APLASTIC OSTEODYSTROPHY WITHOUT ALUMINUM - THE ROLE OF SUPPRESSED PARATHYROID FUNCTION

We evaluated 259 dialysis patients using serum parathyroid hormone (PT H, IRMA; normal range 1 to 5.5 pm or 10 to 55 pg/ml), the deferoxamine infusion test and iliac crest bone biopsy to determine the various fo rms of renal osteodystrophy and their risk factors. Although half of t he biopsied patients had low turnover osteodystrophy, evidence of alum inum toxicity was present in only 1/3 of them. Additional risk factors for this bone lesion included treatment with peritoneal dialysis, ing estion of calcium carbonate, diabetes mellitus and advanced age. The P TH levels in patients with the aplastic lesion were significantly lowe r than in patients with normal or high bone turnover lesions [7.7 +/- 6.1 vs. 36.9 +/- 3.2 pm (77 +/- 61 vs. 369 +/- 32 pg/ml), P < 0.0001]. Aside from hypercalcemia, these patients were relatively asymptomatic . In a second study, 10 patients on peritoneal dialysis with the aplas tic lesion had their dialysate calcium lowered from 1.62 to 1.0 mm. Th is resulted in a significant increase in PTH levels, from [3.7 +/- 0.8 to 10.6 +/- 1.9 pm (37 +/- 8 to 106 +/- 19 pg/ml), P < 0.001] which p ersisted over the nine-month observation period. In conclusion, the ap lastic lesion is the most common form of renal osteodystrophy, with al uminum intoxication implicated in only 1/3 of the cases. In the remain der, factors identified include therapy with peritoneal dialysis using supraphysiological dialysate calcium, oral CaCO3 intake and diabetes mellitus. These factors may modulate their effect by lowering serum PT H to levels which are inadequate in maintaining normal bone turnover. The long-term sequelae of this non-aluminum related lesion remain to b e defined.