Abstract
Renal osteodystrophy is a significant complication in chronic kidney disease. This condition is referred to as mineral and bone disorders in chronic kidney disease, mainly because of its wider ranging impact, including an association with increased mortality and non-bone-related morbidity. Because most of the abnormalities that characterize mineral and bone disorders in chronic kidney disease (e.g., hyperphosphatemia, secondary hyperparathyroidism) are amenable to therapeutic interventions, this field has also been in the cross-hairs of many pharmaceutical companies. The advent of a number of new therapeutic options for mineral and bone disorders in chronic kidney disease has broadened our armamentarium but has also resulted in an intense marketing battle between pharmaceutical companies. The paucity of randomized, controlled trials in this field has allowed the various companies to promote unilaterally data that fit their needs and to attempt to discredit data that support their competitors' products. Although this attitude is expected and regarded as acceptable in a consumer society, on a scientific level, it has resulted in a polarized and often confused audience: The practicing nephrologists. This article provides a historical overview of how the field of mineral and bone disorders in chronic kidney disease has evolved from a pharmaceutical standpoint, with a critical emphasis of the key moments that resulted in the current acrimonious climate. Also assessed is what the key unanswered questions are in this field, and practical solutions to the discussed issues are provided.
Highlights
F ew failing organs have an impact as widespread as the kidneys, but none of the deleterious consequences of chronic kidney disease (CKD) has had such an intriguing and convoluted history as what is referred to as the “mineral and bone disorders” of the CKD (CKD-MBD) [1], which encompasses such traditional concepts as renal osteodystrophy and secondary hyperparathyroidism (SHPT)
As one of the first described complications of uremia, CKD-MBD has enjoyed the undivided attention of the nephrology community. This is because of the beautiful and complex interrelationship of calcium, phosphorus, vitamin D, and parathyroid hormone (PTH) and because of mounting evidence showing a link between various aspects of CKD-MBD and adverse outcomes, especially in patients who undergo maintenance dialysis [2,3]
We provide a critical overview of how the current landscape of CKD-MBD has evolved from a pharmaceutical standpoint and assess what the most pressing issues are for practitioners in this field
Summary
No RCT was ever done to show that interventions to lower PTH or phosphorus improve mortality, even though there is biological plausibility and observational studies show a strong association. Comorbidity profiles, and adverse effects are often limiting factors and make the availability of multiple binders helpful in individualizing therapy. This involves dietary, medication, and dialysate-associated calcium intake. Observational studies show a survival benefit from treatment with activated vitamin D in dialysis patients that is independent of PTH, calcium, or phosphorus level, suggesting that all patients with CKD could benefit from some form of vitamin D replacement therapy. The high price of several medications represents a serious limitation in everyday practice Many of these products have cheaper generic alternatives, but both the economic and the biologic advantages of one versus the other need to be better studied. A balanced, transparent, and hands-off collaboration wherein industry supports the process rather than the specific set of guidelines that involve their products may diminish the perception of conflict of interest
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