Osteomalacia in Chronic Renal Failure: a Syndrome Previously Reported Only with Maintenance Dialysis

Abstract

Osteomalacia without marked elevations of parathyroid hormone (PTH) has been described in maintenance dialysis patients. The proposed etiology has centered upon the transfer of an environmental agent (aluminum) from the dialysis water system. The present report describes an azotemic patient, who, prior to the initiation of dialytic therapy, presented with severe osteomalacia and low PTH concentrations for the severity of renal failure. The osteomalacia was documented by bone histology on two occasions 1 year apart, and aluminum deposits at the osteoid-mineralized bone interface were demonstrated with histologic techniques. PTHconcentrations were within the normal range (less than 0.1 ng/ml) on three widely spaced intervals. No definite statement can be made regarding the etiology of the osteomalacic syndrome in this patient, but maintenance dialysis does not appear to be necessary for its expression.

Hypercalcemia in a Dialysis Patient

“…Few data specifically address this process in hypercalcemic patients. Although serum parathyroid hormone levels tended to be lower in osteomalacic patients with hyper calcemia in one series [24], in our experience, C-terminal parathyroid hormone levels were of no discriminant value [46], The type of osteodystrophy present in the patient under consideration could reliably be determined only with a bone biopsy.…”

Renal Osteodystrophy: Pathophysiology and Treatment

“…1 case of true osteomalacia associated with high plasma aluminum and presence of aluminum at the place of the min eralization front has been so far reported [ 17] with the suspicion that it was due to oral Al(OH):, given as phosphate binder, and histo logical evidence of aluminum is found in 5% of the uremic patients not yet on dialysis [18].…”

“…even if it would be proven efficient (in a control trial versus placebo) in prevent ing osteitis fibrosa and osteomalacia -for the following reasons: (1) la-hydroxylated D me tabolites improve both calcium and phos phate absorption and, therefore, correct hy pocalcemia. but may worsen hyperphosphat emia [22]; (2) prevention of hypercalcemia and hyperphosphatemia is practically diffi cult and needs close monitoring of plasma calcium and phosphate; (3) prevention of hy perphosphatemia needs aluminum-contain ing phosphate binders which may be poten tially harmful on a long-term basis [17,18,23], and (4), as shown by Hack et al [24], phosphate restriction alone may increase plasma l,25-(OH)2 D3 levels.…”

Management of Bone Disease in the Dialysis Patient

“…The agents currently available for phosphate binding include aluminum hy droxide, aluminum carbonate and calcium carbonate. Since ingestion of excessive quan tities of aluminum-containing phosphate binders can lead to aluminum toxicity [3], the use of calcium carbonate may be pre-fcrred [4]. even though it may be somewhat less efTcctive than aluminum hydroxide in reducing intestinal phosphate absorption.…”