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Reflex sympathetic dystrophy syndrome (RSDS) is a rarely described complication after different types of organ transplants. Three out of 147 kidney recipients treated at our center during the last 6 years developed severe bilateral symmetrical pain in the ankles and knees, with great difficulties in walking 2-3 months after kidney transplantation. Clinical examination revealed periarticular soft tissue swelling and vasomotor changes with no effusion. Patchy osteoporotic patterns were seen radiographically in clinically affected areas. Scintigraphy showed increased epiphyseal uptake of 99mTc with a periarticular distribution. Clinical symptoms, radiographic, and scintigraphic signs were compatible with so-called RSDS. The exact cause of the syndrome remained obscure. All patients received standard immunosuppression with cyclosporine A (CyA), azathioprine, and prednisone. Symptoms of RSDS improved when doses of CyA were reduced and blood levels declined; patients were treated with calcitonin and calcium channel blockers simultaneously. Non-steroidal antiinflammatory drugs were not effective in symptom relief. In all three cases, most probably spontaneous complete recovery was achieved over the course of 2-8 months; no one patient progressed to aseptic osteonecrosis.

Reflex sympathetic dystrophy syndrome (RSDS) is a rarely described complication after different types of organ transplants. Three out of 147 kidney recipients treated at our center during the last 6 years developed severe bilateral symmetrical pain in the ankles and knees, with great difficulties in walking 2-3 months after kidney transplantation. Clinical examination revealed periarticular soft tissue swelling and vasomotor changes with no effusion. Patchy osteoporotic patterns were seen radiographically in clinically affected areas. Scintigraphy showed increased epiphyseal uptake of ""' Tc with a periarticular distribution. Clinical symptoms, radiographic, and scintigraphic signs were compatible with so-called RSDS. The exact cause of the syndrome remained obscure. All patients received standard immunosuppression with cyclosporine A (CyA), azathioprine, and prednisone. Symptoms of RSDS improved when doses of CyA were reduced and blood levels declined; patients were treated with calcitonin and calcium channel blockers simultaneously. Non-steroidal antiinflammatory drugs were not effective in symptom relief. In all three cases, most probably spontaneous complete recovery was achieved over the course of 2-8 months; no one patient progressed to aseptic osteonecrosis.

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