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- W120872642 abstract "The fractional urinary excretion of filtered inorganic phosphate (Pi) increases progressively from the normal value of less than 15% up to 80% or more in advanced renal failure. The mechanisms responsible for this adaptation have been examined by several investigators. Slatopolsky et al (1) suggested that a reduction in glomerular filtration led to an increase in plasma Pi, which in turn decreased plasma ionised calcium concentration and stimulated increased parathyroid hormone secretion. Pi retention was thus considered to be responsible for secondary hyperparathyrodism, which in turn decreased tubular Pi reabsorption and tended to correct or minimise the rise in the plasma Pi concentration. Recently Bricker et al (2) have suggested that there is an increased responsiveness to the phosphaturic effect of PTH in renal failure, and that this may contribute to phosphate homeostasis in this circumstance. By contrast, Swenson et al (3) reported that PTH was not required for phosphate homeostasis in renal failure in the dog. In a recent micropuncture study in the rat, Bank et al (4) concluded that, in this species in renal failure, the proximal tubule has a greatly enhanced intrinsic capacity for Pi reabsorption which is unmasked by parathyroidectomy, but is normally suppressed by the secondary hyperparathyroidism of renal failure." @default.
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- W120872642 date "1980-01-01" @default.
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- W120872642 title "Phosphate Handling by the Remnant Dog Kidney in the Presence and Absence of the Contralateral Normal Kidney" @default.
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- W120872642 doi "https://doi.org/10.1007/978-1-4615-9167-2_15" @default.
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