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      Direct Effect of the Correction of Acidosis on Plasma Parathyroid Hormone Concentrations, Calcium and Phosphate in Hemodialysis Patients: A Prospective Study

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          Background: Metabolic acidosis contributes to renal osteodystrophy and together with hyperphosphatemia, hypocalcemia and altered vitamin D metabolism may result in increased levels of intact parathyroid hormone (iPTH) and metastatic calcifications. However, the impact of the correction of metabolic acidosis on iPTH levels and calcium-phosphate metabolism is still controversial. Study Design: The effects of the correction of metabolic acidosis on serum concentrations of iPTH, calcium (Ca), phosphate (PO<sub>4</sub>) and alkaline phosphatase were prospectively studied. Twelve uremic patients on maintenance hemodialysis (HD) for 49 months (median; range 6–243 months) with serum bicarbonate levels ≤20 mmol/l were studied before and after 3 months of oral sodium bicarbonate supplementation. Predialysis serum bicarbonate, arterial pH, ionized calcium, plasma sodium, plasma potassium, serum creatinine, hemoglobin, K<sub>t</sub>/V, postdialysis body weight, predialysis systolic and diastolic blood pressure were also evaluated before and after correction. Results: Serum bicarbonate levels and arterial pH increased respectively from 19.3 ± 0.6 to 24.4 ± 1.2 mmol/l (p < 0.0001) and 7.34 ± 0.03 to 7.40 ± 0.02 (p < 0.001). iPTH levels decreased significantly from 399 ± 475 to 305 ± 353 pg/ml (p = 0.026). No changes in total serum Ca, plasma PO<sub>4</sub>, serum akaline phosphatase, K<sub>t</sub>/V, serum creatinine, hemoglobin, body weight, predialysis systolic and diastolic blood pressures were observed. iCa decreased significantly. Conclusions: Our study demonstrates that the correction of metabolic acidosis in chronic HD patients reduces iPTH concentrations in HD patients with secondary hyperparathyroidism possibly by a direct effect on iPTH secretion.

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          Cloning and characterization of an extracellular Ca(2+)-sensing receptor from bovine parathyroid.

          Maintenance of a stable internal environment within complex organisms requires specialized cells that sense changes in the extracellular concentration of specific ions (such as Ca2+). Although the molecular nature of such ion sensors is unknown, parathyroid cells possess a cell surface Ca(2+)-sensing mechanism that also recognizes trivalent and polyvalent cations (such as neomycin) and couples by changes in phosphoinositide turnover and cytosolic Ca2+ to regulation of parathyroid hormone secretion. The latter restores normocalcaemia by acting on kidney and bone. We now report the cloning of complementary DNA encoding an extracellular Ca(2+)-sensing receptor from bovine parathyroid with pharmacological and functional properties nearly identical to those of the native receptor. The novel approximately 120K receptor shares limited similarity with the metabotropic glutamate receptors and features a large extracellular domain, containing clusters of acidic amino-acid residues possibly involved in calcium binding, coupled to a seven-membrane-spanning domain like those in the G-protein-coupled receptor superfamily.

            Author and article information

            S. Karger AG
            16 March 2001
            : 87
            : 3
            : 257-262
            Division of Nephrology Spedali Civili and Chair of Nephrology, University of Brescia, Italy
            45923 Nephron 2001;87:257–262
            © 2001 S. Karger AG, Basel

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            Page count
            Figures: 3, Tables: 3, References: 26, Pages: 6
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            Original Paper

            Cardiovascular Medicine, Nephrology

            Uremia, Acidosis, Dialysis, PTH, Calcium, Phosphate


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