Hyperparathyroidism / Renal Osteodystrophy

Peter L. Munk, Anthony G. Ryan

A 37-year-old man presented with a complaint of lower back pain.

Figure 125A

Figure 125B

Renal osteodystrophy (secondary hyperparathyroidism).

The pubic abnormalities are Looser’s zones: pseudofractures secondary to osteomalacia. The surgical clips are in relation to a renal transplant (failed).

None.

Renal osteodystrophy is a constellation of clinical, pathologic, and radiologic manifestations seen in patients with chronic renal disease.

The radiological manifestations are diverse and fall into several categories. With the increasing utilization of hemodialysis and aggressive management of patients with renal disease, patients with imaging manifestations of renal osteodystrophy are increasingly encountered. These changes are in many cases reversible following renal transplantation, although they may take years to regress.

These changes can be broadly categorized under several headings.

The osseous changes due to renal osteodystrophy are for the most part due to secondary hyperparathyroidism.

Patients with renal failure often undergo hypertrophy of the hyperparathyroid glands induced by hyperphosphatasemia due to decreased renal excretion. Increased circulating levels of parathyroid hormone (PTH) then alters bone metabolism, leading to a protean constellation of changes. In particular, PTH promotes the development of osteoclasts, osteoblasts, and osteocytes, giving rise to bone resorption, periosteal reactions, and brown tumors. Osteosclerosis, osteoporosis, and osteomalacia may all occur; hence the sobriquet “active bones disease.”

Osteoclastic bone resorption is probably the most consistent feature and may affect any portion of the bone, that is, subperiosteal, cortical, subchondral, trabecular, endosteal, or at entheses.

Patients with renal failure due to chronic disease affecting the glomeruli also develop alterations in vitamin D metabolism, frequently showing decreased sensitivity to the vitamin. This in turn also alters bone metabolism, with osteomalacia or rickets developing. Metabolic interactions become very complex, and often several manifestations of disease are present simultaneously.

• Secondary hyperparathyroidism may occur in patients with renal failure of any etiology.
  
• Resorption of adjacent ligaments and tendons may lead to “spontaneous” tendon rupture.
  
• Rickets may actually be the initial feature for the presence of chronic renal disease in children.
  
• Bone may soften and lead to bowing, particularly of the lower limbs. Hip pain secondary to slipping of the femoral epiphyses due to weakening of the bone may occur. Frank fractures may occur secondary to the weakened bone. Bowing of bone and pathologic fractures may also occur in the mature skeleton. Insufficiency fractures also occur with increased frequency in these patients.