Phosphaturic mesenchymal tumor can cause osteomalacia due to excessive secretion of fibroblast growth factor 23 (FGF23), which disrupts the metabolism of phosphate and vitamin D. These tumors are predominantly benign, but less than 5% of them are malignant forms. This article presents the first clinical case in the Russian Federation of a 69-year-old patient with severe hypophosphatemia due to metastatic prostate cancer. Increased secretion of FGF23 are described in the androgen-resistent prostate cancer, which led to pronounced disorders of mineral metabolism, accompanied by a clinical symptom of weakness, pain in the bones, immobilization of the patient. The condition was regarded as worsening against the background of the progression of the disease. However, symptomatic therapy aimed at increasing the level of phosphate significantly improved the patient’s general condition. The medical community should be aware of the possibility of developing hypophosphatemia in patients with weakness and bone pain, which are not always associated with the progression of metastatic prostate cancer.

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Primary hyperparathyroidism (PHPT) is characterized by hypercalcemia. The only curative treatment is parathyroidectomy. However, patients are often ineligible or decline surgery. Denosumab (Dmab) is an antiresorptive pharmaceutical alternative. The effects of exposure to Dmab in subjects with chronic kidney disease (CKD) and PHPT are unknown.Purpose:We aimed to assess the e cacy and safety of denosumab in postmenopausal women with PHPT-related osteoporosis and CKD.Methods: Women over 50 years of age with PHPT or postmenopausal osteoporosis (PMO) were retrospectively recruited into this longitudinal study. These PHPT and PMO groups were further categorized into four subgroups based on the presence of CKD (Glomerular ltration rate (GFR) <60 mL/min/1.73mBI): patients with PHPT with and without CKD and patients with PMO with and without CKD. All patients were given denosumab over 24 months due to veri ed osteoporosis. The primary outcomes were changes in bone mineral density (BMD) and serum calcium levels.Results: 145 postmenopausal women median age 69 [63;77] were recruited and assigned to one of the subgroups. Denosumab treatment signi cantly increased BMD (median ΔT-score: L1-L4 +0.65 (p<0.001), femur neck +0.3 (p=0.012); radius 33% +0.2 (p<0.05)) in PHPT-related osteoporosis and CKD at 24 months. Changes in BMD were similar in all study groups compared to baseline. A marked decline in calcium was noted in the primary study group of PHPT with CKD (median ΔCa = -0.24 mmol/L p<0.001), compared to PHPT without CKD (median ΔCa = -0.08 mmol/L p<0.001) and PMO with or without CKD.Denosumab treatment was well-tolerated with no serious adverse events. Conclusion: Denosumab treatment was similarly effective at increasing BMD in patients with PHPT and PMO with and without renal insu ciency. The calcium lowering effects of denosumab were most signi cant in patients with PHPT and CKD. The safety of denosumab did not differ among participants with and without CKD.

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