Reversal of Aluminum-Related Bone Disease After Substituting Calcium Carbonate for Aluminum Hydroxide Gavril Hercz, MD, Dennis L. Andress, MD, Henry G. Nebeker, MD, James H. Shinaberger, MD, Donald J. Sherrard, MD, and Jack W. Coburn, MD • Aluminum-related osteodystrophy, a crippling disease in patients with renal failure, can develop from the long- term ingestion of aluminum hydroxide gels. We present a diabetic patient treated with continuous ambulatory peritoneal dialysis (CAPO) who developed markedly elevated plasma aluminum levels but no musculoskeletal symptoms. Bone biopsy revealed features of the aplastic form of aluminum-related disease with significant aluminum staining, decreased osteoblastic osteoid, and decreased bone formation by double tetracycline label- ing, but no excess accumulation of unmineralized osteoid. Aluminum hydroxide gels were discontinued and the patient received calcium carbonate to control hyperphosphatemia; 9 months later, a bone biopsy showed marked improvement of the aluminum-related bone disease, and at 2 to 10 months, plasma aluminum had decreased from 208.7 ± 10.3 (SE) to 55.7 ± 3.9/Lg/L. © 1988 by the National Kidney Foundation, Inc. INDEX WORDS: Plasma aluminum; aluminum toxicity; renal osteodystrophy; aluminum-related bone disease; aluminum hydroxide; calcium carbonate; bone biopsy. A LUMINUM-RELATED osteodystrophy is recognized as a disabling complication oc- curring in a substantial fraction oflong-term dialy- sis patients. Some series have reported a 37% prevalence in asymptomatic patients as detected by bone biopsy. \,2 With time, a significant number of these patients can develp bone pain, fractures, or muscle weakness. \'3 Early studies of aluminum-related bone disease reported the source of aluminum as the water used for the preparation of dialysate. 4.5 However, there is emerging evidence that the disorder can develop from the absorption and accumulation of aluminum from oral aluminum hydroxide gels. 2.6·8 Because of the potential toxicity of the aluminum gels, there has been renewed interest in the use of calcium carbonate, which has been shown to bind phosphate in the intestine. 9 Further studies have demonstrated its effectiveness in dialysis pa- tients lO . l 3; however, there are no data on the ef- fects of the discontinuation of aluminum-contain- From the Medical and Research Services. J.i?terans Adminis- tration Wadsworth Medical Center. and the Department of Medicine. UCLA School of Medicine. Los Angeles; the J.i?terans Administration Medical Center. and The Medical Service. Seat- tle Medical Center; and the Department of Medicine. Uni- versity of Washington School of Medicine. Seattle. Supported in part by research funds from the J.i?terans Ad- ministration. Address reprint requests to Jack W. Coburn. MD, Nephrol- ogy Section (691111lL), Wadsworth Medical Center, Wil- shire and Sawtelle Boulevards, Los Angeles, CA 90073. © 1988 by the National Kidney Foundation, Inc. 0272-6386/88/1101-0014$3.00/0 ing gels on the course of aluminum-related bone disease. We report a patient undergoing continuous am- bulatory peritoneal dialysis (CAPD) who devel- oped asymptomatic aluminum-related osteodystro- phy from the oral absorption of aluminum over a relatively short period; on discontinuation of aluminum hydroxide gel and substitution of cal- cium carbonate as a phosphate-binding agent, the skeletal histology improved markedly. CASE REPORT Therapy with CAPD was initiated in a 65-year-old man with renal failure secondary to noninsulin-dependent diabetes melli- tus. Over a lO-month period, the patient sporadically ingested 4 to 5 gld of the prescribed aluminum hydroxide gels. The pa- tient denied symptoms of bone pain, muscle weakness, or frac- tures. There was no history of treatment with total parenteral nutrition, parenteral albumin products, sucralfate, glucocorti- coids, or anticonvulsants, and he had not taken aluminum hy- droxide before initiation of CAPD. He had not received vi- tamin D sterols and he had not used aluminum cookware. The patient became anuric shortly after starting CAPD. Physical examination was remarkable only for nonproliferative diabetic retinopathy. Neurologic examination revealed normal muscle strength. Plasma samples were collected at 2-week intervals, begin- ning 3 months after CAPD was initiated, for the determination of aluminum, phosphorus, total calcium, and alkaline phospha- tase as part of a protocol involving the study of other CAPD patients.I4 In addition, the serum immunoreactive parathyroid hormone (iPTH) level was measured. With the finding of plasma aluminum levels elevated to 180 to 260 /Lg/L, the pa- tient underwent a bone biopsy to evaluate whether there was evidence of aluminum-related bone disease. At this time, after 10 months of therapy with CAPD, the aluminum hydroxide gels were discontinued. Serum phos- 70 American Journal of Kidney Diseases, Vol XI, No 1 (January), 1988: pp 70-75