Treating the renal patient who has a fracture: Opinion vs evidence

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Managing bone health in patients with chronic kidney disease presents unique challenges. While the common end point—a fracture—is comparable to that in patients with osteoporosis, the underlying metabolic conditions differ from patient to patient with chronic kidney disease and may be dramatically different from those in patients who have osteoporosis without chronic kidney disease.

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Renal osteodystrophy is not osteoporosis

Renal osteodystrophy is not osteoporosis. While osteoporosis in people without kidney disease is defined clinically on the basis of bone mineral density (measured by bone densitometry), renal osteodystrophy is a histologic diagnosis made on bone biopsy: it is a continuum between frankly low-turnoverbone disease—encompassing adynamic bone disease and osteomalacia—and frankly highturnover-bone disease, with severe secondary hyperparathyroid bone disease and osteitis fibrosa. Histologically, there may or may not be low trabecular bone volume or loss of connectivity typical of the bone loss in osteoporosis.

Patients at both ends of the spectrum of bone turnover in renal osteodystrophy may have the same bone mineral density on densitometry. Low bone mineral density may reflect inadequate mineralization (seen in osteomalacia and adynamic bone disease) or increased peritrabecular fibrosis (seen in secondary hyperparathyroid bone disease). High bone mineral density readings may capture extraosseous calcifications, which are very common in chronic kidney disease.

Renal osteodystrophy is part of the syndrome called chronic kidney disease-mineral and bone disease, 1 which is not limited to bone fractures but may also affect vascular health. Abnormal calcium deposits in vascular tissue—consistent with calciphylaxis and associated with increased morbidity and mortality rates in chronic kidney disease—may occur with low bone turnover.

The diagnosis of osteoporosis in the general population is based on clinical evidence: the measured bone mineral density is compared with normalized scores. Histologically, the bone of the osteoporotic patient shows osteopenia with increased bone turnover and a shift toward increased bone resorption, resulting in loss of connectivity of the trabeculae, as well as decreased trabecular volume. These conditions are common in advanced age and in certain pathologic states (eg, steroid therapy, metastatic bone disease, Paget disease of bone).

It is well accepted that the risk of fracture in osteoporosis increases as measured bone mineral density decreases. Conversely, increasing bone mineral density has been correlated with fewer fractures. The clinician is often guided by biomarkers of bone metabolism such as urinary N-terminal cross-linked telopeptides of collagen (NTx) in diagnosing and treating bone breakdown.

Can bisphosphonates be used in chronic kidney disease?

Bisphosphonates are antiresorptive agents that bind to the hydroxyapatite of bone. They poison the osteoclast (the bone-resorbing cell), causing its death and thereby halting the resorption of bone. Osteoblasts—the boneforming cells—are presumably not affected, and the bone continues to make osteoid, which is subsequently mineralized. Bone turnover is dramatically decreased. The net effect is increased bone density in people with osteoporosis. The half-life of these agents is years.

In the general population, bisphosphonate therapy has been associated with decreased risk of fragility bone fractures. However, the long-term effects are not yet known. Indeed, jaw necrosis—possibly due to low bone turnover—is being reported with increasing frequency. 2 Fractures associated with low bone turnover in patients without chronic kidney disease treated with bisphosphonates longterm are now being reported. 3,4

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