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Bisphosphonates and the kidney

  • Jonathan Green

Bone remodelling is a continuous and dynamic process that normally involves the coordinated interplay among 3 types of cells: the bone resorptive osteoclasts, the bone-forming osteoblasts, and osteocytes, which are thought to act as mechano-transducers in bone [1]. The process becomes unbalanced in the elderly, in patients with benign bone disease [2], and in patients with primary bone lesions from multiple myeloma or bone metastases from solid tumours [3, 4]. Bisphosphonates are synthetic analogues of pyrophosphate–a naturally occurring modulator of mineralisation found in plasma, urine, and bone. They inhibit osteoclast-mediated bone resorption through several mechanisms, including inhibition of osteoclastogenesis, disruption of intracellular vesicular trafficking, and induction of osteoclast apoptosis, as well as indirectly via effects on osteoblasts [5]. Bisphosphonates are transported through the bloodstream and are deposited at sites of active bone remodelling, where they bind avidly to the mineralised bone matrix via the bisphosphonate moiety [5]. During bone resorption, bisphosphonates are internalised by osteoclasts, wherein they mediate their antiresorptive effects [5]. Therefore, bisphosphonates have provided increasing clinical utility in the management of patients with pathologies associated with perturbations in bone metabolism [3, 4, 6].

Keywords

Multiple Myeloma Zoledronic Acid Acute Tubular Necrosis Metastatic Bone Disease Skeletal Complication 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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© Springer Science+Business Media, LLC 2008

Authors and Affiliations

  • Jonathan Green
    • 1
  1. 1.Musculoskeletal DiseasesNovartis Institutes for BioMedical ResearchBaselSwitzerland

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