Bisphosphonate therapy in renal osteodystrophy – a review REVIEW

bisphosphonates. For this reason knowledge of the pharmacokinetics of the various bisphosphonates is a mandatory precondition for their use in severe renal impairment or dialysis dependence. Bone disease is a frequent finding in severe renal impairment (Kidney Disease: Improving Global Outcomes [KDIGO] stages IV & V). Most forms are subsumed under the terms renal osteopathy or renal osteodystrophy. However, they do not form a homogeneous syndrome but encompass a whole complex of bone changes characterized on the one hand by chronic vitamin D deficiency and reduced 1-α-hydroxylase activity and on the other by secondary hyperparathyroidism (1). Other critical determinants of bone metabolism include chronic metabolic acidosis, raised ß2-microglobulin levels (2, 3) and regular heparin treatment in dialysis (4) (Fig. 1). Most current treatments in dialysis patients aim to lower parathyroid hormone (PTH) levels into the guideline range (Kidney Disease Outcome Quality Initiative [KDOQI]) (5). Additional aims are to lower calcium and phosphate levels into their predefined target ranges. But since this barely influences the critical determinants just mentioned, such therapy often has a limited impact on bone. Approaches aimed at treating bone metabolism directly are only in their infancy and to be viewed in the main as experimental. Nevertheless, patients in stage IV or V chronic renal failure are known to be at above-average fracture risk even after their PTH levels have been lowered into the KDOQI guideline range (Tab. I) (6). Hence the need to elucidate the feasibility of bisphosphonate use in severe renal impairment or dialysis dependence.