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It has been proposed that the functional adaptations of surviving nephrons in advancing chronic renal failure (CRF) are not random but characterized by an excretory response which varies inversely with the number of surviving nephrons ('magnification phenomenon'). Because validation of this hypothesis in man is incomplete, we undertook to characterize the excretory response to acute volume expansion in patients with CRF. In normals, water immersion to the neck (NI) results in a redistribution of blood volume with preferential central hypervolemia (CV) in the absence of plasma compositional change.

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The rDNA magnification process consists of a rapid and inheritable rDNA increase occurring in bobbed males: in a few generations the bb loci acquire the wild-type rDNA value and reach a bb+ phenotype.--We have analyzed the rDNA magnification process in the repair-recombination-deficient mutant mei9a, both at the phenotypical and rDNA content levels. In mei9a bb double mutants the recovery of bb+ phenotype is strongly disturbed and the rDNA redundancy value fails to reach the wild-type level.

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In chronic renal disease, the addition of a fixed quantity of Na to the extracellular fluid (ECF) will evoke a natriuretic response per nephron which is inversely proportional to the glomerular filtration rate (GFR). One factor that could contribute to this "magnification" phenomenon is an increased sensitivity of residual nephrons to physiologic natriuretic forces. The present studies were designed to examine this possibility.

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