/deletion angiotensin converting enzyme gene polymorphism affects the microvascular structure of the kidney in patients with nondiabetic renal disease.
abstract: OBJECTIVE
  It has been reported that the deletion allele of the insertion/deletion polymorphism of the angiotensin I converting enzyme gene is associated with increased cardiovascular risk and progressive renal disease, including immunoglobulin A nephropathy. We therefore investigated the relationship between angiotensin converting enzyme polymorphism and intrarenal microvascular structure in 56 patients with nondiabetic renal disease.
  
  
  RESULTS
  We determined various cardiovascular hormones of the renin-angiotensin system and angiotensin converting enzyme gene polymorphism in 56 patients with nondiabetic renal diseases who underwent a renal biopsy. The patients were divided into three groups by angiotensin converting enzyme genotype (insertion/insertion, n = 21; insertion/deletion, n = 23; deletion/deletion, n = 12) using polymerase chain reaction methods. The angiotensin converting enzyme insertion/ deletion and deletion/deletion genotypes were associated with a significantly higher interlobular artery wall : lumen ratio than the insertion/insertion genotype (insertion/insertion 0.27 +/- 0.01, insertion/deletion 0.32 +/- 0.01, deletion/deletion 0.33 +/- 0.02; P < 0.05). Afferent arteriolar and tubulo-interstitial injury scores were similar among the three genotypes. Although serum angiotensin converting enzyme activity was higher in the deletion/deletion than in the other two genotypes (insertion/insertion 9.7 +/- 0.7, insertion/deletion 10.7 +/- 0.9, deletion/deletion 14.0 +/- 2.4 IU/I; P < 0.05), other factors of the renin-angiotensin system, including blood pressure and serum creatinine levels, were not different among the three groups.
  
  
  CONCLUSIONS
  The angiotensin converting enzyme deletion/deletion genotype may be considered a risk factor for the development of microvascular wall thickening in nondiabetic renal diseases.
authors: Department of Medicine, Dokkyo University School of Medicine, Tochigi, Japan.
authors: M
authors: M
authors: Teranishi
authors: H
authors: H
authors: Ono
authors: T
authors: T
authors: Ishimitsu
authors: H
authors: H
authors: Matsuoka
mesh_terms: D000328:Adult; D000803:Angiotensin I / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D001706:Biopsy; D004247:DNA / Q000032:analysis; D017931:DNA Primers / Q000737:chemistry; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D017353:Gene Deletion; D005838:Genotype; D006801:Humans; D007674:Kidney Diseases / Q000097:blood / Q000201:enzymology / Q000473:pathology*; D007679:Kidney Medulla / Q000098:blood supply; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012077:Renal Artery / Q000201:enzymology / Q000473:pathology*; D012083:Renin / Q000097:blood
chemical_list: D017931:DNA Primers; D000804:Angiotensin II; D004247:DNA; D000803:Angiotensin I; D007703:Peptidyl-Dipeptidase A; D012083:Renin