It is generally accepted that
aluminium induces
osteomalacia in chronic
hemodialysis patients by binding to the calcification front, thereby inhibiting mineralization of osteoid. Because this form of
osteomalacia is
vitamin D resistant, the condition has often been assumed to be irreversible, although promising results have been achieved recently by using a
chelating agent for removal of
aluminium from the skeleton. In this paper we present four chronic
hemodialysis patients with
aluminium toxicity and histologic
osteomalacia in whom the mineralization defect greatly regressed after the use of reverse osmosis treated-water for dialysis, but without further treatment. In three other patients, also with
aluminium toxicity and histologic
osteomalacia, similarly treated, the histological severity of the
osteomalacia remained static. Those patients in whom bone mineralization status improved developed
hyperparathyroidism after reverse osmosis water-treatment, whereas the static patients remained euparathyroid. The results suggest that resolution of
aluminium related
osteomalacia may occur with reduction in dialysis fluid
aluminium, and that
parathyroid hormone plays a role in the healing of
aluminium related
osteomalacia. The therapeutic implications are twofold: attempts to remove all traces of
hyperparathyroidism may be detrimental to the bone mineralization status; and stimulation of the parathyroid glands by means of a mild reduction in dialysis fluid
calcium may be of value in the management of those cases with persistent
osteomalacia and low bone turnover.