title: Renal outcome and vascular morbidity in systemic lupus erythematosus (SLE): lack of association with the angiotensin-converting enzyme gene polymorphism.
abstract: OBJECTIVE
  The angiotensin-converting enzyme (ACE) gene polymorphism has been associated with worse outcome in various chronic glomerular disorders and in hypertension. Because nephritis and vascular morbidity are prominent determinants of outcome in systemic lupus erythematosus (SLE), we studied the distribution and prognostic effect the ACE genotype might have on the outcome of SLE.
  
  
  METHODS
  Fifty-six consecutive Israeli SLE patients and 48 (sex and ethnic origin matched) healthy individuals were evaluated for the ACE genotype by a polymerase chain reaction-based assay. The clinical and laboratory parameters of the patients as well as the SLE disease activity index (SLEDAI) and the presence of hypertension, diabetes mellitus, ischemic heart disease, congestive heart failure, and stroke were correlated with the ACE genotype.
  
  
  RESULTS
  The distribution of the ACE genotype D/D, D/I, and I/I in the lupus group was 59%, 36%, and 5%, respectively, similar to the distribution in the control group (54%, 31%, and 15%, respectively). We failed to find any significant association between the ACE genotype and disease manifestations, SLEDAI, renal function, or cardiovascular and cerebrovascular morbidity. The clinical and laboratory parameters associated with renal outcome and vascular morbidity in our cohort are described.
  
  
  CONCLUSIONS
  No difference was found between the distribution of the ACE genotype in lupus patients and the general population in Israel. Renal function as well as cardiovascular and cerebrovascular morbidity among Israeli patients with SLE are disease-related and independent of the ACE gene polymorphism.
authors.affiliation: Rheumatology Unit, Schneider Children's Medical Center, Petah Tikva, Israel. ymolad@post.tau.ac.il
authors.forename: Y
authors.initials: Y
authors.lastname: Molad
authors.forename: E
authors.initials: E
authors.lastname: Gal
authors.forename: N
authors.initials: N
authors.lastname: Magal
authors.forename: J
authors.initials: J
authors.lastname: Sulkes
authors.forename: M
authors.initials: M
authors.lastname: Mukamel
authors.forename: A
authors.initials: A
authors.lastname: Weinberger
authors.forename: S
authors.initials: S
authors.lastname: Lalazari
authors.forename: M
authors.initials: M
authors.lastname: Shohat
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D002561:Cerebrovascular Disorders / Q000201:enzymology* / Q000235:genetics; D015331:Cohort Studies; D004247:DNA / Q000032:analysis; D017931:DNA Primers / Q000737:chemistry; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000201:enzymology / Q000235:genetics; D005260:Female; D005838:Genotype; D006333:Heart Failure / Q000150:complications / Q000201:enzymology / Q000235:genetics; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000201:enzymology / Q000235:genetics; D007674:Kidney Diseases / Q000201:enzymology* / Q000235:genetics; D008180:Lupus Erythematosus, Systemic / Q000201:enzymology* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics* / Q000378:metabolism; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D011379:Prognosis; D011446:Prospective Studies; D012720:Severity of Illness Index; D020521:Stroke / Q000150:complications / Q000201:enzymology / Q000235:genetics
chemical_list: D017931:DNA Primers; D004247:DNA; D007703:Peptidyl-Dipeptidase A