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

Bone biomarkers are hard to interpret in chronic kidney disease

In chronic kidney disease, the interpretation of biomarkers of bone metabolism is notoriously unreliable. The usual chemistry values associated with clinical osteoporosis in the general population—ie, elevated levels of urinary NTx, serum C-terminal cross-linked telopeptides of collagen (CTx), osteocalcin, and bone-specific alkaline phosphatase—are not valid in patients with chronic kidney disease, for obvious reasons: with declining renal function, the various markers accumulate in the serum. Urinary NTx does not apply in patients with advanced chronic kidney disease or end-stage renal disease.

How should renal osteodystrophy be treated?

Nephrologists currently focus therapy on reducing hyperphosphatemia (associated with increased morbidity across all stages of chronic kidney disease), replenishing vitamin D as much as possible without causing hyperphosphatemia and hypercalcemia, and suppressing parathyroid hormone secretion.

However, there is not enough evidence on what the goal should be with respect to parathyroid hormone in patients with chronic kidney disease who are not on dialysis. Although in the recent past many believed that parathyroid hormone goals should be 150 to 300 pg/mL in dialysis patients, the latest guidelines suggest that perhaps this goal is too narrow and may lead to more adynamic bone disease. Similarly, there is no consensus on the use of synthetic parathyroid hormone analogues.

Bisphosphonate therapy, particularly with pamidronate (Aredia) and zolendronic acid (Reclast), has been associated with adverse renal effects even in patients without chronic kidney disease. There are no prospective studies of the effects of these agents in patients with depressed renal function.

The patient with chronic kidney disease who has a fracture remains a unique problem for the nephrologist, primary care physician, and subspecialist. Efforts should be concentrated on preventing and treating metabolic bone disease in its entire spectrum, with rational, prospective studies, and should not depend on anecdotal reports. Opinions abound, without adequate evidence to back them up.