HYPOPHOSPHATEMIC OSTEOMALACIA IN A RENAL-ALLOGRAFT RECIPIENT - A CAUSE OF SEVERE OSTEOPOROSIS

Renal osteodystrophy improves after renal transplantation but, after the procedure, other forms of bone disease emerge. We report a male patient that received a renal allograft four years before, who consulted for low back pain secondary to multiple verebral compression fractures. The patient had good renal funtion, a parathormone independent hyperphosphaturia, normal 25-OH cholecalciferol, increased urinary hydroxyproline, decreased osteocalcin, reduced bone density and a bone biopsy revealing osteomalacia. The diagnosis of hypophosphemic osteomalacia was reached and treatment with phosphates and ergocalciferol was started but, despite this, the patient suffered a new fracture two years later. Two mechanisms can produce hypophosphatemia after a renal transplantation: a parathormone excess due to the preview renal failure, that disappears during the first year after the transplantation or a derangement in renal phosphate transport that can be due to a generalized proximal tubule solute transport derangement (Fanconi syndrome), parathormone hypersensitivity or to an ''idiopathic'' hyperphosphaturia. Despite a good treatment, bone mass is not recovered and there is a high fracture risk. Mineral metobolism must be closely monitored after a renal allograft and its alterations must be quickly treated.