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Radiology - Diagnostic

Training Level

Resident PGY 1


Henry Ford Hospital


Introduction: With the advent of dialysis technology, patients with end stage renal disease have improved mortality; however, renal replacement is not without its own burdens, including endocrine disturbances such as secondary hyperparathyroidism. Though patient survival from end stage renal disease has improved in recent years, there is little published information regarding the exact incidence and burden of secondary hyperparathyroidism among renal replacement populations.This case reports examines a patient with secondary hyperparathyroidism secondary to renal osteodystrophy that was mistaken for acute osteomyelitis. Case Presentation: A 59-year-old female patient with a complicated medical history including end-stage renal disease on hemodialysis and HIV presented to an outside hospital with unilateral left knee pain. She had fallen prior to presentation, and the ensuing CAT (CT) scan was concerning for osteomyelitis or septic arthritis. Arthrocentesis was unremarkable for infection. Nevertheless, the outside hospital performed surgical irrigation and drainage of the knee and obtained bone biopsies of the left distal femur and proximal tibia based on suspicious imaging findings. Despite sterile bone cultures, they recommended six weeks of empiric broad spectrum antibiotics for suspected osteomyelitis. The patient presented to Henry Ford Hospital with worsening left knee pain after completing prolonged antibiotics for osteomyelitis and new-onset hip pain. CT of the knee demonstrated further bony erosion. She was admitted for suspected worsening osteomyelitis. Further testing, including pelvic-MRI, demonstrated widespread multifocal osseous resorptive changes; elevated serum PTH levels (2000 pg/mL);and normal serum calcium (9.7 mg/dL).These helped confirm the diagnosis of secondary hyperparathyroidism due to renal osteodystrophy. Discussion: Our patient experienced renal osteodystrophy from secondary hyperparathyroidism, a common sequelae of chronic kidney disease. Secondary hyperparathyroidism can manifest with numerous clinical signs and symptoms including wide spread osseous resorptive changes that can mimic osteomyelitis. In this case, severe knee pain, elevated inflammatory markers and radiography findings misled the outside hospital to an incorrect diagnosis of osteomyelitis, resulting in unnecessary treatment. The known history of end-stage renal disease, arthrocentesis, and surgical findings discordant with infection signaled that further work-up and a broader differential diagnosis were needed in this case. A more comprehensive differential diagnosis and careful work-up could have helped this patient avoid unnecessary invasive surgery and superfluous prolonged antibiotic treatment. Conclusion: Secondary hyperparathyroidism can present in a wide range of clinical presentations, including destructive osseous changes. The successful diagnosis of this patient relied on radiographic imaging and confirmation with laboratory analyses. It is important to remember there are numerous etiologies that can masquerade as osteomyelitis and present with significant osseous pathology. An extensive differential diagnosis and heightened clinical suspicion for endocrine pathology is needed when faced with osseous destruction, especially if the clinical findings do not match the suspected diagnosis in the setting of chronic kidney disease.

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Secondary Hyperparathyroidism Mimicking Osteomyelitis