The suspected diagnosis can be supported by a skin biopsy, usually a punch biopsy, which shows arterial calcification and occlusion in the absence of vasculitis. Excisional biopsy should not be done due to increased risk of further ulceration and necrosis. Bone scintigraphy can be performed in cases where skin biopsy is contraindicated. Results of the study show increased tracer accumulation in the soft tissues. In certain patients, an anti-nuclear antibody test may play a role in diagnosis of calciphylaxis. Plain radiography and mammography may also show calcifications but these tests are less sensitive. Laboratory studies, such as phosphate levels, calcium levels, and parathyroid levels, are nonspecific and unhelpful for diagnosis of calciphylaxis. Treatment
The treatment of calciphylaxis requires a multidisciplinary approach, using the knowledge of nephrologists, plastic surgeons, dermatologists, and wound care specialists working together to manage the disease and its outcomes. The key to treating calciphylaxis is prevention via rigorous control of phosphate and calcium balance and management of risk factors in patients who have increased chances of developing calciphylaxis. There is no specific treatment. Most treatment recommendations lack significant data, and none are internationally recognized as the standard of care. It is generally accepted to apply a multi-pronged approach to each patient. Analgesia and wound management
Pain management and choice of analgesia is a challenging task in managing calciphylaxis. Pain is one of the most severe and pervasive symptoms of the disease and can be unresponsive to high-dose opioids.
Because the tissue has infarcted, wound healing seldom occurs, and ulcers are more likely to become secondarily infected. Many cases of calciphylaxis lead to systemic bacterial infection and death.Calciphylaxis is characterized by the following histologic findings:

systemic medial calcification of the arteries, i.e. calcification of tunica media. Unlike other forms of vascular calcifications (e.g., intimal, medial, valvular), calciphylaxis is characterized also by
small vessel mural calcification with or without endovascular fibrosis, extravascular calcification and vascular thrombosis, leading to tissue ischemia (including skin ischemia and, hence, skin necrosis). Heart of stone
Severe forms of calciphylaxis may cause diastolic heart failure from cardiac calcification, called  heart of stone. Widespread intravascular calcification typical of calciphylaxis lesions occur in the myocardium and prevent normal diastolic filling of the ventricles. Cause
The cause of calciphylaxis is unknown. Calciphylaxis is not a hypersensitivity reaction (i.e., allergic reaction) leading to sudden local calcification. The disease is also known as calcific uremic arteriolopathy; however, the disease is not limited to patients with kidney failure. The current belief is that in end-stage kidney disease, abnormal calcium and phosphate homeostasis result in the deposition of calcium in the vessels, also known as metastatic calcification. Once the calcium has been deposited, a thrombotic event occurs within the lumen of these vessels, resulting in occlusion of the vessel and subsequent tissue infarction. Specific triggers for either thrombotic or ischemic events are unknown.