Microsoft Word - NEF113BF

M. Gonella, MD, Servizio di Nefrologia e Dialisi, Ospedale S. Spirito, I-15033 Casale Monferrato (Italy) Dear Sir, Despite early suggestions about aluminum (Al) absoφtion and toxicity in renal failure [ 1 ], Al hydroxide was widely used as a phosphate binder until a few years ago. In the late 70s, Al metabolism was more deeply investigated and its deposition in various tissues was found to be correlated with serious disorders [2]. Moreover, it was established that Al burden does not only derive from dialysate but also from gut absorption in RDT patients on Al containing phosphate binders [3]. Thus, in order to correct hypeφhospha-temia while avoiding Al intoxication, calcium carbonate, that was already employed as Ca supplement, was also tested as a phosphate binder on the basis of previous observations [4], and it was confirmed as a valid therapy in correcting hypeφhosphatemia in RDT patients. The risk of hypercalcemia can be prevented by adjusting dialysate Ca concentration (dCa) and administering CaCC1⁄8 just before meals [5-8]. In our experience a schedule including a dCa of 3.5 mEq/1 and a mean CaCC1⁄8 dose of 9 ± 3 g given only in the interdialytic days before meals allowed in the long term a good control of divalent ions in all patients [9]. The possible use of magnesium (Mg) salts as phosphate binders, instead of CaCX3⁄4 [10, 11], is hampered by the difficulty of associating a proper dialysate Mg concentration (dMg). In fact, the use of Mg salts, when not associated with a shaφ reduction of dMg, results in hypermagnesemia which can further impair bone mineralization; on the other side, when Mg salts are associated with a negligible dMg, low postdialytic serum Mg can occur with acute harmful effect [12]. Therefore, the use of Ca salts is widely accepted as first choice phosphate binders in RDT patients. However, despite a good control of divalent ions, most RDT patients developed secondary hypeφarathyroidism in the long term. Slatopolsky et al. [13] showed that intravenous boli of calcitriol (CAL) suppress elevated parathyroid hormone (PTH) concentration, probably through the saturation of parathyroid cells, CAL receptors and the consequent suppression of parathyroid activity. Since then a number of papers illustrating the beneficial effect of oral or intravenous CAL boli upon PTH secretion has been published.