BIOCHEMICAL-DIAGNOSIS AND PREVENTION OF A DYNAMIC BONE-DISEASE

Aluminic adynamic bone disease (ABD) is a true demineralizing bone dis ease markedly favoring hypercalcemia, hyperphosphatemia and soft tissu e calcifications. Although it shares common pathogenetic mechanisms wi th non aluminic ABD its main cause is iatrogenic and its prevention re lies on adequate treatment of tap water used for the dialysate and on total exclusion of long term administration of aluminum phosphate bind ers. It should be a story of the past. In patients never exposed to al uminum the histological pattern of ABD may be nevertheless present. It is not a clinical bone disease but it favors the toxicity of subseque nt exposition to factors depressing bone formation like aluminum and c orticosteroids. It also increases the risk of hypercalcemia and soft t issue calcifications but to a much lesser extent than aluminic ABD. It may be diagnosed without the help of aggressive bone biopsy mainly on a plasma intact PTH concentration < 150 pg/ml and a plasma calcium > 2,50 mmol/l. It is intrinsically due to a bone resistance to PTH induc ed by uremia per se and therefore only partially introgenic when the s uppressive treatment of hyperparathyroidism restores normal plasma con centration of PTH. Therefore it can be easily prevented by maintaining predialysis plasma concentrations of intact PTH between 100 - 250 pg/ ml, that of calcium between 2,4 and 2,6 mmol/l, and of phosphate betwe en 1,3 and 1,7 mmol/l thanks to the use as phosphate binder of oral al kaline calcium salts taken with the meals in association with an appro priate dialysate calcium concentration (1,75 to 1,0 mmol/l) and the re strictive use of non hypercalcemic and hyperphosphatemic doses of 1-al pha-OH and vitamin-D-3 derivatives once native vitamin-D-3 deficiency is corrected.