Zinc nutritional status modifies renal osteodystrophy in uremic rats
P L Kimmel1, C B Langman, B Bognar
1Department of Medicine, George Washington University Medical Center, Washington, DC 20037, USA.
Clinical Nephrology
|January 5, 2002
Summary
Zinc deficiency in rats with induced kidney problems reduced parathyroid hormone (PTH) and secondary hyperparathyroidism. This suggests zinc status impacts mineral metabolism in chronic kidney disease.
Area of Science:
- Mineral Metabolism
- Renal Physiology
- Nutritional Biochemistry
Background:
- Previous research indicated zinc depletion lowers calcitriol (1,25(OH)2D) in rats with normal or impaired renal function.
- Calcitriol synthesis is partly dependent on kidney function, necessitating investigation into zinc's role in vitamin D metabolism and related disorders.
Purpose of the Study:
- To investigate the impact of zinc nutritional status and renal function on vitamin D metabolites, parathyroid hormone (PTH) response, mineral balance, and bone histomorphometry in rats.
- To elucidate the relationship between zinc, renal insufficiency, and secondary hyperparathyroidism.
Main Methods:
- Fifty-eight male Sprague-Dawley rats were fed zinc-replete or zinc-deplete diets for two weeks.
- Half of each group underwent nephrectomy (N) or sham (S) surgery, followed by an eight-week observation period.
- Measurements included external mineral balances, plasma levels of creatinine, zinc, calcium, phosphorus, magnesium, 25-hydroxycholecalciferol, calcitriol, PTH, and bone histomorphometry.
Main Results:
- Zinc-depleted rats exhibited lower plasma zinc; nephrectomized rats showed reduced creatinine clearance.
- Plasma calcium, phosphorus, and magnesium levels were comparable across groups at sacrifice, except for magnesium in renal insufficiency.
- Vitamin D metabolite levels were similar; PTH levels increased with nephrectomy but were lower in zinc-depleted nephrectomized rats compared to zinc-replete nephrectomized rats. Zinc deficiency attenuated PTH increase and bone changes in renal insufficiency.
Conclusions:
- Zinc depletion mitigates the rise in plasma PTH and the development of secondary hyperparathyroid bone disease in a rat model of uremia.
- The underlying mechanism remains unclear but may involve zinc's direct effects on PTH synthesis, release, metabolism, action, or bone mineral metabolism.
- Findings suggest zinc nutritional status is relevant to mineral metabolism management in patients with chronic kidney disease and end-stage renal disease.
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