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Nephrol Dial Transplant (2003) 18: 874-877
© 2003 European Renal Association-European Dialysis and Transplant Association

Invited Comment

Bone disease after renal transplantation

Heide Sperschneider and Günter Stein

Department of Internal Medicine IV, Friedrich-Schiller-University, Jena, Germany

Keywords: ß2 microglobulin amyloidosis; bone disease; hyperparathyroidism; osteoporosis; renal transplantation

The first 150 words of the full text of this article appear below.

Introduction

Kidney transplantation largely restores defective exocrine and endocrine renal function in patients with end-stage renal disease (ESRD). This in turn is expected to lead to a progressive correction of established renal bone disease. This widely held assumption, however, lacks convincing evidence from experimental and clinical data published thus far. A major obstacle to the investigation of renal osteodystrophy in transplant recipients has been its unpredictable evolution under the multiple biochemical and hormonal influences that regulate mineral metabolism and bone turnover independently. The clinical and histological features of the pre-existing uraemic bone disease at the time of kidney transplantation are highly variable. Moreover, its course after transplantation depends on persisting abnormalities such as hypercalcaemia, hypophosphataemia and hypomagnesaemia as well as on the type, dose and duration of immunosuppressive medications that are needed to minimize allograft rejection. These factors operate additively and their effects are often difficult to dissociate from the already . . . [Full Text of this Article]

Persistent secondary hyperparathyroidism (HPT)

Post-transplant osteoporosis

Pain in the distal extremities [‘symmetric bone pain syndrome’; ‘calcineurin inhibitor-induced pain syndrome’ (CIPS)]

Spontaneous femoral head necrosis/localized osteonecrosis

ß2 Microglobulin (ß2M) amyloidosis

Conclusion


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