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Bisphosphonates and the kidney

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Clinical Nephrotoxins

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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].

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  1. Musculoskeletal Diseases, Novartis Institutes for BioMedical Research, Basel, CH-4002, Switzerland

    Jonathan Green

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  1. Laboratory of Pathophysiology Universiteitsplein 1, University of Antwerp, Wilrijk, B-2610, Belgium

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  2. Division of Nephrology, Hypertension and Clinical Pharmacology, Oregon Health Sciences University, 3181 SW Sam Jackson Park Road, Portland, OR, 97201, USA

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Green, J. (2008). Bisphosphonates and the kidney. In: De Broe, M.E., Porter, G.A., Bennett, W.M., Deray, G. (eds) Clinical Nephrotoxins. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-84843-3_24

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  • DOI: https://doi.org/10.1007/978-0-387-84843-3_24

  • Publisher Name: Springer, Boston, MA

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