title: Role of genetic polymorphism in the SA gene on the blood pressure and prognosis of renal function in patients with immunoglobulin A nephropathy.
abstract: The SA gene has been shown to be much more highly expressed in the kidneys of spontaneously hypertensive rats than in the corresponding wild-type strain. Genetic polymorphism of this gene has been shown to play a role in human hypertension, although the details of this association remain controversial. We investigated the possible associations between SA gene polymorphism and both hypertension and the prognosis of renal function in patients with immunoglobulin A nephropathy (IgAN). Genomic DNA was isolated from the peripheral blood of 367 individuals, including 274 patients with histologically proven IgAN and 100 controls without any history of renal disease. The SA genotype was determined by polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) with Pst I. The frequencies of genotypes and alleles were not different between the patients with IgAN and those without renal disease. In the group without renal disease, the SA gene polymorphism was not associated with hypertension. However, in the patients with IgAN the A1 allele frequency was significantly higher in the hypertensives than in the normotensives. The renal survival of the patients with the A2 allele tended to be better than that of those without the A2 allele. The findings thus suggest that SA gene polymorphism may be associated with the renal prognosis of IgAN through its effect on blood pressure. Further, they suggest that the sensitivity to this gene polymorphism increases in patients with renal injury.
authors.affiliation: Division of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan. naritai@med.niigata-u.ac.jp
authors.forename: Ichiei
authors.initials: I
authors.lastname: Narita
authors.forename: Noriko
authors.initials: N
authors.lastname: Saito
authors.forename: Shin
authors.initials: S
authors.lastname: Goto
authors.forename: Arimasa
authors.initials: A
authors.lastname: Shirasaki
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Morioka
authors.forename: Song
authors.initials: S
authors.lastname: Jin
authors.forename: Kentaro
authors.initials: K
authors.lastname: Omori
authors.forename: Minoru
authors.initials: M
authors.lastname: Sakatsume
authors.forename: Masaaki
authors.initials: M
authors.lastname: Arakawa
authors.forename: Fumitake
authors.initials: F
authors.lastname: Gejyo
mesh_terms: D000368:Aged; D000483:Alleles; D001794:Blood Pressure / Q000502:physiology*; D003066:Coenzyme A Ligases; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D005922:Glomerulonephritis, IGA / Q000235:genetics* / Q000503:physiopathology*; D006801:Humans; D007668:Kidney / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic / Q000502:physiology*; D011379:Prognosis; D011506:Proteins / Q000235:genetics*; D012016:Reference Values; D016019:Survival Analysis
chemical_list: D011506:Proteins; C081817:Acsm3 protein, rat; D003066:Coenzyme A Ligases