A 51-year-old man is evaluated in the outpatient clinic for an 8-month history of progressive proximal muscle weakness and diffuse bone pain. He reports difficulty climbing stairs and rising from a chair. He recently sustained a right-sided rib fracture from a minor coughing fit. His medical history is significant for gastroesophageal reflux disease, for which he frequently takes over-the-counter aluminum hydroxide. He took a short course of oral bisphosphonates 2 years ago for suspected osteoporosis but discontinued it. Vital signs are within normal limits. Physical examination reveals proximal muscle weakness of the lower extremities and marked tenderness over the ribs, pelvis, and shins.
Laboratory studies show the following:
| Test | Result | Reference Range |
|---|---|---|
| Serum calcium | 9.1 mg/dL | 8.4 - 10.2 mg/dL |
| Serum phosphate | 1.6 mg/dL | 2.5 - 4.5 mg/dL |
| Parathyroid hormone (PTH) | 45 pg/mL | 15 - 65 pg/mL |
| 25-hydroxyvitamin D | 38 ng/mL | 20 - 50 ng/mL |
| 1,25-dihydroxyvitamin D | 12 pg/mL | 18 - 72 pg/mL |
| Alkaline phosphatase | 280 U/L | 40 - 120 U/L |
| Serum creatinine | 0.8 mg/dL | 0.7 - 1.3 mg/dL |
Urinalysis reveals a fractional excretion of phosphate of 25% (normal < 5% in the setting of hypophosphatemia). Urine tests for glucose and amino acids are negative.
Which of the following is the most likely primary molecular mechanism responsible for this patient's clinical and laboratory findings?
- Secretion of a circulating factor that downregulates renal sodium-phosphate cotransportersCevap
- BGastrointestinal binding of dietary phosphate by a heavy metal-containing antacid
- CEctopic production of a peptide structurally homologous to parathyroid hormone
- DIntratubular deposition of monoclonal light chains causing generalized proximal tubular dysfunction
- EPharmacologic inhibition of osteoclastic bone resorption leading to impaired bone remodeling