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      Renal 31-Phosphorus-Magnetic Resonance Spectral Changes in Experimental Uremia

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          Abstract

          Altered renal cellular phosphate (P<sub>i</sub>) homeostasis may be involved in disturbed regulation of lα,25-dihydroxyvitamin D<sub>3</sub> [1,25(OH)<sub>2</sub>D<sub>3</sub>] production in chronic renal failure. To assess cytoplasmic concentrations of P<sub>i</sub> and other phosphate metabolites in uremia, phosphorus-magnetic resonance spectroscopy (<sup>31</sup>P-MRS) studies were carried out in vivo in rat remnant kidney. Five-sixths-nephrectomized animals (Nx, n = 8, serum creatinine 1.28 ± 0.18 mg/ dl) and sham-operated control animals (n = 8) were pair-fed a high-phosphate diet (1.6% phosphate, 1.0% calcium) for 19 days. In both remnant and intact kidneys, <sup>31</sup>P-magnetic resonance spectra displayed six major peaks: phospho-monoesters (PME), P<sub>i</sub>, phosphodiesters, and adenosine triphosphate (ATP)-γ -α, and -β. Phosphocreatine was absent. The relative intensity of the renal γATP signal was comparable between the remnant kidney in Nx and the sham-operated kidney in control animals and was, therefore, used as the internal standard to assess the P<sub>i</sub>/γATP ratio. The P<sub>i</sub>/γATP ratio was significantly (p < 0.05) increased in the remnant kidney as compared to the sham-operated control kidney (0.97 ± 0.24 in Nx vs. 0.75 ± 0.12 in sham-operated controls; means ± SE). Similarly, the PME/γATP ratio was significantly increased in Nx (p < 0.01), whereas the relative intensities of other phosphate metabolite signals were not altered in Nx. Mean serum 1,25(OH)<sub>2</sub>D<sub>3</sub> concentrations were 62 pg/ml for Nx and 93 for sham-operated controls (p < 0.05); mean serum phosphate levels were 4.35 mmol/l for Nx and 2.61 for sham-operated controls (p < 0.01). The pH in the remnant kidneys was 7.20 ± 0.06 (mean ± SE, n = 8), whereas the pH in intact kidneys was 7.29 ± 0.05 (n = 8, p < 0.05). To examine the contribution of blood cells to <sup>31</sup>P-magnetic resonance spectra, an exchange transfusion with a fluorocarbonated oxygen carrier (to a final hematocrit of 8%) was carried out, while animals (n = 5) were monitored by MRS. This did not significantly change the relative intensities of phosphate metabolite peaks, indicating that blood phosphorus did not measurably contribute to the renal P<sub>i</sub> signal. The data suggest that intrarenal P<sub>i</sub> concentration is elevated in renal failure. This could inhibit 25-hydroxyvitamin D<sub>3</sub>-1 α-hydroxylase activity and thus have some relevance for pathogenesis of renal hyperparathyroidism.

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          Author and article information

          Journal
          NEF
          Nephron
          10.1159/issn.1660-8151
          Nephron
          S. Karger AG
          1660-8151
          2235-3186
          1996
          1996
          19 December 2008
          : 73
          : 1
          : 27-33
          Article
          188994 Nephron 1996;73:27–33
          10.1159/000188994
          8742953
          © 1996 S. Karger AG, Basel

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          Page count
          Pages: 7
          Categories
          Original Paper

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