Effects of Antiresorptive Treatment on Bone Mineral Density and Bone Turnover Markers in a Child With Steroid‐Resistant Nephrotic Syndrome: A Case Report

Glucocorticoid-induced osteoporosis (GIOP) is a significant complication of prolonged glucocorticoid treatment in paediatric nephrotic syndrome, but the optimal treatment strategy remains unclear. We report the case of a 17-year-old boy with steroid-resistant nephrotic syndrome due to focal segmental glomerulosclerosis who developed progressive bone fragility during high-dose glucocorticoid treatment. Four months after initiation of glucocorticoids, his lumbar bone mineral density (BMD) decreased 9.2%, serum alkaline phosphatase (S-ALP) decreased 22% and serum tartrate-resistant acid phosphatase-5b (S-TRACP-5b) increased 47% compared with baseline, indicating compromised bone strength. Oral alendronate (35 mg/week) was initiated to prevent progression of GIOP. One month after antiresorptive treatment, S-TRACP-5b decreased 87% from the level measured at 4 months. BMD and S-ALP initially continued to decline slightly until 7 months but subsequently demonstrated sustained recovery. S-TRACP-5b levels were lower than baseline levels to a greater extent than the S-ALP levels between 5 and 28M, corresponding to progressive improvement in the BMD. No fragility fractures or adverse events occurred, and remission of nephrotic syndrome was maintained. This case suggests that alendronate rapidly suppresses bone resorption, promotes a bone formation-dominant state in conjunction with glucocorticoid tapering and may prevent bone fragility in paediatric GIOP. A ≥ 34% increase in S-TRACP-5b accompanied by a ≥ 22% decrease in S-ALP from baseline may indicate the appropriate timing for initiating antiresorptive treatment. Further investigations are warranted to establish evidence-based management strategies for paediatric GIOP.