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The role of ACE gene polymorphism in progression of kidney disease in patients with primary glomerulonephritis

Objective:Assessment of the role of ACE gene polymorphism in progression of kidney disease in patients with primary glomerulonephritis (PGN) classified according to the basal value of serum creatinine. Design and Methods:ACE genotype was determined by PCR in 148 patients with PGN; 110 of them were followed up for 29.1 months. They were divided into two groups:A) patients with basally normal creatinine (N=58), and B) basally elevated creatinine (N=52). Progression was considered to be found in patients with creatinine elevated above normal value limit (>130 mmol/l) or with doubled creatinine at already basally elevated values. Results:There is no significant difference in genotype distribution between patients with PGN and control group (N=73); D allele freguency in PGN is 0.577 vs. 0.541 in the control group (p>0.01). During the follow-up period 46 patients were non-progressors and 12 were progressors in group A. There is no significant difference in the D allele frequency between progressors and non-progressors, but statistically significantly lower frequency of II genotype was found in progressors (p=0.044). In B group, 42 patients were observed to be progressors and 10 were non-progressors during the follow-up period. There is no significant difference in ACE genotype distribution between progressors and non-progressors (p>0.05). However, the number of progressors in significantly higher in B group than in group A, independently of ACE genotype (42 vs.12; p <0.001). Conclusion: The progression of renal disease is independent of ACE genotype in patients with PGN and basaly elevated serum creatinine. The presence of II genotype in patients with basally normal renal function implicates a favourable clinical outcome.

ACE gene polymorphism; primary glomerulonephritis

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