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SUMMARY
Rats of different strains raised on a semipurified casein—sugar diet, develop a nephrocalcinosis in which deposits composed principally of calcium and phosphorus accumulate at the corticomedullary junction of the kidney. To determine whether the development of this nephrocalcinosis was in any way related to the activity of the parathyroid glands, female weanling 21-day-old rats were parathyroidectomized (PTX) or sham-operated and fed the semipurified diet for 3 weeks. Absorption, retention and excretion of Ca, P and Mg were studied during a 14-day balance period. The effects of injecting PTX rats with a small amount of parathyroid extract (15 U.S.P. units Lilly Para-thor-mone, every 12 h for 1 week) were examined.
Compared with sham-operated animals PTX rats showed: lower serum Ca and higher P concentrations; a lower urinary excretion (% intake) of Ca, P and Mg; a higher retention (% intake) of P and Mg; a higher concentration of Mg in bone (% femur ash). Administration of parathyroid extract (PTE) tended to reverse changes induced by parathyroidectomy but PTE-treated animals remained slightly hypocalcaemic. Sham-operated and PTE-treated PTX rats developed nephrocalcinosis but untreated PTX rats did not do so.
The results indicate that nephrocalcinosis did not develop in rats fed the semipurified diet in the absence of parathyroid hormone. It is postulated that although some activity of the parathyroid glands is needed for mineral deposition in the renal tubules, excessive activity is not necessarily a prerequisite to the development of this type of renal calcification.
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Department of Medicine and Biochemistry Research Group, University of Otago Medical School, Dunedin, New Zealand
(Received 7 October 1974)
High doses of disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) inhibit bone mineralization, induce hypercalcaemia and diminish intestinal absorption of calcium in the rat (Gasser, Morgan, Fleisch & Richelle, 1973; Goulding & McChesney, 1974). This hypercalcaemia, either by a direct effect or by inhibiting secretion of parathyroid hormone (PTH), may suppress renal synthesis of 1,25-dihydroxycholecalciferol (1,25(OH)2D3) and hence explain the diminished intestinal absorption of calcium (Bonjour, DeLuca, Fleisch, Trechsel, Matejowee & Omdahl, 1973; Hill, Lumb, Mawer & Stanbury, 1973). Parathyroid hormone affects the renal production and excretion of cyclic AMP (Chase & Aurbach, 1967) and cyclic AMP enhances the synthesis of 1,25(OH)2D3 (Rasmussen, Wong, Bikle & Goodman, 1972; Larkins, MacAuley, Rapoport, Martin, Tullock, Byfield, Matthews & Maclntyre, 1974). Thus reduced production of cyclic AMP after administration of EHDP may be important in diminishing renal synthesis