Calcific uremic arteriolopathy--the argument for hyperbaric oxygen and sodium thiosulfate
Related Experiment Video
Updated: Jun 14, 2026

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
Published on: November 7, 2017
Natasha M Rogers1, P Toby H Coates
1Department of Nephrology and Transplantation Services, The Queen Elizabeth Hospital, Woodville, South Australia, Australia.
Abstract:
Calcific uremic arteriolopathy (CUA) is a rare event primarily in patients with end-stage kidney disease which is characterized by small vessel media calcification, panniculitis, dermal necrosis producing exquisitely painful difficult to heal wounds. Mortality rates may be as high as 80%, predominantly due to intervening sepsis. This clinical phenomenon is being increasingly reported and treated with a widening number of agents. Recent case reports highlight the benefit of two modalities that have been employed as adjuvant therapy with significant success in the treatment of CUA. Hyperbaric oxygen (HBO) is capable of enhancing oxygen delivery to the ulcerating lesions that characterize CUA. Chronic hypoxia can be reversed using HBO to facilitate growth factor production, neoangiogenesis, fibroblast proliferation, and collagen synthesis that may facilitate all aspects of wound healing. Sodium thiosulfate appears to chelate and solubilize calcium ions, reducing the calcium vascular load that appears to participate in the obliterative small vessel disease. There is a rapid analgesic effect and slower regression of cutaneous calcific nodules. The authors advocate for aggressive treatment of CUA, using all available therapies.
Related Concept Videos
Treatment for Pulmonary Arterial Hypertension: Oxygen Therapy for Respiratory Failure
Oxygen therapy is vital in increasing and maintaining blood oxygen levels in PAH patients. As a result, it aids in reducing fatigue, improving...
Venous Thrombosis III: Interprofessional Care
Peripheral Artery Disease III: Interprofessional Care
Acute Kidney Injury IV: Diagnostic Studies and Prevention
Ischemic Stroke ll: Pathophysiology
Heart Failure VI: Adjunct Therapies