Review
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World J Nephrol. Oct 6, 2012; 1(5): 127-133
Published online Oct 6, 2012. doi: 10.5527/wjn.v1.i5.127
Metabolic bone diseases in kidney transplant recipients
Rubin Zhang, Kanwaljit K Chouhan
Rubin Zhang, Kanwaljit K Chouhan, Section of Nephrology, Department of Medicine, Tulane University School of Medicine, New Orleans, LA 70112, United States
Author contributions: Zhang R contributed to the design of the paper, acquisition, analysis and interpretation of the data from various studies which are reviewed in this paper and revised it critically for important intellectual content; Chouhan KK contributed to the conception and design of the paper, revised and drafted the paper and contributed to the final approval of the version to be published.
Correspondence to: Rubin Zhang, MD, FASN, Professor, Medical Director of Kidney and Pancreas Transplantation, Section of Nephrology, Department of Medicine, Tulane University School of Medicine, 1415 Tulane Ave, TW-35, New Orleans, LA 70112, United States. rzhang@tulane.edu
Telephone: +1-504-9881457 Fax: +1-504-9881105
Received: July 3, 2011
Revised: June 1, 2012
Accepted: September 25, 2012
Published online: October 6, 2012
Abstract

Metabolic bone disease after kidney transplantation has a complex pathophysiology and heterogeneous histology. Pre-existing renal osteodystrophy may not resolve completely, but continue or evolve into a different osteodystrophy. Rapid bone loss immediately after transplant can persist, at a lower rate, for years to come. These greatly increase the risk of bone fracture and vertebral collapse. Each patient may have multiple risk factors of bone loss, such as steroids usage, hypogonadism, persistent hyperparathyroidism (HPT), poor allograft function, metabolic acidosis, hypophosphatemia, vitamin D deficiency, aging, immobility and chronic disease. Clinical management requires a comprehensive approach to address the underlying and ongoing disease processes. Successful prevention of bone loss has been shown with vitamin D, bisphosphonates, calcitonin as well as treatment of hypogonadism and HPT. Novel approach to restore the normal bone remodeling and improve the bone quality may be needed in order to effectively decrease bone fracture rate in kidney transplant recipients.

Keywords: Uremic osteodystrophy, Bone loss, Fracture, Kidney transplantation