Acute and long-term effects of corticosteroid therapy on bone metabolism in patients with kidney diseases.

Aim: The aim of our study was to examine parameters of bone metabolism during pulse and long-term methylprednisolone (MP) treatment in patients with kidney diseases.

Methods: In 13 patients with RPGN, treated with intravenous MP pulses, followed by tapering oral doses, osteocalcin (OC) and β-CrossLaps (β-CL) were measured before treatment, after the 3rd pulse, then 1 and 3 months later ("acute study"). In a separate set of analyses serum markers of bone metabolism and bone mineral density (BMD) were studied in 40 patients on maintenance MP therapy ("chronic study").

Results: Immediately after the 3rd MP pulse serum OC decreased to 38 ± 23%, β-CL increased to 200 ± 121% of the baseline (p = 0.002 for OC and p = 0.003 for β-CL, respectively), and the OC/β-CL ratio decreased from 55 ± 35 to 9 ± 7 (p = 0.002). OC remained below and β-CL above baseline even at 3 months post pulse steroid treatment. Patients in the "chronic study" who were on maintenance oral steroid therapy received 13,844 ± 7,454 mg MP over 53 ± 47 months. BMD at the end of follow-up revealed reduced bone mineral density in 72.5% of the participants. Z-scores both at the hip and at the lumbar spine were significantly correlated with duration of steroid treatment and also with the cumulative steroid dose.

Conclusion: MP pulse causes immediate, profound suppression of osteoblast function, and significant increase of osteoclast activity, suggesting uncoupling of bone formation and resorption. Prolonged high dose steroid treatment causes significant bone loss in patients with chronic kidney disease. Appropriate systematic follow up of bone metabolism, preventive measures and therapy when needed would be important for the bone health of this patient population.