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Abstract: TH-PO137

Histologic Specificity in Calciphylaxis

Session Information

Category: Bone and Mineral Metabolism

  • 502 Bone and Mineral Metabolism: Clinical

Authors

  • O'Neill, W. Charles, Emory University School of Medicine, Atlanta, Georgia, United States
  • Cheeley, Justin Thomas, Emory University School of Medicine, Atlanta, Georgia, United States
  • Ellis, Carla L., Emory University School of Medicine, Atlanta, Georgia, United States
  • Jagannathan, Geetha, Emory University School of Medicine, Atlanta, Georgia, United States
Background

Skin biopsy is often used to support the diagnosis of calciphylaxis, otherwise termed calcific uremic arteriolopathy (CUA), but the specificity is unknown. We previously showed that many of the findings ascribed to CUA were also present in amputation specimens of patients without CUA. To better understand the specificity of histology in CUA and thus the underlying pathophysiology, we prospectively compared involved and uninvolved tissue from 18 subjects with a clinical diagnosis of CUA.

Methods

16 patients undergoing skin biopsies for CUA consented for a biopsy of uninvolved skin, usually on the contralateral extremity. In an additional 2 cases, skin samples were obtained at autopsy. Sections were stained with hematoxylin and eosin and von Kossa calcium stain. The clinical diagnosis was made by the consulting dermatologist, who also performed the punch biopsies. The biopsies were reviewed by one of two pathologists and scored for the following: calcification, thrombosis, or intimal hyperplasia of small arteries or arterioles, and extravascular calcification.

Results

The characteristics of the subjects were as follow: age, 58 +/- 3 years; gender, 67% female; end-stage renal disease, 89%; warfarin use, 50%. Locations of the biopsies were thigh (11), lower leg (4), arm (1), abdominal wall (1), and mons pubis (1). Small vessel calcification was seen in half of the lesional samples and 44% of control samples. Extravascular calcification was seen in 44% of lesional samples and 22% of control samples. In contrast, thrombosis (50%) and intimal hyperplasia (33%) of small vessels were observed only in lesional samples. Of the lesional biopsies with thrombosis or intimal hyperplasia, small vessel calcification was present in 78% and 83% respectively. There were nondiagnostic histologic findings in 6 lesional biopsies and 7 control biopsies.

Conclusion

The similar proportions of small vessel calcification in lesional and control biopsies indicate a lack of any specificity and suggest that this is not sufficient to cause of CUA. Thrombosis or intimal hyperplasia were specific to lesional biopsies, suggesting a pathogenic role and consistent with the ischemic nature of the lesions. While not a specific finding, calcification was present in most of the lesional biopsies with thrombosis or intimal hyperplasia, suggesting a contributory role.

Funding

  • Clinical Revenue Support