Abstract
INTRODUCTION: Osteomalacia is an often-overlooked manifestation of post-transplant bone disease that may persist or newly develop in kidney transplant recipients because of pre-existing chronic kidney disease-mineral and bone disorder, ongoing immunosuppression, and alterations in calcium-phosphate metabolism. Severe vitamin D deficiency, hypophosphatemia, and secondary hyperparathyroidism create a metabolic milieu that favors osteoid mineralization defect and leads to debilitating skeletal pain and fragility fractures. OBJECTIVE: This case report documents the clinical course, diagnostic work-up, and therapeutic response of a kidney-transplant recipient with severe vitamin D deficiency, with the aim of raising awareness of this condition and outlining practical management strategies. CASE REPORT: A 61-year-old woman underwent living-donor kidney transplantation in 2020. Four months later, she presented with diffuse bone pain, progressive gait impairment, and laboratory evidence of hypercalcemic hyperparathyroidism (PTH 130 pg/mL), severe vitamin D deficiency (25[OH]D 7 ng/mL), and hypophosphatemia (2.8 mg/dL). Very high levels of bone-specific alkaline phosphatase may reflect both bone mineralization defect and high bone turnover. Imaging supported the diagnosis of osteomalacia, revealing bone-marrow edema of both knees, Looser zones, and focal radiotracer uptake on ^99mTc-MDP scintigraphy. The patient started treatment with high-dose cholecalciferol (60,000 IU/day) followed by monthly calcifediol, together with continued cinacalcet and subsequent oral bisphosphonate therapy; this regimen normalized 25(OH)D (42 ng/mL), reduced bone-turnover markers, and enabled the recovery of independent ambulation within 9 months. Follow-up dual-energy X-ray absorptiometry showed lumbar BMD improvement (T-score -3.7 to -2.6) and stabilization of femoral osteopenia at 26 months post-transplant. CONCLUSION: Early recognition of osteomalacia after kidney transplantation and aggressive correction of vitamin D deficiency, phosphate wasting, and hyperparathyroidism can result in rapid symptomatic relief and partial reversal of bone loss. Routine monitoring of mineral metabolism and bone turnover markers should therefore be integrated into post-transplant care to prevent delayed diagnosis. Controlled studies are warranted to define optimal supplementation protocols and thresholds in this population.