Prevention of Enhanced Parathyroid Hormone Secretion, Synthesis and Hyperplasia by Mild Dietary Phosphorus Restriction in Early Chronic Renal Failure in Rats: Possible Direct Role of Phosphorus

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Abstract
In order to evaluate the effect of dietary phosphorus (P) restriction on the pathogenesis of secondary hyperparathyroidism (2°HPT) in chronic renal failure (CRF), we studied parathyroid function and parathyroid cell proliferation in 5/6 nephrectomized rats (CRF rats) fed with three different dietary P contents (0.6, 0.3 and 0.1%). Four weeks after 5/6 nephrectomy, serum immuno-reactive parathyroid hormone (PTH) concentration, PTH mRNA level in parathyroid glands and the size of parathyroid glands were increased in CRF rats compared to those of sham-operated rats when both groups of rats were fed with normal P (0.6%) diet. These changes were not accompanied by any detectable changes of serum concentrations of calcium (Ca), inorganic phosphate (Pi) or calcitriol. In contrast, such evidence of 2°HPT was obliterated in CRF rats fed with 0.3 or 0.1% P diet. In rats fed with 0.3% P diet, serum concentrations of Ca, Pi, and calcitriol were not different from those of sham-operated rats or from CRF rats fed with normal P diet. In contrast, serum Ca and calcitriol concentrations increased and serum Pi decreased in CRF rats fed with 0.1% P diet. These data suggest that 2°HPT can be completely prevented at the levels of PTH secretion, synthesis and parathyroid cell proliferation by mild dietary P restriction (0.3%) alone, and that such effects may not depend upon the changes in serum concentrations of Ca, Pi or calcitriol, but may depend on reduced dietary P content per se. Thus, mild dietary P restriction from the early stage of CRF may be clinically effective for the prevention of 2°HPT.

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