Logo CIN CIN '2007 - 4º CONGRESO DE NEFROLOGIA EN INTERNET

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Bone disease after renal tranplantation

Dr Jose Weisinger

Departments of Medicine, Universidad Central de Venezuela, and Division of Nephrology and Renal Transplantation, Hospital Universitario de Caracas

Abstract

It has been well established that a rapid decrease in bone mineral density (BMD) occurs in the first six to 12 months after a successful renal transplantation, and persists, albeit at a lower rate, for many years. This rapid BMD loss significantly increases the fracture risk of these patients to levels even higher than chronic kidney disease stage 5 (CKD-5) patients on dialysis. The presence of low BMD as a predictor of risk fracture is controversial. Indeed, there is not a compelling correlation between the decline in BMD and skeletal fractures. However, Bone disease after renal transplantation probably represents a unique bone disorder that must be differentiated from renal osteodystrophy. In fact, this syndrome results from multiple factors that include pre-transplant bone status, use of glucocorticoids and other immunosuppressive drugs, hypophosphatemia and alterations of the calcium-vitamin D axis. Recent studies have demonstrated decreased osteoblast number, reduced bone formation rate, delayed mineralization and increased osteoblast and osteocytes apoptosis. Bisphosphonates and vitamin D metabolites may be valuable in preventing or diminishing the early bone loss. However be should be careful with the use of bisphosphonates and over suppression of bone, especially in patients with low bone turnover. New prospective controlled trials are required to confirm the real efficacy of these drugs, particularly in the long-term renal transplant patients.

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