Modulation of renal osteodystrophy by extrarenal production of calcitriol

James A. Delmez, Adriana S. Dusso, Eduardo Slatopolsky, Steven L. Teitelbaum

Research output: Contribution to journalArticle

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Abstract

We report a patient with severe chronic renal failure who developed spontaneous bone fractures. He was found to have hypercalcemia, normal calcitriol levels (probably due to extrarenal production by noncaseating granulomas), and functional hypoparathyroidism. The bone biopsy showed low bone turnover and the presence of noncaseating granulomas. Treatment with corticosteroids decreased the calcium and calcitriol levels and the parathyroid hormone levels rose. No further fractures occurred. A repeat bone biopsy revealed the presence of osteitis fibrosa. Renal osteodystrophy may be modulated by extrarenal production of calcitriol. In this case, excessive suppression of parathyroid hormone by endogenous calcitriol presumably caused an adynamic bone lesion and spontaneous fractures.

Original languageEnglish
Pages (from-to)85-89
Number of pages5
JournalAmerican Journal of Nephrology
Volume15
Issue number1
DOIs
StatePublished - Jan 1 1995

Keywords

  • Calcitriol
  • Osteodystrophy
  • Parathyroid hormone
  • Renal failure

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