As progressive renal failure develops, phosphate excretion per functioning nephron increases, thus preserving homeostasis. To test whether dietary phosphate supply might contribute to the regulation of renal phosphate excretion in the uremic setting, groups of male Sprague-Dawley rats that were either parathyroidectomized (PTX) or sham PTX (S-PTX) and either five-sixths nephrectomized (Nx) or sham Nx (S-Nx) were studied following a 4-wk dietary regimen consisting of 0.1 or 0.7% phosphate. For Nx rats fed the 0.7% phosphate diet the fractional excretion of phosphate (FE(Pi)) was enhanced (47 ± 6 vs. 21 ± 3%) and the maximum tubular reabsorption of phosphate per milliliter GFR (Tm(Pi)/GFR) was suppressed (1.65 ± 0.19 vs. 2.33 ± 0.19 μmol/ml). FE(Pi) was unchanged by PTX in these Nx animals (42 ± 6 vs. 47 ± 6%). Tm(Pi)/GFR remained suppressed in PTX, NX animals when compared with S-Nx, PTX controls (3.38 ± 0.33 vs. 5.07 ± 0.41 μmol/ml). For rats fed the 0.1% phosphate diet Nx did not affect Tm(Pi)/GFR in either S-PTX (5.40 ± 0.43 vs. 4.97 ± 0.34 μmol/ml) or PTX (7.03 ± 0.23 vs. 6.98 ± 0.21 μmol/ml) animals. For both S-Nx and Nx animals the effects of PTX and dietary phosphate restriction on Tm(Pi)/GFR were independent and additive. In all groups of animals, tubular reabsorption of phosphate per milliliter GFR (TR(Pi)/GFR) dropped acutely with continued infusion of phosphate once Tm(Pi)/GFR was achieved. Thus, a resetting of TR(Pi)/GFR occurs among Nx rats in response to both chronic dietary phosphate deprivation and acute intravenous phosphate loading. Renal adaptive mechanism(s) maintaining phosphate excretion in uremia include(s) those mechanisms affecting tubular phosphate reabsorption when phosphate supply is altered.
|Original language||English (US)|
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|State||Published - 1985|
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