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ACE gene polymorphism in focal glomerulosclerosis and membranous glomerulonephritis - Is observed difference of clinical significance.

Background and purpose: The renin angiotensin system has been considered one of the probable pathophysiologic mechanisms governing disease progression. Genetic polymorphism of the renin-angiotensin system have been associated with the clinical course of renal disease. One of the genetic polymorphisms is a deletion or insertion of a 287 base pair fragment in intron 16 of the ACE gene. Therefore, the purpose of this study was to evaluate the association between genetic polymorphism of the ACE gene and the prevalence and clinical course of focal segmental glomerulosclerosis (FSGS) and idiopathic membranous glomerulonephritis (MGN) in our patient population. Material and methods: In the study were included 39 patients (22 m, 17f) with biopsy proven primary FSGS and in 30 patients (23 m, 7f) with MGN. The mean age of patients with FSGS was 40.6+18.2 years while in MGN was aged on the average 47.8+/- 14.2 years. 31 patients with FSGS and 30 patients with MGN had follow-up average 38.4+/-17.9 months (range 3-168 months). The control group consisted of 73 healthy persons. ACE genotypes were determined by PCR method. Results: The frequency of DD, ID and II genotype was 28.2%, 48.7% and 23.7% in patients with FSGS, 36.6%, 53.3% and 10% in MGN, while 32.8%, 42.4% and 24.8% in control healthy population, respectively. There was no difference in genotype frequencies between patients and control population. Also, there was no difference in the allele frequencies between patients and the control group. In FSGG, the patients with II genotype had lower proteinuria in comparison to the patients with DD genotype (p>0.05), while patients with DD genotype showed significant increase in plasma creatinine in comparison to the patients with II genotype (p=0.07) at the end of follow-up. The time to reach the remission of the disease was shorter in patients with II genotype (p<0.05). In MGN, there were no significant differences in the degree of proteinuria and in the levels of plasma creatinine at the end of the follow-up period in relation to basal values within individual ACE genotypes (NS). Conclusion: We failed to find differences in ACE genotype distribution between observed groups of primary glomerulonephritis and control group indicating that this polymorphism does not predispose to the development of renal disease. However, there were some differences in the clinical course in FSGS considering ACE genotype while no indication that D allele is a predictor of a more rapid progression of renal disease in MGN was found. It is difficult to say whether these differences are really a consequence of different disease nature. Further investigations with more patients followed for a longer period are needed.

ACE gene polymorphism; focal segmental glomerulosclerosis; membranous nephropathy

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