RENAL OSTEODYSTROPHY IN DIALYSIS PATIENTS - DIAGNOSIS AND TREATMENT

This article reviews the clinical, biological, radiological, and patho logical procedures and their respective indications for the practical diagnosis of the following various histological patterns of renal oste odystrophy: osteitis fibrosa due to parathyroid hormone (PTH) hypersec retion; osteomalacia or rickets due to native vitamin D deficiency and /or aluminum overload; and adynamic bone disease (ABD) due to aluminum overload and/or PTH secretion oversuppression. Our advice regarding b one biopsy is to restrict it to patients with symptoms and hypercalcem ia, especially those who have been previously exposed to aluminum. In other cases, we propose relying merely on the determination of the pla sma concentrations of calcium, protide, phosphate, bicarbonate, intact PTH, aluminum, 25(OH)D-3, and alkaline phosphatase (total and bony if hepatic disease is associated) to choose the appropriate treatment. B ecause of the danger of the desferrioxamine treatment necessary to che late and remove aluminum, the suspicion of aluminic bone disease (oste omalacia or ABD) will always be confirmed by a bone biopsy. In the cas e of nonaluminic osteomalacia, correction of the vitamin D deficiency by native vitamin D or 25(OH)D,, and of the calcium deficiency and aci dosis by alkaline salts of calcium and if necessary sodium bicarbonate are sufficient to cure the disease. In the case of nonaluminic ABD, t he stimulation of PTH secretion by the discontinuation of Icr hydroxyl ated vitamin D and the induction of a negative calcium balance during dialysis by decreasing the calcium concentration in the dialysate will allow an increase of the CaCO3 dose to correct for hyperphosphatemia without inducing hypercalcemia. For hyperparathyroidism, i.e., plasma intact PTH levels greater than two- or four-fold the upper limit of no rmal levels (according to the absence or presence of previous aluminum exposure), the treatment will consist in increasing the CaCO3 dose to correct for hyperphosphatemia together with a decrease of the calcium concentration in the dialysate if the dose of CaCO3 is so high that i t induces hypercalcemia. When the hyperphosphatemia has been corrected and there is still a low or normal corrected plasma calcium level, la (OH)D, in an oral bolus 2 or 3 times a week should be given at the min imal dose of 1 mu g. When the PTH level stays above 400 pg while hyper calcemia occurs and hyperphosphatemia persists, surgical subtotal para thyroidectomy is recommended or the injection of calcitriol into the b ig nodular hyperplastic parathyroid glands under sonography control in high surgical risk patients. Special recommendations are given for ch ildren.