Marc D. Cohen, MD
Division of Rheumatology
Mayo Clinic
Jacksonville, FL

Renal Osteodystrophy

Renal osteodystrophy can be divided according to the rate of bone turnover. Secondary hyperparathyroidism is the classic high-bone turnover condition. The low-bone turnover entities include osteomalacia, aluminum-related bone disease, and adynamic bone disease (ABD). The term adynamic is confusing because, although it implies low-bone turnover, ABD is one of several causes of low-bone turnover conditions.

Hyperparathyroidism secondary to chronic kidney disease has several etiologic factors (Table 1) (1,5); among them, hyperphosphatemia, calcium balance, and 1,25 dihydroxyvitamin D deficiency are typical targets for intervention.

The low turnover states probably have a final common pathogenesis; factors that have been implicated are listed in Table 2 (5). Osteomalacia and adynamic bone disease are distinguished pathologically by the volume of osteoid (increased in osteomalacia, normal in ABD). The pathogenesis of aluminum-related bone disease is most well-characterized (6), and the finding of aluminum in the mineralization front suggested that it may directly interfere with mineralization (7).

Most patients with renal osteodystrophy are asymptomatic. Symptoms of an acute arthritis may be the presenting complaint (pain, edema, erythema, warmth, decreased range of motion). The diagnostic possibilities include gout, pseudogout, hydroxyapatite, or oxalate crystalline arthritis (see below), with confirmation by joint aspiration or synovial biopsy. Bone pain is rare, is seen usually with osteomalacia, but it can occur within any of the syndromes. Some aspects of pain may be related to pseudofracture. There may be skeletal deformities (eg, genu valgum) in adults, but these are more common in uremic children.

Recently, interest in spontaneous tendon ruptures (8), which has been considered a classic finding of primary hyperparathyroidism, but are rare in dialysis populations, has increased; the most commonly affected tendons are quadriceps, triceps, and the extensor tendons of the fingers (5, 8). It appears that the most important risk factor is the hyperparathyroidism itself (9).

Some pain syndromes may worsen while on dialysis (eg, bone cysts due to amyloidosis), whereas others may not (eg, brown tumors [see below]).

The classic radiographic finding of secondary hyperparathyroidism is subperiosteal bone resorption and erosions. The earliest findings usually occur on the radial (lateral) aspect of the middle phalanx of the second and third digits of the dominant hand, but can progress to include proximal tibia, distal clavical, radius, and ulna, and humeral and femoral necks (10). These lesions, if biopsied, typically demonstrate osteitis fibrosa cystica.

Brown tumors, or osteoclastomas, may be seen on plain film as radiolucent, cystic regions, often within cortical bone (10). They must be distinguished from metastases, lesions of dialysis related amyloidosis, or primary bony malignant tumors. Pathologically, these demonstrate osteitis fibrosa cystica.

Other radiographic findings may include osteosclerosis (typically of the axial skeleton, with a striped appearance on lateral spine films demonstrating alternating areas of radiopacity and radiolucency, the so-called “rugger jersey spine”) and osteopenia. There are far fewer characteristic findings of osteomalacia in adults, although Looser zones or pseudofractures (bands of radiolucency often perpendicular to the long axis of the bone) are nearly pathognomonic of the entity in adults (10).