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Aluminum-induced bone disease in uremic patients receiving dialysis was first described a little more than 10 years ago. The epidemic form of the disease was seen in centers where there was a high aluminum content in the water dialysate. Although this problem has been corrected, sporadic forms of the disease continue to be noted in dialyzed and nondialyzed patients. Multiple fractures are a radiological feature of aluminum-related bone disease. Fractures of the ribs and hips and vertebral crush fractures are the usual manifestations. We present four patients whose nontraumatic fractures involved large bones, without evidence of multiple fractures. In two of the patients symptoms were vague and subacute; a third patient with a subcapital fracture was ambulatory. Only in one patient (fractured dens) were symptoms acute enough to warrant immediate radiography. One of the patients had no symptoms pertaining to a fracture of C5 with retrolisthesis. Rib fractures are common in this condition but were seen in only one patient, in whom they were detected 8 years previously. Healing was not seen in any of the fractures. In patients receiving dialysis the presence of spontaneous fractures of large bones or cervical vertebrae, which may be clinically silent or vaguely symptomatic, should raise the possibility of aluminum-induced osteomalacia even if these fractures are solitary.

We present two cases of growth plate injury of the hand and wrist in young patients with renal rickets and osteodystrophy but no history of antecedent trauma. The postulated mechanism of injury is subclinical biomechanical stress on the involved extremity superimposed on the already weakened metaphysis and growth plate. Thus, the findings may be viewed as an insufficiency injury to the metaphysis and growth plate. Physicians should be aware that, in the absence of unusual athletic activity, epiphysiolysis of the upper extremity is uncommon and requires a search for underlying metabolic bone disease.

A recent publication showed the earliest signs of renal osteodystrophy in patients on maintenance hemodialysis (MHD) to occur in the tufts [1]. We present three patients on MHD, in two of whom the earliest unequivocal radiographic improvement was seen in the tufts. The third patient had been on MHD and, following subtotal parathyroidectomy, showed significant osseous improvement in the hands with relatively equal improvement in the hands with relatively equal improvement in the tufts and middle phalanges. It appears that, with the use of routine primary or secondary magnification, the tufts are radiographically a highly sensitive site for both the early occurrence and improvement of osteodystrophy in patients on MHD. We are not aware of any previous publication pointing out exclusive improvement in the tufts in patients on MHD with virtually no change in the mid-phalanges. Two of these three cases illustrate that renal osteodystrophy is reversible by maintenance hemodialysis alone.

Normal and rachitic, skeletally immature arctic foxes (Alopex lagopus) were subjected to physical examination, roentgenographic studies, and in some cases histologic studies. The involved animals had active rickets coupled with antecedent normal diaphyseal bone formation. Evaluation of all the long bones showed highly variable manifestations of the disease, which undoubtedly reflect different rates of physeal endochondral transformation and metaphyseal remodeling. Histologic examination showed distinct patterns of widening of the physes and variable osteodystrophy in the trabecular and cortical bone of the metaphyses and epiphyseal ossification centers. These aforementioned factors certainly would necessitate different regional calcium needs and, therefore, different regional responses to the most rapid deficiency. The physes involved in the most rapid growth rates of this period showed the most widening of the growth plate, and the most dystrophic changes in the metaphysis. Skeletal injuries, including metaphyseal fractures and slow-down of longitudinal growth (particularly in the ulna) were also evident. Because of apparent dietary differences in the affected and normal fox kits, this juvenile-onset disease was presumed due to calcium-deficient intake following weaning. To the best of our knowledge this is the first report of spontaneously occurring rickets in a wild animal in its nautral habitat. There are several possible mechanisms for the variable widening of the physis and the loss of bone mineralization in these fox kits: calcium-deficient diet, binding of calcium in the bowel by high phosphorus intake, secondary hyperparathyroidism, and vitamin A toxicity.