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Hyperparathyroidism Secondary to Renal Osteodystrophy

Sarah E Maier, MD candidate
Attending???

Presentation

A 50-year-old man with end-stage renal disease and hypertension presented after a hypotensive episode and temperature spike following dialysis.

Imaging Findings

PA chest radiograph
Lateral chest radiograph

PA and lateral chest films demonstrate radiographic signs of chronic secondary hyperparathyroidism. This included the "rugger-jersey" spine and subligamentous bone resorption of the distal clavicle.

Differential Diagnosis

Radiographically, there are five characteristic signs of hyperparathyroidism

Subperiosteal resorption of bone on the radial aspects of the middle phalanges of the fingers is the earliest feature of hyperparathyroidism and is virtually diagnostic. Later in the disease, medial margins of the femoral neck and the inner aspect of the proximal tibia demonstrate evidence subperiosteal resorption. Subligamentous bone resorption most often affects the inferior aspect of the distal clavicle at which the coracoclavicular ligament attaches. Generalized osteopenia typically accompanies hyperparathyroidsim which is best seen with a skull film. Brown tumors are usually found only in hyperparathyroidism. They contain fibrous tissue, giant cells, osteoclasts and blood. Radiographically they appear as lucent cyst- like lesions most frequently occurring in either the mandible, pelvis or femurs. Most heal once the serum level of parathyroid hormone is decreased.

Osteosclerosis rarely occurs in primary hyperparathyroidism and therefore coupled with the other radiographic finding suggest that there is renal failure. Alternatively, brown tumors are an infrequent finding in secondary hyperparathyroidism.

Diagnosis

Secondary Hyperparathyroidism due to renal osteodystrophy

Discussion

Parathyroid hormone promotes the release of calcium into the blood from bone by osteolysis. When there is excess amounts of this hormone in the serum, it is categorized as either being primary or secondary hyperparathyroidism. In primary hyperparathyroidism, excess amounts of parathyroid hormone is released because of a tumor of the parathyroid gland, usually an adenoma. Secondary hyperparathyroidism usually results from a dysfunctional kidney. Vitamin D fails to be converted into its active form because the kidney, which is responsible for this reaction, is non- functioning. This in turn decreases the absorption of calcium from the gut and an overall decrease in serum calcium. In addition, the serum phosphate levels increase because of lack of excretion by the kidney. The combination of overall decreased serum calcium and phosphate stimulates the parathyroid gland to produce excess amounts of parathyroid hormone stimulating osteolysis in an effort to raise the serum calcium. Renal osteodystrophy is a term used to describe the combination of kidney abnormalities coupled with hyperparathyroidism and the associated soft tissue and skeletal changes.

References

Juhl JH, Paul ??. Paul and Juhl's essentials of radiologic imaging. Crummy AB, ed??. Philadelphia: Lippincott, 1993, 237-243.


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