Printed in U.S.A. Bone Mineral Metabolism and Osteodystrophy in Uremia1’2

been frequently reported in European literatitre, it has not been a major prob-lem in this coutfltr). However, with the in-creased! use of long-term hemodialysis in time nmanagement of utremic patients and the colmsequent prolongation of their lives, a nmost virulent form of renal osteodystrophy and disordered! calcium and phosphorus nmetabolism has appeared in such patients (1-4). Altimough numerous studies imave been carried out dealing with different aspects of this problem, time nature of the mecha-nisnms involved in the development of these abnormalities is still poorly under-stood!. Furthermore, it is becoming increas-ingly apparent that time usual conservative measures (high calcium intake, alkali ad-nmi nistration, and phosphate restriction combined with phosphate-binding antac-ids) do not always correct hypocalcemia or improve time bone pathology or sympto-matology. While such conservative meas-ures, including chronic dialysis, may make the patient feel better, it is also possible timat they may contribute to a further de-terioration in the osseous pathology and abnormal deposition of calcium salts in the soft tissues. We may decrease the effects o