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Dott. Massimo Bertoli, Riviera S. Benedetto, 124, I-35100 Padova (Italy) Dear Sir, Aseptic osteonecrosis of the femur head, a disabling disease which strikes about 16% of renal transplant recipients, seems clearly related to steroid therapy as its incidence drops sharply with the use of new immunosuppres-sants such as cyclosporin [1]. Several etiological factors related to corticosteroid treatment have been implicated, such as fat embolism in the small subchondral arteries associated with hyperîipidemia, or steroid-induced osteoporosis due to reduced osteogenesis as well as reduced interstinal calcium absorption, which may aggravate secondary hyperparathyroidism. Hypercoagulabil-ity related to steroid therapy may also lead to thrombosis of the bone arterioles with consequent avascular osteonecrosis. However, a recent editorial concluded that ‘there are no suitable biochemical or hormonal markers for predicting which patients will develop aspetic osteonecrosis after transplant surgery’ [1]. In our opinion, uremic neuropathy may also facilitate the onset of transplant osteonecrosis, which, in fact, has been described in pathologic situations characterized by severe peripheral nervous system disease, such as alcoholism [2], diabetes [3], familial dysautonomia [4] and in the uremic patient undergoing periodic dialysis [5]. Sixteen patients, 12 males and 4 females, ranging in age from 24 to 57 years, underwent renal transplantation and were treated with conventional immunotherapy (prednisolone and azathioprine). In addition to routine periodic laboratory tests, an electromyogram of the external popliteal sciatic nerve (velocity of neuromotor conduction) was performed once annually before and at 6 months following transplantation. Five patients in this group (31.2%) developed osteonecrosis; in 4 cases onset occurred within 10 months of transplantation, and in 1 after 38 months. One patient also developed aseptic necrosis of a metacarpal epiphy-sis. No significant differences were observed between patients with and without osteonecrosis regarding the biochemical parameters examined (hematocrit, serum alkaline phosphatase, calcium, phosphorus, cholesterol and triglycerides) and total steroid dose. From a neurological point of view, however, motor conduction velocity of the sciatic-popliteal nerve was significantly slower (p < 0.05) in patients with osteonecrosis before and also 6 months after renal transplantation (41.05 ± 1.4 and 41.25 ± 0.96 m/s, respectively), while in patients without osteonecrosis, values were 45.5 ± 1.96 and 46.8 ± 5.59 m/s, respectively.