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Nephrol Dial Transplant (2000) 15: 945-950
© 2000 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

The role of cytokines in skeletal remodelling: possible consequences for renal osteodystrophy

Esther A. González

Division of Nephrology, Saint Louis University, St Louis, Missouri, USA

Introduction

The pathogenesis of renal bone disease, a common complication encountered in patients with renal insufficiency, has centred around perturbations in the parathyroid hormone–vitamin D axis [1]. Thus, excess parathyroid hormone (PTH) can give rise to the high bone turnover state of osteitis fibrosa, and conversely, relatively low levels of PTH are associated with the low bone turnover state of adynamic bone. However, there are many observations which imply that the protean manifestations of renal bone disease cannot be explained simply by abnormalities of PTH or vitamin D metabolites. For example, levels of PTH correlate relatively poorly with various parameters of bone histology, and there is clearly a wide scatter of the data points for any given level of PTH [2,3]. While low levels of calcitriol are clearly important in the pathogenesis of hyperparathyroidism, and the administration of vitamin D metabolites is a key component . . . [Full Text of this Article]

Bone remodelling

The RANK/RANKL/OPG system

Effects of uraemia on skeletal biology

Summary

Acknowledgments

Notes

References


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