Quantitative trait loci for compensatory renal hypertrophy in the mouse.
Reduction in numbers of nephrons or decrease in kidney function due to a variety of diseases results in compensatory renal hypertrophy (CRH). Recently, it has been proposed that CRH may be a prerequisite for progression of renal injury; genetic dissection of CRH may be therefore helpful in understanding the process whereby people with partial renal insufficiency progress to end-stage renal disease. Since genetic analysis of CRH in humans is quite limited, we searched for genetic determinants of CRH after unilateral nephrectomy using a total genome scan of the mouse BXD recombinant inbred strains. We demonstrated that CRH is a highly heritable trait and we identified a quantitative trait locus on mouse chromosome 11 near the D11Mit14 marker that exerts a major effect on CRH (lod score = 3.4) and is responsible for approximately 52% of genetic variation in CRH. This marker maps near Ace, Gh, and Ngfr positional candidate genes.[1]References
- Quantitative trait loci for compensatory renal hypertrophy in the mouse. Zídek, V., Musilová, A., Vorlíèek, J., Simáková, M., Pravenec, M. Biochem. Biophys. Res. Commun. (1998) [Pubmed]
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