Bone Pain in Transplant Recipients Responsive to Calcium Channel Blockers

Bouteiller and colleagues [1] and Lucas and colleagues [2] have reported a bone pain syndrome in the epiphyseal regions of 17% of patients who received renal transplantation. This syndrome occurred only in patients receiving cyclosporine in addition to corticosteroids and not in patients treated only with azathioprine and prednisone alone [2, 3]. The episodes of pain were temporally related to increased cyclosporine levels, were relieved when the dose was decreased, and returned with rechallenge [1, 2]. Although multiple toxicities have been attributed to the vasoconstrictive properties of cyclosporine [4], the pathophysiology of these patients' bone pain syndrome remains unknown.

We describe 15 consecutive patients who received transplants and presented with an acute bone pain syndrome similar to that described by Lucas and colleagues [2] but that resolved when treated with calcium channel blockers. During the study period, 18 patients were referred from the kidney, liver, lung, and pancreas transplant services for evaluation of severe joint or bone pain. Inclusion criteria were the presence of severe, unexplained, usually bilateral, deep aching bone pain occurring in the lower extremities that began or worsened with recumbency. Three patients did not meet the criteria for inclusion and were diagnosed with gout or tendonitis. The transplant team ordered imaging studies (radiographs, bone scan, and magnetic resonance imaging) as appropriate for clinical evaluation of the symptoms. The treating physicians determined the selection and dosing of calcium channel blockers Table 1 to control hypertension or to successfully treat recurrent episodes of bone pain. The following cases show the character of this bone pain syndrome.