201 - Renal osteodystrophy

2013 whose GFR is reduced due to intrinsic parenchymal damage as opposed to age-related reductions in GFR without another specific intrinsic renal diagnosis. At each level of CKD there may exist a specific form of renal osteodystrophy. The earliest form of renal bone disease (secondary hyperparathyroidism) may be defined by quantitative histomorphometry and/or biochemical profiling (elevated 1-84 intact parathyroid hormone [PTH]) as early as stage 3 CKD (GFR 30 to 60 mL/min). Even though there is an exponential relationship between the declining level of GFR and the height of the endogenous PTH, elevated PTH levels (secondary hyperparathyroidism) may also be seen in patients with various forms of osteoporosis due to many other possible causes that may not be related to reduced GFR (e.g., low 25-hydroxyvitamin D levels, calcium malabsorption, hypercalciuria). Only after correcting other reversible factors that may also lead to secondary hyperparathyroidism while the PTH remains elevated in association with reduced GFR can the secondary hyperparathyroidism be attributed to the reduction in renal function. The KDOQI guidelines (both opinionand evidence-based) provide suggestions concerning the management of secondary hyperparathyroidism when due to intrinsic renal damage. In addition, there are published suggestions for the management of patients with postmenopausal, male, and glucocorticoid-induced osteoporosis who have secondary hyperparathyroidism not related to reduction in renal function. The other forms of renal bone disease (osteomalacia, mixed renal osteodystrophy, adynamic renal bone disease, and aluminum bone disease) are rare until stage 5 CKD (end-stage renal disease with GFR less than 15 mL/min or on dialysis). The classification of renal bone disease is most objectively defined by double tetracycline-labeled quantitative histomorphometry, and quantitative histomorphometric criteria for defining the specific form of renal bone disease (standardized nomenclature) have been published. Hence, here the means by which renal osteodystrophy is first defined is divided into quantitative bone histomorphometry, then biochemical profiling, and, finally, clinically. In addition, the challenge of defining osteoporosis, a common metabolic bone disease in the CKD population, will be discussed. Finally, the therapeutic options that are available to treat specific forms of renal bone disease and osteoporosis associated with CKD will be presented.