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  • Author: Julia R Nunley, MD; Chief Editor: Dirk M Elston, MD  more...
Updated: Feb 08, 2016


Calciphylaxis is a poorly understood and highly morbid syndrome of vascular calcification and skin necrosis. Bryant and White first reported it in association with uremia in 1898. However, the significance of this relationship became uncertain when vascular calcification was subsequently shown to be prevalent in uremia, yet the syndrome of vascular calcification with cutaneous necrosis remained rare.

In 1962, Selye[1] constructed an experimental model and was able to precipitate systemic calcification, somewhat analogous to this syndrome, in nephrectomized rats. He was the first to coin the term calciphylaxis to characterize this enigma. Over the years, many other names have been suggested to characterize the pathogenic process, which has remained elusive. Interestingly, the clinical importance of this syndrome was not recognized until a 1976 report by Gipstein et al.[2] Since then, a multitude of case reports of calciphylaxis have documented data outlining its morbidity and therapeutic dilemmas, as well as a quest to better understand its etiology and pathogenesis. Unfortunately, it remains a conundrum.[3]



The pathogenesis of calciphylaxis remains obscure and is likely the result of a multiplicity of comorbid factors or events. Disorders that are most often implicated in the pathogenesis of calciphylaxis include chronic renal failure, obesity, diabetes mellitus, hypercalcemia, hyperphosphatemia, an elevated calcium-phosphate product, secondary hyperparathyroidism, and perhaps a variety of hypercoagulable states. Yet, although these abnormalities are extremely common in patients with end-stage renal disease (ESRD), calciphylaxis is relatively rare.

Using a rat model, Selye[1] demonstrated that a series of events might be necessary for the formation of calciphylaxis. He defined calciphylaxis as a condition of hypersensitivity induced by a set of "sensitizing" agents, in which calcinosis occurred only in those subsequently subjected to a group of "challengers" and only after a critical lag time. Experimental sensitizing events and agents included nephrectomy and exposure to parathyroid hormone (PTH) and vitamin D. Substances used as challengers included egg albumin and metallic salts. Calciphylaxis was the end result.[4]

Although extrapolation of animal data to humans is conjectural, it seems to be true that serial events, most consistently involving renal failure–induced abnormalities in calcium homeostasis, are required to occur over time for calciphylaxis to develop. The cause of calciphylaxis has been elusive, most likely because it is the common endpoint of a heterogeneous group of disorders.

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.[5, 6] Uremia-induced defects in this system may predispose to calciphylaxis.[7] Corticosteroids, aluminum, hyperparathyroidism, liver disease, warfarin therapy, and a variety of inflammatory processes all can alter this balance and promote vascular calcification.[8, 9] Chronic inflammatory conditions may predispose to calciphylaxis by reducing serum levels of fetuin-A, an important inhibitor of calcification produced in the liver.[10, 11, 12] 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.[13]

Many investigators have noted that vascular occlusion and thrombosis are uniformly present and result in cutaneous ischemia[14, 15, 16] ; however the factors associated with thrombosis are not uniform.




Calciphylaxis is an uncommon condition that affects 1-4% of the population with ESRD.[17, 18] A concern exists that the incidence has increased during the last decade because of a number of possible factors, including more widespread use of parenteral vitamin D and iron dextran. No good data are available regarding the incidence of calciphylaxis in the general population without ESRD, but it is probably exceedingly rare.


Although the disease may affect persons of any race, it appears to be more prevalent in whites.


Females are affected more often than males, with a female-to-male ratio of approximately 3:1. Females also appear to be more commonly affected with nonuremic calciphylaxis.


Calciphylaxis has been reported in individuals ranging in age from 6 months to 83 years. From a large series of patients, a mean patient age of 48 years (±16 y) has been calculated. Individuals seemingly more predisposed are younger patients who have had a longer duration of renal replacement therapy.

Contributor Information and Disclosures

Julia R Nunley, MD Professor, Program Director, Dermatology Residency, Department of Dermatology, Virginia Commonwealth University Medical Center

Julia R Nunley, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Society of Nephrology, International Society of Nephrology, Medical Dermatology Society, Medical Society of Virginia, National Kidney Foundation, Phi Beta Kappa, Women's Dermatologic Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Board of Dermatology<br/>Co-Editor for the text Dermatological Manifestations of Kidney Disease .

Specialty Editor Board

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD Associate Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.


Smeena Khan, MD Private Practice, Adult and Pediatric Dermatology Associates

Smeena Khan, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

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Several lesions of calciphylaxis that occurred on the lower extremity of a patient undergoing dialysis. These lesions developed in areas of livedo reticularis and followed the path of the vasculature.
An isolated lesion of calciphylaxis manifesting as an enlarging necrotic plaque on the lower extremity of a patient undergoing dialysis. The stellate purpuric morphology can be appreciated surrounding the area of necrosis.
Calciphylaxis may manifest as rapidly progressive, diffuse and extensive, cutaneous necrosis, as is seen in this patient with chronic renal failure. Bullae may also be seen as a rare manifestation of calciphylaxis.
Radiologic findings of a hand in a patient with calciphylaxis. Extensive calcification of the radial and ulnar arteries is readily visible.
Histologically, calcification of the blood vessels, as well as the subcutis, can be seen in calciphylaxis.
Demonstrated here is the characteristic circumferential medial calcific deposit in an arteriole with subintimal edema. Histologic images courtesy of Steve A. McClain, MD, Department of Dermatology SUNY-Stony Brook.
This image shows circumferential medial calcific deposits obliterating the external elastica of an arteriole. Histologic images courtesy of Steve A. McClain, MD, Department of Dermatology SUNY-Stony Brook.
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