title: Angiotensin-converting enzyme polymorphism gene and evolution of nephropathy to end-stage renal disease.
abstract: Genetic polymorphisms of the renin-angiotensin system (RAS) have been implicated in the pathogenesis of nephropathy and end-stage renal disease (ESRD). The association between angiotensin-converting enzyme (ACE) gene polymorphism and nephropathy evolution was studied. A random sample of 161 subjects from the Nephrology Department (of Hospital de Sant Pau) were divided into two groups: (i) 117 with end-stage renal disease; (ii) 44 with established nephropathy; and (iii) control groups of 129 subjects. The ACE gene polymorphism was performed by using polymerase chain reaction. High DD genotype presentation was observed in the two groups of subjects with nephropathy (46.12 and 61.37%, respectively vs 35.66% in controls; P < 0.0482), and also, a decrease was observed in the II genotype (6.4 and 4.54%, respectively vs 13.17% in controls, P < 0.0404). Glomerular filtration rate (GFR) was evaluated after 44 months of follow up. An important decrease of GFR was observed in patients with DD polymorphism versus other genotypes (initial, 32.3 +/- 7.9 and at 44 months, 18.35 +/- 3.3 mL/min vs 31.4 +/- 11.9 and 11.7 +/- 3.2 mL/min; P < 0.039). In a non-longitudinal study of patients in ESRD, patients with an ACE-DD genotype had a lower period of time between diagnosis of nephropathy and ESRD than patients with other genotypes (10.45 +/- 9.32 vs 19.5 +/- 8.4 years; P < 0.034). In conclusion, the ACE gene that controls RAS response may influence the development and progression of nephropathy to ESRD. Patients who develop several types of nephropathy have a higher risk of severe evolution if they have a profile of ACE-DD genotype.
authors.affiliation: Department of Endocrinology, Hospital de la Santa Creu i Sant Pau, Autonomous University of Barcelona, Avn. Sant Antoni Ma. Claret 167, Barcelona 08025, Spain.
authors.forename: M Angels
authors.initials: MA
authors.lastname: Ortiz
authors.forename: Anna
authors.initials: A
authors.lastname: De Prado
authors.forename: Teresa
authors.initials: T
authors.lastname: Doñate
authors.forename: Lluis
authors.initials: L
authors.lastname: Gallart
authors.forename: Helena
authors.initials: H
authors.lastname: Claramunt
authors.forename: Marta
authors.initials: M
authors.lastname: Hernández
authors.forename: Joaquin
authors.initials: J
authors.lastname: Martínez
authors.forename: Esther
authors.initials: E
authors.lastname: Martínez
authors.forename: Jose M
authors.initials: JM
authors.lastname: Pou
mesh_terms: D018450:Disease Progression; D005260:Female; D006801:Humans; D007674:Kidney Diseases / Q000150:complications / Q000235:genetics*; D007676:Kidney Failure, Chronic / Q000209:etiology / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic
chemical_list: D007703:Peptidyl-Dipeptidase A