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E1440. Musculoskeletal Findings in Secondary Hyperparathyroidism due to Chronic Renal Disease
Authors
  1. Siddharth Pandya; Creighton University Arizona Health Alliance
  2. Bryant Brown; Creighton University Arizona Health Alliance
  3. Madisen Rosztoczy; University of Arizona - College of Medicine - Phoenix
  4. Dan Gridley; Creighton University Arizona Health Alliance
Background
Hyperparathyroidism (HPT) is defined as an excess in serum parathyroid hormone (PTH). HPT due to chronic renal disease is termed secondary hyperparathyroidism and affects approximately 900,000 patients in the United States annually. In normal physiology, a low serum calcium level triggers the production of PTH which leads to increased bone resorption and augmented serum calcium levels. The increased bone resorption results in a myriad of classic osseous findings, termed renal osteodystrophy, which we present in this exhibit.

Educational Goals / Teaching Points
To identify and describe the numerous musculoskeletal radiologic findings of chronic renal disease and secondary HPT. To understand the pathophysiology that results in the osseous findings of renal osteodystrophy.

Key Anatomic/Physiologic Issues and Imaging Findings/Techniques
In renal failure, the diminished ability to produce Vitamin D leads to decreased calcium absorption in the intestines. As a result, decreased serum calcium results in excess PTH secretion. This positive feedback loop results in the disease known as secondary HPT. The bony resorption associated with HPT most commonly occurs in the subperiosteal and subchondral locations and can be seen radiographically. When this subperiosteal resorption occurs in the spine, sclerotic poorly developed bone is formed preferentially within the superior and inferior endplates of the vertebral bodies resulting in alternating bands of sclerosis and lucency colloquially termed a “rugger jersey” appearance. In addition, when this resorption occurs in the skull, multiple punctate lucent foci give rise to a “salt and pepper” appearance. Furthermore, throughout the skeleton as trabecular bone is resorbed, the void may fill with fibrous and hemorrhagic material. These foci appear as lytic lesions radiographically and are known as brown tumors. Further increased bone turnover leads to generalized osteopenia and osteomalacia, which predisposes patients to fractures and gives the "superscan" appearance on bone scintigraphy. Finally, as these patients go on to renal transplantation or are on hemodialysis long-term they develop dense periarticular soft tissue calcifications.

Conclusion
Secondary HPT due to chronic renal disease is a common medical condition with high incidence and prevalence in the United States. While nonspecific in isolation, the musculoskeletal sequelae of subperiosteal resorption due to prolonged PTH elevation leads to pathognomonic imaging findings of renal osteodystrophy.