Calciphylaxis Clinical Presentation

  • Author: Julia R Nunley, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Jun 24, 2011
 

History

Most patients with calciphylaxis have a long-standing history of chronic renal failure and renal replacement therapy. On rare occasions, calciphylaxis may occur in a patient with chronic renal failure prior to the initiation of replacement therapy. Very rarely, it may occur in an individual without a history of chronic renal failure.

Many persons who develop calciphylaxis have undergone renal allograft transplantation. The allograft may still be functional when calciphylaxis develops. Frequently, patients have been noncompliant with dietary, medical, and/or dialysis prescriptions prior to the onset of calciphylaxis.

Lesions of calciphylaxis typically develop suddenly and progress rapidly. Lesions may be singular or numerous, and they generally occur on the lower extremities (see image below); however, lesions also may develop on the hands and torso. Intense pain is a constant finding.

Several lesions of calciphylaxis that occurred on 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.

The patient's history may reveal an event that is a suspected trigger or risk factor for the development of calciphylaxis. These triggers include the following[4, 7, 6, 14, 15, 16, 17, 18, 19] :

  • Long-term obesity
  • Recent and sudden weight loss
  • Malnutrition
  • Infusion of medications such as iron dextran
  • Remote and/or recent use of immunosuppressive agents, especially corticosteroids
  • Liver disease
  • Diabetes mellitus and insulin injections
  • Use of vitamin D and calcium-based phosphate binders
  • Elevated aluminum levels
  • Concomitant vascular disease
  • Concurrent use of warfarin anticoagulation: Current data suggest that warfarin therapy may lower protein C concentrations, leading to a procoagulant condition in the calcified vessel. Warfarin may also inhibit carboxylation of matrix Gla protein, an important inhibitor of calcification, thus promoting calcification

Review of the patient's medical record usually reveals a history of hyperphosphatemia with hyperparathyroidism and hypoalbuminemia.[2] Patients with nonuremic calciphylaxis frequently have a history of primary hyperparathyroidism, malignancy, alcoholic liver disease, or underlying connective-tissue disease or pro-inflammatory condition.[14, 15, 20, 21, 22]

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Physical

Early lesions of calciphylaxis manifest as nonspecific violaceous mottling; as livedo reticularis; or as erythematous papules, plaques, or nodules. More developed lesions have a stellate purpuric configuration with central cutaneous necrosis (see the image below).

An isolated lesion of calciphylaxis manifesting asAn 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.

Multiple lesions of variable age may be present, following the path of the vasculature. Less commonly, lesions may manifest as either bullae (see the image below) or distinct subcutaneous, erythematous nodules suggestive of erythema nodosum. Lesions are excruciatingly tender and extremely firm.

Calciphylaxis may manifest as rapidly progressive,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.

The distribution of the lesions may be characterized as proximal or distal. Ninety percent of lesions of calciphylaxis occur on the lower extremities. Distal lesions are those that occur below the knee; proximal lesions occur on the thighs or the trunk. Proximally distributed lesions occur in 44-68% of patients, with lesions developing predominantly on the thighs, the buttocks, and the lower part of the abdomen. Distal and visceral involvement are not uncommon.

An intact peripheral pulse helps to distinguish acral calciphylaxis from atherosclerotic peripheral vascular disease. Ulceration is considered a late finding and is associated with a higher mortality rate.

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Causes

Disorders associated with the development of calciphylaxis include the following[2, 4, 15, 16, 17] :

  • Common associations include chronic renal failure, hypercalcemia, hyperphosphatemia, elevated calcium-phosphate product, hyperparathyroidism, and vascular calcification.
  • Speculative associations include aluminum toxicity, coagulation abnormalities, and iron dextran infusion.
  • Associations suggested from clinical observations include renal transplantation, immunosuppressive agents, corticosteroid use, and obesity.
  • Systemic inflammation appears to be a predisposing factor.[10, 11]

The cause of calciphylaxis remains obscure. Most cases occur in the setting of chronic renal failure, abnormal calcium-phosphate homeostasis, and hyperparathyroidism. Both hypercalcemia and hyperphosphatemia may be present, and the calcium-phosphate product frequently exceeds 60-70 mg2/dL2. However, calciphylaxis may occur in the setting of normal, or minimally elevated, calcium and phosphate levels.

Case reports exist of calciphylaxis occurring in primary hyperparathyroidism, cirrhosis, Crohn disease, malignancy, and rheumatoid arthritis, without renal disease. The pathogenesis of calciphylaxis in these cases is uncertain.[14, 15, 20, 21] The exact role of PTH is uncertain because calciphylaxis may occur after total parathyroidectomy, in the absence of measurable PTH levels.

Patients at an increased risk appear to be those who are obese and those who have been exposed to immunosuppressive agents, including glucocorticoids.[15] Calciphylaxis occurs more frequently in areas where body fat is most abundant, such as the thighs, the buttocks, and the lower part of the abdomen.[16, 17] Fatty areas may be at higher risk for thrombosis, owing to lower blood flow or the increased potential for vascular kinking.

Persons with diabetes mellitus may also be at an increased risk;[15, 16, 17] insulin injections may be an independent risk due to trauma to the subcutis.

The clinical appearance of the lesions of calciphylaxis (livedo reticularis and stellate purpura) suggests that the common endpoint of the process is small vessel occlusion. Indeed, microthrombi are found in most cases. Note the following:

  • Hypercoagulable conditions, including protein C and protein S deficiencies, and the presence of a circulating anticoagulant have been described in a number of patients.[23, 24, 25, 26, 27] However, conditions of hypercoagulability are not found uniformly. If they do exist, they could possibly precipitate or exacerbate calciphylaxis in a predisposed patient.
  • Vascular calcification is a constant finding in cases of calciphylaxis. Theoretically, various pathologic roles may be attributed to this vascular calcification. First, calcification of the vascular endothelium may alter the local interaction of procoagulant and anticoagulant factors, predisposing to a microenvironment of hypercoagulability. Alternatively, extensive endothelial calcification and intimal hyperplasia, which are known to compromise the luminal size of vessels in calciphylaxis, may result in vascular occlusion. Finally, data suggest that the uremic milieu may promote calcification through inhibition of various endogenous inhibitors of calcification such as alpha2-Heremans-Schmid glycoprotein/fetuin A (AHSG), osteopontin, and matrix Gla protein. These theories remain speculative.[6, 9]
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Contributor Information and Disclosures
Author

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, and Women's Dermatologic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

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, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD  Assistant 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, and Texas Dermatological Society

Disclosure: Nothing to disclose.

Joel M Gelfand, MD, MSCE  Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania

Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology

Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

Dirk M Elston, MD  Director, Department of Dermatology, Geisinger Medical Center

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