Interaction between gene polymorphisms of nitric oxide synthase and renin-angiotensin system in the progression of membranous glomerulonephritis

Stratta, Piero; Bermond, Francesca; Guarrera, Simonetta; Canavese, Caterina; Carturan, Sonia; Dall'Omo, Annamaria; Ciccone, Giovannino; Bertola, Laura D.; Mazzola, Gina; Fasano, Edvige; Matullo, Giuseppe

doi:10.1093/ndt/gfg604

Cited by 18 publications

(13 citation statements)

References 16 publications

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“…Prior studies related the incidence of MGN and several gene polymorphisms: TNF-a gene G-308A, ACE insertion or deletion (ACE I/D), angiotensin II Type 1 receptor (AT1R 1166A/C), angiotensinogen (AGT M235T), and NOS (ecNOS4b/a). [21][22][23] This study focused on IL-6 C-572G (rs1800796) SNP previously investigated for abdominal aortic aneurysms (AAAs) and coronary heart disease. 24,25 We found strong correlation between MGN and IL-6 C-572G SNP: C allele and CC genotype frequency at IL-6 C-572G SNP was definitely higher in MGN patients.…”

Section: Discussionmentioning

confidence: 99%

Effect ofIL-6C-572G polymorphism on idiopathic membranous nephropathy risk in a han chinese population

Chen

Huang

et al. 2010

Renal Failure

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Membranous glomerulonephritis (MGN) is viewed as an immune-mediated glomerular disease, with immunologic expression occurring in genetically susceptible persons. The cytokine interleukin-6 (IL-6) gene polymorphism is known to impair intracellular signaling pathways following adaptive immune response. Our study gauged the effects of IL-6 C-572G (rs1800796) single nucleotide polymorphism (SNP) on MGN among Taiwan's Han Chinese population, as analyzed in 265 controls and 106 MGN patients. Genotyping for IL-6 C-572G SNP was performed by restriction fragment length polymorphism assay. Data showed stark differences in genotype and allele frequency distributions at IL-6 C-572G SNP between MGN patients and controls (p = 1.6E-04 and 1.7E-04, respectively). People with C allele or with CC genotype at IL-6 C-572G SNP showed higher risk of MGN (odds ratio = 2.42 and 2.71, respectively; 95% confidence interval = 1.51-3.87 and 1.60-4.60, respectively). These point to IL-6 C-572G polymorphism as the underlying cause of MGN; polymorphism merits further investigation.

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Section: Discussionmentioning

confidence: 99%

Effect ofIL-6C-572G polymorphism on idiopathic membranous nephropathy risk in a han chinese population

Chen

Huang

et al. 2010

Renal Failure

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“…A 27-bp long repeat in the fourth intron of endothelial NOS (eNOS) designated as the 4a/4b polymorphism has been reported that in the presence of ACE I/D or M235T polymorphism increased the risk of renal disease progression (52).…”

Section: Interaction Of Ace I/d Polymorphism With Enos Gene Polymorphismmentioning

confidence: 99%

ACE insertion/deletion (I/D) polymorphism and diabetic nephropathy

Rahimi¹

2012

J Nephropathol

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Implication for health policy/practice/research/medical education:The presence of angiotensin converting enzyme (ACE) insertion/deletion (I/D) polymorphism affects the plasma level of ACE. ACE DD genotype is associated with highest systemic and renal ACE levels, compared with the lowest ACE activity in carriers of II genotype. Most studies confirmed that ACE I/D polymorphism is involved in the susceptibility to overt nephropathy with protective role of ACE II genotype against the disease in both type 1 and 2 diabetes mellitus. In this review focus has been performed on the study of ACE I/D polymorphism in various populations and its influence on the risk of onset and progression of diabetic nephropathy. Results:The presence of ACE insertion/deletion (I/D) polymorphism affects the plasma level of ACE. ACE DD genotype is associated with the highest systemic and renal ACE levels compared with the lowest ACE activity in carriers of II genotype. Conclusions: In this review focus has been performed on the study of ACE I/D polymorphism in various populations and its influence on the risk of onset and progression of diabetic nephropathy. Also, association between ACE I/D polymorphism and response to ACE inhibitor and angiotensin II receptor antagonists will be reviewed. Further, synergistic effect of this polymorphism and variants of some genes on the risk of development of diabetic nephropathy will be discussed.Review Article

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“…Again, results of genetic studies were contrasting, with some authors showing an association with the progression of IgA nephropathy (89) that was not confirmed by others (90). Of note, however, in a combined gene analysis of eNOS 4a/4b, ACE I/D, AGT M235T, and AT1R A166C polymorphisms in a large cohort of patients with idiopathic membranous nephropathy, Stratta et al found that the combination of aaϩba of eNOS 4a/4b genotypes with IIϩID ACE I/D or TTϩMT AGT M235T genotypes was associated with accelerated renal disease progression, whereas the same eNOS polymorphism had no predictive role when considered alone (91). This finding suggests that in some circumstances a single gene variant may result in appreciable phenotypic changes only upon combination with other polymorphisms that may result in additional or synergistic effects on the same metabolic pathways.…”

Section: Other Non-ras Polymorphisms and Their Interactions With The mentioning

confidence: 99%

Angiotensin Converting Enzyme Insertion/Deletion Polymorphism and Renoprotection in Diabetic and Nondiabetic Nephropathies

Ruggenenti

Bettinaglio

Pinares

et al. 2008

Clinical Journal of the American Society of Nephrology

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Despite the huge amount of studies looking for candidate genes, the ACE gene remains the unique, well-characterized locus clearly associated with pathogenesis and progression of chronic kidney disease, and with response to treatment with drugs that directly interfere with the renin angiotensin system (RAS), such as angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor antagonists (ARA). The II genotype is protective against development and progression of type I and type II nephropathy and is associated with a slower progression of nondiabetic proteinuric kidney disease. ACE inhibitors are particularly effective at the stage of normoalbuminuria or microalbuminuria in both type I and type II diabetics with the II genotype, whereas the DD genotype is associated with a better response to ARA therapy in overt nephropathy of type II diabetes and to ACE inhibitors in male patients with nondiabetic proteinuric nephropathies. The role of other RAS or non-RAS polymorphisms and their possible interactions with different ACE I/D genotypes are less clearly defined. Thus, evaluating the ACE I/D polymorphism is a reliable tool to identify patients at risk and those who may benefit the most of renoprotective therapy with ACE inhibitors or ARA. This may guide pharmacologic therapy in individual patients and help design clinical trials in progressive nephropathies. Moreover, it might help optimize prevention and intervention strategies at population levels, in particular, in countries where resources are extremely limited and 1 million patients continue to die every year of cardiovascular or renal disease.

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Interaction between gene polymorphisms of nitric oxide synthase and renin-angiotensin system in the progression of membranous glomerulonephritis

Cited by 18 publications

References 16 publications

Effect ofIL-6C-572G polymorphism on idiopathic membranous nephropathy risk in a han chinese population

Effect ofIL-6C-572G polymorphism on idiopathic membranous nephropathy risk in a han chinese population

ACE insertion/deletion (I/D) polymorphism and diabetic nephropathy

Angiotensin Converting Enzyme Insertion/Deletion Polymorphism and Renoprotection in Diabetic and Nondiabetic Nephropathies

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