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Nephrol Dial Transplant (2000) 15: 565-568
© 2000 European Renal Association-European Dialysis and Transplant Association


Editorial Comments

Use of corticosteroids in nephrology — risk and prevention of osteoporosis induction

Peter M. Jehle and Daniela R. Jehle

Department of Internal Medicine II, Division of Nephrology, University of Ulm, Germany

Clinical significance of corticosteroid-induced osteoporosis

Although recognized for almost 60 years, corticosteroid-induced osteoporosis (COP) is a major problem. Corticosteroids (Cs) particularly affect the axial skeleton and the proximal femur. They may induce bone loss as well as osteonecrosis. Cs-induced bone loss is biphasic with a rapid initial phase of approximately 10–15% during the first few months and a slower phase of approximately 2–5% annually. Daily prednisone doses of >=7.5 mg cause significant bone loss and a doubling in the risk of fracture [1]; however, even lower doses (e.g. 6.3 mg/day [2]) or inhaled steroids may also induce bone loss [1]. In the UK, over 250 000 patients take continuous oral Cs, yet no more than 14% receive any therapy to prevent bone loss. The majority of patients on long-term Cs have low bone mineral density (BMD), an estimated 50% of them develop osteoporosis, and over 25% sustain osteoporotic fractures . . . [Full Text of this Article]

Pathophysiology of COP

Diagnostic approach

Pharmacological strategies for the prevention and therapy of COP

Calcium

Vitamin D

1{alpha}-hydroxylated vitamin D metabolites

Hormone replacement therapy

Bisphosphonates

Calcitonin

Fluoride

PTH/IGF-1

General recommendations to prevent COP in renal failure patients

Future therapeutic strategies in COP

Notes

References


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Longitudinal follow-up of bone mineral density in children with nephrotic syndrome and the role of calcium and vitamin D supplements
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[Abstract] [Full Text] [PDF]