What molecular and chemical factors are involved in the pathophysiology of calciphylaxis?

Updated: Feb 24, 2020
  • Author: Julia R Nunley, MD; Chief Editor: Dirk M Elston, MD  more...
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Many molecular and cytochemical factors have been identified as crucial in bone metabolism. The receptor activator of nuclear factor-kB (RANK), RANK ligand, and osteoprotegerin appear to regulate skeletal and extraskeletal mineralization. [6, 7] Uremia-induced defects in this system may predispose to calciphylaxis. [8] Corticosteroids, aluminum, hyperparathyroidism, liver disease, warfarin therapy, and a variety of inflammatory processes all can alter this balance and promote vascular calcification. [9, 10] Chronic inflammatory conditions may predispose to calciphylaxis by reducing serum levels of fetuin-A, an important inhibitor of calcification produced in the liver. [11, 12, 13] Other authors have recently suggested that calciphylaxis is an active form of osteogenesis with up-regulation of bone morphogenic protein 2 (BMP-2), Runx2, its target gene, and its indirect antagonist sclerostin. [14]

Most investigators note that the common endpoint of calciphylaxis is vascular occlusion and thrombosis, which results in cutaneous ischemia [15, 16, 17] ; however, the factors associated with thrombosis are not uniform.

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