We present a case of adynamic bone disease in a patient with chronic kidney disease on haemodialysis, with subsequent renal transplantation.

Mr PW is a 69 year old man with end-stage renal failure secondary to diabetic nephropathy, requiring renal replacement therapy for five years prior to his cadaveric renal transplant in August 2012.  His renal disease was complicated by hyperphosphataemia and secondary hyperparathyroidism treated with sevelamer and calcitriol.  Post-transplant, he was commenced on immunosuppression with mycophenolate mofetil, tacrolimus and a reducing dose of prednisolone from 30 mg daily to 7.5 mg daily over four months.  In September 2012, he had severe lower back pain after slipping off a low stool, and x-ray of spine demonstrated a new fracture at L1 with 50% loss of anterior vertebral height.  Femoral neck bone mineral density (BMD), measured by dual energy x-ray absorptiometry, was in the osteoporosis range (T-score -2.7).  Lumbar spine BMD T-score was elevated by the presence of degenerative sclerosis (T-score +0.3).  The serum 25-hydroxyvitamin D level was low at <20 nmol/L (normal range, 75-150 nmol/L) which increased to 126 nmol/L with vitamin D3 3000 IU daily.  The serum PTH level reduced from 673 pg/ml to 62 pg/ml (normal range, 12-65 pg/ml) four months post-renal transplant.  A summary of his biochemical results is shown in the table.  Mr PW underwent tetracycline-labelled bone biopsy of the iliac crest in April 2013 which showed absence of osteoblasts and osteoclasts and low rate of bone formation, consistent with adynamic bone disease.  Bone was well mineralized and there was no aluminium staining. 

This case highlights the importance of excluding adynamic bones disease prior to antiresorptive treatment in patients with chronic renal failure.  We will review the literature on treatment of adynamic bone disease, including teriparatide, an anabolic agent that simulates bone formation.