Meany et al. present a novel cause of a current major problem in clinical medicine, difficulty in accurately diagnosing chronic kidney disease–mineral bone disorder (CKD-MBD), a term coined by the Kidney Disease: Improving Global Outcomes foundation to replace ROD. The basis for the change in terminology stems from the realization that the skeletal and mineral disorders complicating kidney disease are critical in the pathogenesis of the excess cardiovascular mortality risk associated with CKD. The cardiovascular risk for the presented 64-year-old woman, who was on dialysis after 2 failed kidney transplants and had severe osteoporosis, was extreme. In this patient’s CKD-MBD, diagnosis of the skeletal remodeling disorder was going to guide critical therapy. The case presentation portrays the weakness in the current standard practice, which is in the process of being replaced. The current practice is that iPTH assays are used to relate to past bone biopsy studies and to predict the state of bone remodeling. A bone biopsy would have been indicated in the patient presented, but this is not the standard practice in 2009. Multiple studies have defined the weakness of the standard practice employed here, and the various assays for iPTH used to estimate bone remodeling have numerous problems in addition to the novel biotin interference discovered in this case.
The finding of the adynamic bone disorder would have been associated with attempts to increase bone remodeling by correcting the hypercalcemia and increasing the actions of PTH. The increased PTH concentration results from the reference laboratory and the high alkaline phosphatase concentration confirmed that the patient actually had high-turnover CKD-MBD contributing to her osteoporosis. This finding diametrically changes the treatment strategy to controlling the effects of CKD on the cardiovascular system by decreasing the serum phosphorus and on the PTH concentration by using a calcimimetic agent, because the presence of hypercalcemia contraindicates increasing the dose of vitamin D analogs.
Author Contributions: All authors confirmed they have contributed to the intellectual content of this paper and have met the following 3 requirements: (a) significant contributions to the conception and design, acquisition of data, or analysis and interpretation of data; (b) drafting or revising the article for intellectual content; and (c) final approval of the published article.
Authors’ Disclosures of Potential Conflicts of Interest: Upon manuscript submission, all authors completed the Disclosures of Potential Conflict of Interest form. Potential conflicts of interest:
Employment or Leadership: None declared.
Consultant or Advisory Role: K. Hruska, Genzyme, Shire, Fresenius, and Stryker.
Stock Ownership: None declared.
Honoraria: None declared.
Research Funding: K. Hruska, Shire, and Genzyme.
Expert Testimony: None declared.
Role of Sponsor: The funding organizations played no role in the design of study, choice of enrolled patients, review and interpretation of data, or preparation or approval of manuscript.
- © 2009 The American Association for Clinical Chemistry