OBJECTIVES: The aging process affects responsiveness and other functions of endothelium and vascular smooth muscle cells, predisposing the old vessels to the development of atherosclerotic lesions. Endothelial nitric oxide synthase (ecNOS) gene polymorphisms were shown to affect the occurrence of acute myocardial infarction (AMI). We hypothesized that aging may affect the association between the ecNOS gene polymorphism and AMI. METHODS: We investigated the age-related distribution of the ecNOS gene a/b polymorphism in 121 male AMI patients and 206 age-matched healthy male controls. RESULTS: The aa, ab and bb genotypes were found in 1, 49 and 156 cases among the control subjects and 5, 23 and 93 cases among the AMI patients, respectively. There was a significant correlation between the ecNOS polymorphism and AMI (p +AD0- 0.045). When the correlation was analyzed by age, the significance remained only in the group below the age of 51 (p +AD0- 0.009). The proportion of smokers was increased in the young patients when compared to the old patients (p +AD0- 0.033), indicating that smoking also has greater effect on the younger population. The incidences of hypertension and diabetes mellitus, however, were similar in both populations. CONCLUSION: Our work provides the first evidence that links ecNOS polymorphism to the risk of AMI in relation to age. Young persons who smoke or have ecNOSaa genotype may have an increased risk of developing AMI. The functional as well as structural changes associated with aging in the vascular endothelium may mask the effect of the ecNOS polymorphism in the development of AMI in old persons.
Adult ; Age Distribution ; Aged ; Aged, 80 and over ; Aging/physiology+ACo- ; Chi-Square Distribution ; Comorbidity ; Diabetes Mellitus/epidemiology ; Endothelium, Vascular/enzymology+ACo- ; Genotype ; Human ; Hypertension/epidemiology ; Korea/epidemiology ; Male ; Middle Age ; Myocardial Infarction/physiopathology+ACo- ; Myocardial Infarction/epidemiology ; Nitric-Oxide Synthase/metabolism+ACo- ; Nitric-Oxide Synthase/genetics+ACo- ; Polymerase Chain Reaction ; Polymorphism (Genetics)+ACo- ; Risk Assessment ; Statistics, Nonparametric

We examined the renal responsiveness to ACE inhibitor in IgA nephropathy (IgAN) patients according to the grouping of ACE gene polymorphism. Sixty one patients diagnosed as IgAN by renal biopsy and prescribed with ACE inhibitors were enrolled. Genomic DNA was extracted from whole blood and PCR was performed. The I/D polymorphism was determined by the presence of the 287 bp fragment in intron 16 of chromosome 17. During the follow-up period (mean+ADs- 44.6 months, median: 44.5 months, 5 to 113 months), the blood pressure of 61 patients was controlled below 130/80 mmHg. The renal responsiveness was determined by the degree of changes of proteinuria at 12 months after initiation of ACE inhibitors and by the slope of reciprocal variation of the serum creatinine against follow-up duration ?(1/Cr2-1/Cr1)/durations?. The distribution of the II, ID and DD genotype among 61 patients was 21, 16 and 24 patients, respectively. There were no differences among three genotypes in age, sex, the number of patients with initial blood pressure over 140/90 mmHg, initial serum creatinine level, the number of patients with initial azotemia (+AD4- 1.4 mg/dL) and with initial 24-hr proteinuria amount over 2.0 g. Significant anti-proteinuric effect of ACE inhibitor was found in IgAN (p +AD0- 0.001), but no significant difference was found among genotypes. Significant difference (p +AD0- 0.011) was noticed between II type and DD type in the slope of reciprocal variation of the serum creatinine against follow-up duration. In conclusion, efficacy of ACE inhibitors on renal function preservation in IgAN was more pronounced in DD genotype than II genotype.
Adolescence ; Adult ; Analysis of Variance ; Angiotensin-Converting Enzyme Inhibitors/administration +ACY- dosage+ACo- ; Comparative Study ; Female ; Glomerulonephritis, IGA/genetics+ACo- ; Glomerulonephritis, IGA/drug therapy+ACo- ; Human ; Kidney Function Tests ; Male ; Middle Age ; Peptidyl-Dipeptidase A/genetics+ACo- ; Polymorphism (Genetics)+ACo- ; Probability ; Prognosis ; Retrospective Studies ; Treatment Outcome

Renin-angiotensin system is considered important in the genesis of hypertension and development of end-stage renal disease (ESRD) in autosomal dominant polycystic kidney disease (ADPKD). The angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism has been associated with susceptibility to the development of some renal diseases. We investigated the association of ACE gene polymorphism with the progression to hypertension and ESRD in 108 patients with ADPKD. The ACE I/D polymorphism was amplified with the flanking primers by polymerase chain reaction. In patients genotyped for ACE gene polymorphism, the frequencies of DD (15+ACU-), ID (51+ACU-) and II (34+ACU-) genotypes were similar to those of the general population. Of the 108 patients, 64 (59+ACU-) developed hypertension and 24 (22+ACU-) reached ESRD at the time of study. The prevalence of hypertension was not significantly different among the three genotypes. The mean renal survival time was 53-6 yr in II genotype, 5510 yr in ID genotype and 529 yr in DD genotype which was not significantly different among them. Cumulative renal survival was not significantly different either. There was no association of ACE gene polymorphism with the prevalence of hypertension and renal survival in ADPKD. We suggest that ACE I/D polymorphism is not an important modifying gene in the progression of ADPKD.
Adult ; Aged ; Comparative Study ; Disease Progression ; Female ; Genetic Predisposition to Disease ; Genotype ; Human ; Hypertension, Renal/etiology ; Hypertension, Renal/epidemiology ; Kidney Failure, Chronic/etiology ; Kidney Failure, Chronic/epidemiology ; Korea/epidemiology ; Male ; Middle Age ; Peptidyl-Dipeptidase A/genetics+ACo- ; Polycystic Kidney, Autosomal Dominant/genetics+ACo- ; Polycystic Kidney, Autosomal Dominant/epidemiology ; Polycystic Kidney, Autosomal Dominant/enzymology ; Polycystic Kidney, Autosomal Dominant/complications ; Polymerase Chain Reaction ; Polymorphism (Genetics)+ACo- ; Prevalence

Renin-angiotensin system is considered important in the genesis of hypertension and development of end-stage renal disease (ESRD) in autosomal dominant polycystic kidney disease (ADPKD). The angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism has been associated with susceptibility to the development of some renal diseases. We investigated the association of ACE gene polymorphism with the progression to hypertension and ESRD in 108 patients with ADPKD. The ACE I/D polymorphism was amplified with the flanking primers by polymerase chain reaction. In patients genotyped for ACE gene polymorphism, the frequencies of DD (15+ACU-), ID (51+ACU-) and II (34+ACU-) genotypes were similar to those of the general population. Of the 108 patients, 64 (59+ACU-) developed hypertension and 24 (22+ACU-) reached ESRD at the time of study. The prevalence of hypertension was not significantly different among the three genotypes. The mean renal survival time was 53-6 yr in II genotype, 5510 yr in ID genotype and 529 yr in DD genotype which was not significantly different among them. Cumulative renal survival was not significantly different either. There was no association of ACE gene polymorphism with the prevalence of hypertension and renal survival in ADPKD. We suggest that ACE I/D polymorphism is not an important modifying gene in the progression of ADPKD.
Adult ; Aged ; Comparative Study ; Disease Progression ; Female ; Genetic Predisposition to Disease ; Genotype ; Human ; Hypertension, Renal/etiology ; Hypertension, Renal/epidemiology ; Kidney Failure, Chronic/etiology ; Kidney Failure, Chronic/epidemiology ; Korea/epidemiology ; Male ; Middle Age ; Peptidyl-Dipeptidase A/genetics+ACo- ; Polycystic Kidney, Autosomal Dominant/genetics+ACo- ; Polycystic Kidney, Autosomal Dominant/epidemiology ; Polycystic Kidney, Autosomal Dominant/enzymology ; Polycystic Kidney, Autosomal Dominant/complications ; Polymerase Chain Reaction ; Polymorphism (Genetics)+ACo- ; Prevalence