Poster Presentation Annual Meetings of the Endocrine Society of Australia and Society for Reproductive Biology and Australia and New Zealand Bone and Mineral Society 2016

How low can you go: bone metabolism in chronic kidney disease (#340)

Angela Sheu 1 2 , Jackie Center 1 2 , Grahame Elder 1 2 3
  1. Endocrinology Department, St Vincent's Hospital, Sydney, NSW, Australia
  2. Osteoporosis and Bone Biology Division, The Garvan Institute, Sydney, NSW, Australia
  3. Renal Department, Westmead Hospital, Sydney, NSW, Australia

Differentiating between high and low bone turnover in chronic kidney disease (CKD) is essential; both have serious complications yet polarised management strategies. We present a case of a 59-year-old man with recurrent fractures in the context of end stage renal disease, secondary to lupus nephritis with failed renal transplantation, renal calculi, vascular calcification and severe dilated cardiomyopathy.

The patient developed lupus nephritis at age 21, requiring intermittent high dose corticosteroids. At age 27, he required a total hip replacement (THR) for left hip avascular necrosis. At age 39, bone scan revealed rib and clavicle fractures. As renal function declined, calcitriol was used to control hyperparathyroidism; this was complicated by renal calculi with brittle calcium and phosphate control. At age 40, he commenced dialysis, before receiving a cadaveric renal transplant at age 45. This was complicated by post-transplant lymphoproliferative disease and graft failure, and he returned to dialysis at age 54.

At the time of transplantation, bone mineral density (BMD) by dual energy x-ray absorptiometry revealed osteoporosis and he commenced alendronate. Subsequent BMD improved, but alendronate dosing was reduced due to biochemical evidence of low bone turnover. He then sustained a left peri-prosthetic fracture following a fall from standing height. When he returned to dialysis, alendronate was ceased and concurrent hypogonadism was treated with testosterone replacement.  He continued fracturing, with 2 unprovoked lumbar vertebral fractures and a right atypical femoral fracture. Imaging also revealed severe vascular calcifications.  Right total hip BMD was osteopenic. Biochemistry suggested low bone turnover, with parathyroid hormone 7.1pmol/L, alkaline phosphatase 73U/L, calcium 2.42mmol/L and phosphate 0.84mmol/L. His fractures were managed conservatively and with changes to his dialysate and calcitriol cessation, his biochemistry improved.

We present a case of recurrent fractures due to low bone turnover in CKD and discuss the optimal management to reduce the associated complications.