Vitamin K antagonist treatment and liver dysfunction accompany the development of calciphylaxis, researchers confirm.

To better understand calciphylaxis’ pathogenesis, Phillip Russ, MD, and colleagues from the University Hospital of Marburg in Germany, studied 15 white patients (mean age 65; 9 female) with biopsy-proven disease. Criteria for diagnosis included intimal hyperplasia, micro thrombi, or von Kossa stain positive media calcification. Of the 15 patients, 12 had stage 4 or 5 chronic kidney disease, including 10 with end-stage renal disease.

Three quarters of patients (73.3%) died within a year, according to results published in BMC Nephrology. The team could not identify a single pathway to development of the life-threatening disease. However, they did confirm some clinically significant concomitant factors. Along with secondary hyperparathyroidism (present in 87%), female gender and obesity appeared influential. Twelve patients had a body mass index (BMI) exceeding 30 kg/m2. More importantly, 86.7% of patients took vitamin K antagonists (VKA) for atrial fibrillation. Other relevant medications included proton pump inhibitor (PPI) use (80% of patients), vitamin D (67%), oral calcium supplements (40%), and corticosteroids (33%). In addition, at diagnosis, 10 patients presented with hypoalbuminemia, which likely contributed to liver impairment.

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According to Dr Russ and his colleagues, “treatment with vitamin K antagonists and liver dysfunction are [the] most important concomitant factors in development of calciphylaxis. As progression and development of calciphylaxis are chronic rather than acute processes, early use of DOAC

[direct oral anticoagulants]

instead of VKA might be beneficial and reduce the incidence of calciphylaxis.”

Vitamin K antagonists inhibit the posttranslational gamma-carboxylation of matrix Gla protein, which is responsible for inhibiting calcification.

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Russ P, Russwurm M, Kortus-Goetze B, Hoyer J, and Kamalanabhaiah S. Phenprocoumon based anticoagulation is an underestimated factor in the pathogenesis of calciphylaxis. BMC Nephrol. DOI:10.1186/s12882-019-1301-6