Abstract
The incidence of renal osteodystrophy (ROD) increases with deteriorating kidney function, affecting virtually every patient on chronic dialysis treatment. ROD can persist after kidney transplantation and may be aggravated by immunosuppressants, mainly glucocorticoids. Fracture risk, including hip fractures, is markedly elevated in patients with renal disease compared to the general population. Depending on the type of ROD, high or low bone turnover can be found. Because of poor positive and negative predictive values of serological markers of bone turnover and limited technical capabilities of various bone imaging modalities, the only reliable method to correctly classify ROD is the transiliac bone biopsy. Elevated bone turnover can be successfully treated with active vitamin D, cinacalcet, or parathyreoidectomy, but all of these therapies may lead to oversuppression of bone metabolism. Currently, no specific therapy is available for low turnover bone disease. Bisphosphonates can be a therapeutic option for selected patients after renal transplantation.
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