Adipocytes have been shown to calcify vascular smooth muscle cells when exposed to high phosphate levels in vitro, mediated by vascular endothelial growth factor A (VEGF-A) and leptin released by adipocytes. Given that calciphylaxis tends to affect adipose tissue, this may be a contributing explanation. Another theory has been proposed that vitamin K deficiency contributes to the development of calciphylaxis. Vitamin K acts as an inhibitor of calcification in vessel walls by activating matrix Gla protein (MGP), which in turn inhibits calcification. End-stage kidney disease patients are more likely to have vitamin K deficiency due to dietary restrictions meant to limit potassium and sodium. Many end-stage kidney disease patients are also on a medication called warfarin, a vitamin K antagonist, that limits vitamin K recycling in the body.Reported risk factors include female sex, obesity, elevated calcium-phosphate product, medications such as warfarin, vitamin D derivatives (e.g. calcitriol, calcium-based binders, or systemic steroids), protein C or S deficiency, low blood albumin levels, and diabetes mellitus. Patients who require or have undergone any type of vascular procedures are also at increased risk for poor outcomes. Diagnosis
There is no diagnostic test for calciphylaxis. The diagnosis is a clinical one. The characteristic lesions are the ischemic skin lesions (usually with areas of skin necrosis). The necrotic skin lesions (i.e. the dying or already dead skin areas) typically appear as violaceous (dark bluish purple) lesions and/or completely black leathery lesions. They can be extensive and found in multiples.
Many of the other drugs have a low to very low risk to develop DIL. The following table shows the risk of development of DIL of some of these drugs on a high to very low scale. High risk:
Procainamide (antiarrhythmic)
Hydralazine (antihypertensive)
Moderate risk:
Quinidine (antiarrhythmic)
Low to Very Low Risk:
Infliximab anti (TNF-α)
Etanercept anti (TNF-α)
Isoniazid (antibiotic)
Minocycline (antibiotic)
Pyrazinamide  (antibiotic)
D-Penicillamine (anti-inflammatory)
Carbamazepine (anticonvulsant)
Oxcarbazepine (anticonvulsant)
Phenytoin (anticonvulsant)
Propafenone (antiarrhythmic)
Chlorpromazine (antipsychotic)
Minoxidil (antihypertensive vasodilator)

Diagnosis
Antinuclear antibodies are usually positive in drug-induced Lupus. Anti-Neutrophil Cytoplasmic antibodies (ANCA) can also be positive in association with certain drugs. Furthermore, anti-histone antibodies can also be positive in drug-induced lupus.Anti-Histone antibodies are positive in up to 95% of patients with drug induced lupus. The most common medications associated with drug induced lupus are hydralazine, procainamide, isoniazid, methyldopa, chlorpromazine, quinidine, and minocycline. Treatment
It is important to recognize early that these drugs are causing DIL like symptoms and discontinue use of the drug. Symptoms of drug-induced lupus erythematosus generally disappear days to weeks after medication use is discontinued. Non-steroidal anti-inflammatory drugs (NSAIDs) will quicken the healing process. Corticosteroids may be used if more severe symptoms of DIL are present. See also
Anti-histone antibody
Lupus erythematosus
Hydralazine
Discoid lupus erythematosus
List of cutaneous conditions

References
External links
eMedicine