ACE gene polymorphism and IgA nephropathy: An ethnically homogeneous study and a meta-analysis

Schena, Francesco Paolo; D’Altri, Christian; Cerullo, Giuseppina; Manno, Carlo; Gesualdo, Loreto

doi:10.1046/j.1523-1755.2001.060002732.x

Cited by 73 publications

(53 citation statements)

References 37 publications

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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). The DD genotype of the ACE gene occurs infrequently in Indigenous Australians (Lester et al, 1999), in whom no significant influence on renal disease has been demonstrated.…”

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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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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“…23 Although linkage analysis of familial IgAN revealed close association with the five loci, 17,24,25 precise causative genes have not been identified. Moreover, many candidate genes have been associated with IgAN, such as those for human leukocyte antigen, 26 MHC, 27 uteroglobin, [28][29][30] Ig mu-binding protein 2, 31 polymeric Ig receptor, 32 selectin, 16 and angiotensinconverting enzyme 33,34 ; however, none of these studies have been sufficiently replicated or confirmed functionally. It is noteworthy that the combined effect of multiple susceptibility genes may contribute to the development of IgAN.…”

Section: Discussionmentioning

confidence: 99%

Development of a Model of Early-Onset IgA Nephropathy

Okazaki

Suzuki

Otsuji

et al. 2012

Journal of the American Society of Nephrology

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“…others have reported no correlation between genotype and outcome. 37,38 In a case-control study from India, 39 22 patients with IgAN were divided into progressors (n = 13) and non-progressors (n = 9) based on whether there was at least a 20% decline in renal function at last follow-up. DD genotype of ACE gene was shown to predispose the individual to IgAN in Indian population besides having an impact on disease progression and may explain the poor prognosis of IgAN in India.…”

Section: Gene Polymorphisms: Susceptibility and Progressionmentioning

confidence: 99%

IgA Nephropathy in India: What We Do Know

Chacko

2011

Renal Failure

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ACE gene polymorphism and IgA nephropathy: An ethnically homogeneous study and a meta-analysis

Abstract: Our study and meta-analysis suggest caution in the interpretation of results from association studies enrolling heterogeneous populations. Further studies using new tests, which are free of the bias due to population stratification and ethnicity, are warranted.

Cited by 73 publications

References 37 publications

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

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

Development of a Model of Early-Onset IgA Nephropathy

IgA Nephropathy in India: What We Do Know

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