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Original ArticleOpen Access
The Renin -Angiotensin System Gene Polymorphisms and Clinicopathological Correlations in lgA Nephropathy
OngAjyooth S 
,
OngAjyooth L ,
Limmongkon A ,
Tiensingh A ,
Parichatikanon P ,
Nilwarangkur S
,
OngAjyooth L ,
Limmongkon A ,
Tiensingh A ,
Parichatikanon P ,
Nilwarangkur S Genetic variability in the renin-angiotensin system (RAS) may modify renal responses
to injury and disease progression. We examined whether RAS alleles affect severity of IgA
nephropathy. These genetic variants include angiotensin I converting enzyme deletion polymorphism
in intron 16 (ACE liD), a point mutation in the angiotensinogen (AGT) gene resulting
in a methionine to threonine substitution at residue 235 (M235T) and an angiotensin receptor type
I (ATR) A to C transition at bp 1166 (A 1166 C). A total of 53 patients with biopsy-proven
IgA nephropathy and 80 normal control subjects were recruited for study. These patients were
classified into two groups according to serum creatinine at renal biopsy. Group I patients (n = 40)
had normal renal function, serum creatinine ≤ 1.5 mg/dl and group 2 patients ( n = 13) had renal
insufficiency with serum creatinine > 1.5 mg/dl. The blood pressure and urinary protein of
group 2 patients were higher than group 1 (p < 0.01). The mean scores of histological parameters
including mesangial proliferation, glomerular sclerosis (global and segmental), the interstitial
fibrosis and crescent formation in group 2 patients were significantly higher than in group I
patients (p < 0.05). The most frequent genotype in IgA patients was ID (47%) genotype, followed by II
(45%) and DD (8%) genotype of ACE gene. The mean serum ACE activity in the DD group was
significantly higher than in the II group (p < 0.05) but was not significantly different from that of
the ID group. No statistically significant differences were found with respect to allele frequencies
between IgA group I, group 2, or between controls and all IgA patients. Furthermore, no significant
difference in AGT alleles, ATR alleles frequencies was detected between groups of IgA patients,
although a trend for a higher frequency of DO genotype and AGT-TT genotype were noted in
lgA group 2. The combined analysis of the ACE-DO and AGT-TT genotypes did not show
any genetic influence on the risk of the disease susceptibility. To resolve the true role of ACE
genotype and any dependent effect on progression, larger collaborative studies are required.
Key word : RAS Gene Polymorphism, IgA Nephropathy, Clinicopathology
to injury and disease progression. We examined whether RAS alleles affect severity of IgA
nephropathy. These genetic variants include angiotensin I converting enzyme deletion polymorphism
in intron 16 (ACE liD), a point mutation in the angiotensinogen (AGT) gene resulting
in a methionine to threonine substitution at residue 235 (M235T) and an angiotensin receptor type
I (ATR) A to C transition at bp 1166 (A 1166 C). A total of 53 patients with biopsy-proven
IgA nephropathy and 80 normal control subjects were recruited for study. These patients were
classified into two groups according to serum creatinine at renal biopsy. Group I patients (n = 40)
had normal renal function, serum creatinine ≤ 1.5 mg/dl and group 2 patients ( n = 13) had renal
insufficiency with serum creatinine > 1.5 mg/dl. The blood pressure and urinary protein of
group 2 patients were higher than group 1 (p < 0.01). The mean scores of histological parameters
including mesangial proliferation, glomerular sclerosis (global and segmental), the interstitial
fibrosis and crescent formation in group 2 patients were significantly higher than in group I
patients (p < 0.05). The most frequent genotype in IgA patients was ID (47%) genotype, followed by II
(45%) and DD (8%) genotype of ACE gene. The mean serum ACE activity in the DD group was
significantly higher than in the II group (p < 0.05) but was not significantly different from that of
the ID group. No statistically significant differences were found with respect to allele frequencies
between IgA group I, group 2, or between controls and all IgA patients. Furthermore, no significant
difference in AGT alleles, ATR alleles frequencies was detected between groups of IgA patients,
although a trend for a higher frequency of DO genotype and AGT-TT genotype were noted in
lgA group 2. The combined analysis of the ACE-DO and AGT-TT genotypes did not show
any genetic influence on the risk of the disease susceptibility. To resolve the true role of ACE
genotype and any dependent effect on progression, larger collaborative studies are required.
Key word : RAS Gene Polymorphism, IgA Nephropathy, Clinicopathology
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