Abstract: TH-PO1120
Diffuse Dermal Angiomatosis Mimicking Uremic Calciphylaxis in ESKD
Session Information
- Pathology and Lab Medicine
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Pathology and Lab Medicine
- 1700 Pathology and Lab Medicine
Authors
- Alagar, Jayalakshmi, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania, United States
- Raiyani, Henish K., Temple University Health System Inc, Philadelphia, Pennsylvania, United States
- Gillespie, Avrum, Temple University Health System Inc, Philadelphia, Pennsylvania, United States
Introduction
Calciphylaxis is a life-threatening and progressive vasculopathy most often seen in end-stage kidney disease (ESKD) patients. It has an infrequent association with diffuse dermal angiomatosis (DDA), a rare, acquired vascular disorder.
Case Description
We describe a 59-year-old man on hemodialysis for 3 years for ESKD from Diabetes Mellitus. He also has morbid obesity, numerous failed arteriovenous grafts, and severe peripheral vascular disease with amputations and infections. He presented to the dermatology clinic for a 1-month history of non-healing, painful lesions on the left lower abdomen with recent rupture, malodor, and size increase. Based on macroscopic assessment, clinical context, and previous history of calciphylaxis adjacent to a brachial-axillary graft a few months prior, calciphylaxis was presumed. Skin biopsies were taken at multiple sites. The large number of small slit-like vessels stained with CD31, in conjunction with a Von Kossa stain lacking calcium deposition, favored a diagnosis of DDA. Out of concern for superimposed infection, levofloxacin and cephalexin were prescribed. The lesions completely healed 6 months after initiation of sodium thiosulfate, cinacalcet, a 2.0 mEq/L calcium dialysis bath, and care from a wound care specialist. Calcitriol and calcium acetate binders were discontinued.
Discussion
In calciphylaxis, arteriolar calcium deposition leads to skin and subcutis necrosis. An association with DDA has been described previously in 23 patients. To our knowledge, there was only one patient reported like ours, with clinical features simulating uremic calciphylaxis in the context of ESKD and histopathological findings consistent with DDA. Calciphylaxis may predispose to DDA by inducing low-grade ischemia or occluding larger dermal vessels to drive vascular endothelial growth factor-mediated angiogenesis. For both, managing ischemia, a shared driver of pathogenesis, is key. This includes pain control for calciphylaxis and reducing atherosclerosis and associated risk factors for DDA. In our patient, the combination of ESKD and severe peripheral vascular disease likely contributed to DDA. Our case underscores the continuing need for multi-disciplinary involvement in calciphylaxis work-up and management. In the absence of universally accepted diagnostic criteria or pathognomonic features, recognition of atypical presentations is essential.