Presentation
Multiple bilateral hand gangrenous ulcers and digital infarcts with recent right middle finger resection. History of end stage renal on peritoneal dialysis due to IgA nephropathy.
Patient Data
Bilateral vascular calcification. Loss of bone beyond distal right middle phalanx. No focus of bone or joint destruction.
Bilateral vascular calcification. No focus of bone or joint destruction.
Heavily calcified brachial arteries with no evidence of arterial occlusion to the level of the antebrachial fossa. Distally, bilateral radial and ulnar arteries are grossly calcified with only segmental arterial flow visualized. Unable to exclude occluded segment.
Case Discussion
The underlying etiology for the digital infarcts and vascular calcification is not known in this patient.
The prevalence and severity of vascular calcification increases with advancing disease and falling renal function/glomerular filtration rate 1. In chronic kidney disease, vascular calcification occurs in both the intimal and medial layer of the vessel, however it is far more common in the medial layer 2. This process is multifactorial and includes age, time on dialysis, disruption in mineral homeostasis (hypercalcemia and hyperphosphatemia), vitamin D therapy, diabetes, hypercholesterolemia, vitamin k antagonists, uremia and oxidative stress 1-4. Once thought to be due to elevated phosphate and calcium, there is now an appreciation of an active cell mediated process due to shifts in key inhibitors and inducers that favor a osteochondrogenic phenotype in vascular smooth muscle cells 1-4.
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