Oral Presentation ESA-SRB Conference 2015

Renal bone disease - how to assess and manage (#169)

Grahame Elder 1
  1. Westmead Hospital, Sydney, NSW, Australia

Patients with chronic kidney disease (CKD) have a high incidence of fracture, which should be evaluated as a component of CKD mineral and bone disorder (MBD). Abnormalities of klotho and FGF23 occur early in CKD, with subsequent changes in PTH and 1,25-vitamin D. Autonomic and peripheral neuropathy alter the neural innervation of bone, and changes in semaphorin 3A have been reported. In addition, CKD is a highly inflammatory state, patients are often treated with glucocorticoids that induce osteocyte apoptosis and altered values of RANKL, OPG and sclerostin may affect bone.  These changes result in abnormal bone turnover, mineralisation, volume, and microarchitectural deterioration. In addition, sarcopenia, peripheral neuropathy and drug effects increase falls risk. Assessment and management vary with CKD stage (1-5D or transplant) and should take into consideration the inter-relationship of bone, vascular and soft tissue calcification, cardiac function and mortality. In CKD stages 1-3, BMD assessment by DXA, use of standard turnover markers, PTH and 25OHD can all assist in directing therapy. Interventions to maintain normal bone turnover, mineralisation and volume may all reduce subsequent risks. In CKD stages 4-5D, DXA is less predictive. Bone-specific ALP, TRAcP 5b and PTH give useful information on turnover. Bone histomorphometry remains the gold standard for diagnosis in CKD 4-5D and may show low turnover due to endogenous and iatrogenic factors, high turnover due to hyperparathyroidism, or often mixed uraemic osteodystrophy, combining abnormalities of turnover and mineralisation. Management includes maintenance of normal serum phosphate, avoidance of positive calcium balance (supplements, phosphate binders and dialysate), careful use of calcitriol or analogues and cinacalcet or parathyroidectomy in situations of high turnover with hypercalcaemia or calciphylaxis. Antiresorptives can induce ‘hungry bone’ or worsen low turnover states, but can be used. In CKD stage 5D, the place of newer anabolics and older therapies such as calciferol and vitamin C is unclear.