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

Renal osteodystrophy improves after renal transplantation but, after t he procedure, other forms of bone disease emerge. We report a male pat ient 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 hyper phosphaturia, normal 25-OH cholecalciferol, increased urinary hydroxyp roline, decreased osteocalcin, reduced bone density and a bone biopsy revealing osteomalacia. The diagnosis of hypophosphemic osteomalacia w as reached and treatment with phosphates and ergocalciferol was starte d but, despite this, the patient suffered a new fracture two years lat er. Two mechanisms can produce hypophosphatemia after a renal transpla ntation: a parathormone excess due to the preview renal failure, that disappears during the first year after the transplantation or a derang ement in renal phosphate transport that can be due to a generalized pr oximal tubule solute transport derangement (Fanconi syndrome), paratho rmone hypersensitivity or to an ''idiopathic'' hyperphosphaturia. Desp ite a good treatment, bone mass is not recovered and there is a high f racture risk. Mineral metobolism must be closely monitored after a ren al allograft and its alterations must be quickly treated.