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      Genetic Susceptibility to Renal Injury in Hypertension

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          Substantial evidence indicates that hypertension plays a predominant role in the progression of most chronic renal diseases including diabetic nephropathy. Nevertheless, significant differences are observed in the susceptibility to develop hypertension-associated renal damage between individuals, racial groups and animal strains despite comparable hypertension. Recent studies employing a variety of genetic methods both in humans and in experimental models, have provided strong support for the potential importance of genetic factors and have suggested that genes influencing susceptibility to renal damage may be inherited separately from genes that influence blood pressure. However, due to the genetic complexity involved in a multifactorial trait such as the susceptibility to hypertensive renal damage, very limited progress has been achieved thus far in attempts to link such susceptibility to specific genetic mechanisms, chromosome regions and/or candidate genes. It is anticipated that the rapid recent advances in molecular genetic techniques and the simultaneous use of multiple complementary strategies, as is currently under way, will greatly facilitate this search and provide fundamental new insights into the pathogenesis of hypertensive renal damage.

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          Most cited references 6

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          Chromosomal mapping of quantitative trait loci contributing to stroke in a rat model of complex human disease.

          Stroke is a complex disorder with a poorly understood multifactorial and polygenic aetiology. We used the stroke-prone spontaneously hypertensive rat (SHRSP) as a model organism, mated it with the stroke-resistant spontaneously hypertensive rat (SHR) and performed a genome-wide screen in the resultant F2 cohort where latency until stroke, but not hypertension (a major confounder) segregated. We identified three major quantitative trait loci, STR1-3, with lod scores of 7.4, 4.7 and 3.0, respectively, that account for 28% of the overall phenotypic variance. STR2 colocalizes with the genes encoding atrial and brain natriuretic factor, peptides with important vasoactive properties. Our results demonstrate the existence of primary, blood pressure-independent genetic factors predisposing to a complex form of stroke.
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            Genetics of diabetic nephropathy: evidence for major and minor gene effects.

             A Krolewski (1999)
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              Genetic susceptibility to end-stage renal disease.

              New methods have been developed to uncover the genotypes that result in complex diseases. End-stage renal disease is a complex disease, without a simple correspondence between genotype and phenotype. Both population-based and family-based epidemiological studies and analysis of model organisms suggest that the pathogenesis of end-stage renal disease may have a genetic component. A number of studies have analyzed candidate nephropathy genes with little success, but recently several well-designed studies of multiplex families with diabetic nephropathy have identified candidate nephropathy susceptibility loci. To date, kidney disease-oriented research has focused on effector mechanisms responsible for the initiation and progression of chronic renal disease. However, because end-stage renal disease is a complex disease, interruption of a single effector pathway is unlikely to result in significant therapeutic benefit. Further understanding of the pathogenesis of kidney disease and the development of new kidney disease therapies will require continued application of genetic and genomic tools to kidney disease research.

                Author and article information

                Nephron Exp Nephrol
                Cardiorenal Medicine
                S. Karger AG
                07 November 2001
                : 9
                : 6
                : 360-365
                aLoyola University Medical Center and Hines VA Hospital, Maywood, Ill., bWayne State University, Detroit, Mich., and cUniversity of California, San Francisco, Calif., USA
                52633 Exp Nephrol 2001;9:360–365
                © 2001 S. Karger AG, Basel

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                Page count
                Figures: 3, References: 16, Pages: 6
                Self URI (application/pdf):

                Cardiovascular Medicine, Nephrology

                Rat strains, Hypertension, Genetics, Kidney, Nephrosclerosis


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