Original Article
Kidney International (2008) 74, 319–327; doi:10.1038/ki.2008.180; published online 7 May 2008
Treatment of experimental renal osteodystrophy with pamidronate
Jarkko Jokihaara1,2, Ilkka H Pörsti2,3, Peeter Kööbi2,4, Pasi M Jolma2,5, Jukka T Mustonen2,3, Heikki H T Saha3, Harri Sievänen6, Pekka Kannus2,6, Urszula T Iwaniec7, Russell T Turner7 and Teppo L N Järvinen2,8
- 1Department of Orthopaedics, University of British Columbia, Vancouver, British Columbia, Canada
- 2Medical School and the Institute of Medical Technology, 33014 University of Tampere, Tampere, Finland
- 3Department of Internal Medicine, Tampere University Hospital, Tampere, Finland
- 4Department of Ophthalmology, Tampere University Hospital, Tampere, Finland
- 5Department of Neurology and Rehabilitation, Tampere University Hospital, Tampere, Finland
- 6Bone Research Group, UKK-Institute, Tampere, Finland
- 7Department of Nutrition and Exercise Sciences, Oregon State University, Corvallis, Oregon, USA
- 8Department of Trauma, Musculoskeletal Surgery and Rehabilitation, Division of Orthopaedics and Traumatology, Tampere University Hospital, Tampere, Finland
Correspondence: Teppo LN Järvinen, University of Tampere, Medical School, 33014 Tampere, Tampere, Finland. E-mail: teppo.jarvinen@uta.fi
Received 24 September 2007; Revised 6 February 2008; Accepted 19 February 2008; Published online 7 May 2008.
Abstract
We evaluated the effects of the bisphosphonate pamidronate on bone histomorphometry, structure and strength in male rats with uninephrectomy or with chronic renal disease induced by 5/6 nephrectomy. In rats with chronic renal disease the plasma urea, phosphate and parathyroid hormone levels were significantly increased compared to rats with a uninephroctomy and none of these parameters was affected by pamidronate treatment. In the femoral midshaft, chronic renal disease reduced cortical bone mineral density and content. No difference was observed in the breaking load of the femoral midshaft. In the distal femur, a high-turnover renal osteodystrophy was found but pamidronate suppressed this bone turnover and increased bone mineral content. Treatment had no effect on chronic disease-induced augmentation of osteoid volume or fibroblast surface. These studies show that in this model of stage 3 renal disease, pamidronate increased mineral content in the femoral midshaft and distal metaphysis primarily by adding bone to endocortical and trabecular surfaces but did not reduce osteitis fibrosa.
Keywords:
bone, biomechanics, bisphosphonates, chronic renal insufficiency, histomorphometry
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