title: Angiotensin-converting enzyme gene polymorphism and N-Acetyl-β-D-glucosaminidase excretion in endemic nephropathy.
abstract: BACKGROUND
  Tubular proteinuria and enzymuria are hallmarks of endemic nephropathy (EN). The role of I/D angiotensin convertase (ACE) gene polymorphism has not yet been elucidated in this peculiar chronic tubulointerstitial nephritis, and our aim was to investigate the role of this polymorphism in EN focusing on the urinary N-acetyl-β-D-glucosaminidase (NAG) excretion, a biomarker of proximal tubular damage.
  
  
  METHODS
  ACE genotype and allele frequencies were determined in 229 farmers (147 women and 82 men) from an endemic Croatian village. The farmers were stratified according to the WHO criteria into the following subgroups: those 'at risk' for EN (n = 37), 'suspected of having EN' (n = 57), and 'others' (n = 135).
  
  
  RESULTS
  There were 74 (32.3%) subjects homozygous for the D allele, 99 (43.2%) heterozygous (ID genotype) and 56 (24.4%) homozygous for the I allele. No differences in allele frequency were found between the established WHO subgroups (p > 0.05). In the whole group, DD subjects had significantly higher values of diastolic blood pressure (p = 0.003) and urinary NAG than subjects with ID and II genotype (5.5 ± 1.2 vs. 4.0 ± 3.0 vs. 3.8 ± 4.2, respectively; p = 0.023). The highest values of serum creatinine (p = 0.02), proteinuria (p = 0.03) and urinary NAG (6.0 ± 3.7 vs. 3.7 ± 2.1 vs. 3.0 ± 1.6, respectively; p = 0.008) were observed in those suspected of having EN group with the DD genotype.
  
  
  CONCLUSIONS
  ACE gene polymorphism is not a risk factor for EN. However, it might influence the clinical course of EN, and increased excretion of NAG might be a prognostic marker of this chronic tubulointerstitial nephritis.
authors.affiliation: Department of Nephrology, Arterial Hypertension and Dialysis, University Hospital Center Zagreb, School of Medicine, University of Zagreb, Croatia.ivanpecin@yahoo.com
authors.forename: Ivan
authors.initials: I
authors.lastname: Pećin
authors.forename: Dubravka
authors.initials: D
authors.lastname: Cvorišćec
authors.forename: Marica
authors.initials: M
authors.lastname: Miletić-Medved
authors.forename: Zivka
authors.initials: Z
authors.lastname: Dika
authors.forename: Ante
authors.initials: A
authors.lastname: Cvitković
authors.forename: Ksenija
authors.initials: K
authors.lastname: Vitale
authors.forename: Ninoslav
authors.initials: N
authors.lastname: Leko
authors.forename: Dinko
authors.initials: D
authors.lastname: Novaković
authors.forename: Jadranka
authors.initials: J
authors.lastname: Sertić
authors.forename: Jelena
authors.initials: J
authors.lastname: Kos
authors.forename: Bojan
authors.initials: B
authors.lastname: Jelaković
mesh_terms: D000118:Acetylglucosaminidase / Q000652:urine*; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000483:Alleles; D001449:Balkan Nephropathy / Q000201:enzymology / Q000235:genetics*; D001794:Blood Pressure; D003404:Creatinine / Q000097:blood; D017523:Croatia; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D011507:Proteinuria; D055815:Young Adult
chemical_list: D003404:Creatinine; D000118:Acetylglucosaminidase; D007703:Peptidyl-Dipeptidase A