The pathogenesis of calciphylaxis remains unclear, but the reduced blood ow is thought to rstly result from the calcication of dermal and subcutaneous arterioles. Medial calcication is caused by ectopic bone formation by vascular smooth muscle cells. These cells transform, in response to hyperphosphatemia, hypercalcemia, and hyperglycemia, into osteoblast-like cells capable of producing hydroxyapatite crystals. Moreover, there also exists a relative deciency of calcication inhibitors including matrix gla protein, whose carboxylation is vitamin K depen­dent, and fetuin-A, which is decreased in chronic inammatory conditions such as chronic kidney disease [1, 5]. Finally, thrombosis develops in the lumens of these vessels leading to tissue ischemia and infarction. Thrombosis could be promoted by a local prothrombotic state due to endothelial dysfunction and intimal brosis, but it can also be explained by systemic hypercoagulable condi­tions. It has been demonstrated that calciphylaxis patients have high prevalence of protein C and S deciency, lupus anticoagulant, and antithrombin deciency [10].