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Methods for Analyzing the Impacts of Natural Uranium on In Vitro Osteoclastogenesis
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Physiological doses of calcium regulatory hormones do not normalize bone cells in uraemic rats

A Szabó1, M G Freesmeyer, K Abendroth

  • 1C. Ruprecht University Heidelberg, Germany; I. Semmelweis University Budapest, Hungary.

European Journal of Clinical Investigation
|June 3, 1999
PubMed
Abstract

Insights

In experimental renal failure, parathyroid hormone (PTH) and calcitriol normalize osteoblast activity but not osteoclast surface. This suggests abnormal bone cell responses contribute to skeletal issues in kidney disease.

Area of Science:

  • Nephrology
  • Endocrinology
  • Bone Biology

Background:

  • Patients with end-stage renal failure often exhibit low bone turnover despite normal parathyroid hormone (PTH) levels.
  • Uremia is known to cause hyporesponsiveness to the calcaemic action of hormones.
  • Hyporesponsiveness of bone surface cells in bone modeling in uremia has not been previously demonstrated.

Purpose of the Study:

  • To investigate if PTH and calcitriol can normalize bone surface cell activity in a rat model of moderate renal failure.
  • To determine if hormonal doses that correct serum calcium levels also affect bone modeling in uremic rats.

Main Methods:

  • Subtotally nephrectomized (SNX) and parathyroidectomized (PTX) rats were treated with either a solvent or a combination of calcitriol and rat PTH.
  • Histomorphometric measurements of bone parameters were performed on vertebral bodies (L5).
  • Serum calcium levels were monitored.

Main Results:

  • Calcitriol and PTH administration modestly increased serum calcium in SNX/PTX rats, within the normal range.
  • Osteoclast surface per cent was significantly lower in solvent-treated SNX/PTX rats and was not normalized by PTH and calcitriol.
  • Osteoblast surface and osteoid surface per cent increased in treated rats, leading to a significant increase in bone volume.

Conclusions:

  • PTH and calcitriol, at doses that increase serum calcium, failed to normalize osteoclast surface in experimental renal failure.
  • These hormones were effective in increasing osteoblast number and volume.
  • The findings suggest abnormal bone cell responses to hormones or other factors contribute to skeletal abnormalities in renal failure.

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