Polymorphisms in angiotensin-converting-enzyme gene and progression of IgA nephropathy

Harden, P. N.; Rowe, P. A.; Rodger, R. S. C.; Junor, B. J. R.; Briggs, J. D.; Jardine, Alan G.; Geddes, Colin C.; Boulton-Jones, Michael; Mcllroy, J.H; Connell, John

doi:10.1016/s0140-6736(95)91088-3

Cited by 207 publications

(114 citation statements)

References 8 publications

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“…In contrast to the significant association of the I/D polymorphism with diabetic nephropathy, our current meta-analysis as well as published reports did not support an association of the I/D polymorphism with diabetic retinopathy, suggesting that the ACE locus is unlikely to contribute to susceptibility to retinopathy. Alternatively, since the I/D polymorphism is associated with progression of other renal diseases [34,35], the ACE locus may determine the susceptibility to renal damage in general, and, in coexistence with diabetes, it may act to increase the risk for diabetic nephropathy. The observed difference in the associations between retinopathy and nephropathy suggests that the genetic factors responsible for the two types of microangiopathy are different.…”

Section: Discussionmentioning

confidence: 99%

Meta-analysis of association of insertion/deletion polymorphism of angiotensin I-converting enzyme gene with diabetic nephropathy and retinopathy

et al. 1998

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Several lines of evidence from family and twin studies have strongly suggested that genetic factors are involved in the development of diabetic microangiopathy [1--3]. Several candidate genes have been investigated to elucidate genetic factor(s) responsible for the vascular complications, but little is known about the genetic basis of these complications [4,5]. Elucidation of the genetic factors predisposing to chronic vascular complications in diabetes mellitus will permit identification of individuals genetically predisposed to the complications and, in turn, will allow us an effective intervention tailored to the specific underlying abnormalities.The renin-angiotensin system regulates the systemic circulation and local haemodynamics, and also regulates cell growth and matrix production via its action on angiotensin II production. Angiotensin I-converting enzyme (ACE; EC 3.4.15.1) is not only a key enzyme in the renin-angiotensin system but also regulates kinin metabolism [6]. The plasma ACE level is under genetic control and is strongly associated with an insertion/deletion (I/D) polymorphism of the ACE gene, defined by the presence or absence of the 287 base-pair Alu -repetitive sequence in intron 16 [7]. Accordingly, the I/D polymorphism has been investigated as a strong candidate marker for genetic predisposition to diabetic vascular complications. Association studies of the ACE genotype with diabetic complications, however, have yielded conflicting results. Diabetologia (1998) 41: 47--53 Meta-analysis of association of insertion/deletion polymorphism of angiotensin I-converting enzyme gene with diabetic nephropathy and retinopathy Summary An insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene has repeatedly been shown to be associated with ischaemic heart disease, but the association of this genetic marker with diabetic microangiopathy is controversial. To assess the association of the genotypes with the development of diabetic nephropathy or retinopathy, we performed a meta-analysis of data from the literature, using Mantel-Haenszel method followed by the Breslow-Day test for assessing homogeneity among data. In a total of 4773 diabetic patients from 18 studies with (n = 2495) and without (n = 2278) renal complications, the D allele was significantly associated with diabetic nephropathy (p < 0.0001) in a dominant model (summary odds ratio 1.32, 95 % confidence interval: 1.15 to 1.51). There was no significant evidence against homogeneity of the odds ratios (c 2 = 18.9, 20 df; p = 0.53). The association was significant both in non-insulin-dependent (p < 0.005) and in insulin-dependent diabetes mellitus (p < 0.05). Likewise, in a total of 2010 diabetic patients with (n = 1008) and without (n = 1002) retinopathy, there was no association of the I/D polymorphism with diabetic retinopathy. These data suggest that the ACE I/D polymorphism affects the risk for diabetic nephropathy, but not for diabetic retinopathy. [Diabetologia (1998) 41: 47--53]

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Section: Discussionmentioning

confidence: 99%

Meta-analysis of association of insertion/deletion polymorphism of angiotensin I-converting enzyme gene with diabetic nephropathy and retinopathy

et al. 1998

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“…It has been postulated that, in Caucasians, the DD genotype of the angiotensin-I-converting enzyme (ACE) gene is an independent risk factor for renal disease (Dudley, Keavney, Stratton, Turner, & Ratcliffe, 1995), associated with an increased rate of progression of kidney damage in diabetes (Parving et al, 1996;Yoshida et al, 1996) and IgA glomerulonephritis (Harden et al, 1995). However, others have failed to replicate these associations (Schena, D'Altri, Cerullo, Manno, & Gesualdo, 2001;Schmidt, Schone, & Ritz, 1995).…”

Section: Genetic Explanationsmentioning

confidence: 99%

Exploring the pathways leading from disadvantage to end-stage renal disease for Indigenous Australians

Cass

Cunningham

Snelling³

et al. 2004

Social Science & Medicine

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Indigenous Australians are disadvantaged, relative to other Australians, over a range of socio-economic and health measures. The age-and sex-adjusted incidence of end-stage renal disease (ESRD) -the irreversible preterminal phase of chronic renal failure -is almost nine times higher amongst Indigenous than it is amongst non-indigenous Australians. A striking gradient exists from urban to remote regions, where the standardised ESRD incidence is from 20 to more than 30 times the national incidence. We discuss the profound impact of renal disease on Indigenous Australians and their communities. We explore the linkages between disadvantage, often accompanied by geographic isolation, and both the initiation of renal disease, and its progression to ESRD. Purported explanations for the excess burden of renal disease in indigenous populations can be categorised as:(1) primary renal disease explanations; (2) genetic explanations; (3) early development explanations; and (4) socio-economic explanations.We discuss the strengths and weaknesses of these explanations and suggest a new hypothesis which integrates the existing evidence. We use this hypothesis to illuminate the pathways between disadvantage and the human biological processes which culminate in ESRD, and to propose prevention strategies across the life-course of Indigenous Australians to reduce their ESRD risk.Our hypothesis is likely to be relevant to an understanding of patterns of renal disease in other high-risk populations, particularly indigenous people in the developed world and people in developing countries. Furthermore, analogous pathways might be relevant to other chronic diseases, such as diabetes and cardiovascular disease. If we are able to confirm the various pathways from disadvantage to human biology, we will be better placed to advocate evidence-based interventions, both within and beyond the scope of the health-care system, to address the excess burden of renal and other chronic diseases among affected populations.

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“…Although the ACE DD genotype increases the plasma ACE concentration and the risk for numerous cardiovascular-renal diseased states, such as myocardial infarction (Cambien et al, 1992), cardiomyopathy (Marian et al, 1993), IgA nephropathy (Harden et al, 1995), and diabetic nephropathy (Marre et al, 1994), the findings from case-control studies have not been consistently positive.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin converting enzyme I/D, angiotensinogen T174M-M235T and angiotensin II type 1 receptor A1166C gene polymorphisms in Turkish hypertensive patients

Ağaçhan

İsbır²,

Yılmaz³

et al. 2003

Exp Mol Med

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A bstractEssential hypertension is a m ultifactorial disease in w hich genetic and envirom ental factors play an im portant role. These factors differ in each population. As there are no existing data for the Turkish population, w e investigated four Renin Angiotensin System (RAS) gene polym orphism s, the angiotensin converting enzym e (ACE), angiotensinogen (AG N) M 235T/T174M and angiotensin II type 1 receptor A1166C polym orphism in 109 hypertensive and 86 norm otensive Turkish subjects. Polym erase Chain Reaction (PCR) and Restriction Fragm ent Length Polym orphism (RFLP), and agarose gel electrophoresis tecniques w ere used to determ ine these polym orphism . The frequencies of person that carry ACE D allel (DD+ID) w as significantly higher in hypertensive group (99.1% ) than controls (80%) (P 0.000). M235T TT genotype was also found significantly higher in hypertensives than control group (20% vs 2.7% ; P 0.001). The frequency of AG N 174M allele w as higher in the hypertensive group than control subjects (8.76% vs 4.81% ). Frequency of ATR1 C allele (AC+CC genotypes) w as found higher hypertensives than controls (39.4% vs 25.9% ; P = 0.054). O ur results suggest that an interaction exists between the RAS genes and hypertension in Turkish population.

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Polymorphisms in angiotensin-converting-enzyme gene and progression of IgA nephropathy

Cited by 207 publications

References 8 publications

Meta-analysis of association of insertion/deletion polymorphism of angiotensin I-converting enzyme gene with diabetic nephropathy and retinopathy

Meta-analysis of association of insertion/deletion polymorphism of angiotensin I-converting enzyme gene with diabetic nephropathy and retinopathy

Exploring the pathways leading from disadvantage to end-stage renal disease for Indigenous Australians

Angiotensin converting enzyme I/D, angiotensinogen T174M-M235T and angiotensin II type 1 receptor A1166C gene polymorphisms in Turkish hypertensive patients

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