Vascular ossification – calcification in metabolic syndrome, type 2 diabetes mellitus, chronic kidney disease, and calciphylaxis – calcific uremic arteriolopathy: the emerging role of sodium thiosulfate

Melvin R Hayden¹ , Suresh C Tyagi² , Lisa Kolb³ , James R Sowers⁴ and Ramesh Khanna⁵

¹Department of Family and Community Medicine University of Missouri Columbia, Missouri PO BOX 1140 Lk. Rd. 5-87 Camdenton, Missouri 65020 USA

²Department of Physiology and Biophysics 500 South Preston Street University of Louisville Louisville, Kentucky 40292 USA

³Capital City Medical Associates 1505 Southwest Blvd Jefferson City, Missouri 65109 USA

⁴Department of Internal Medicine University of Missouri School of Medicine Health Sciences Center, MA410, DC043.00 Columbia, Missouri 65212 USA

⁵Department of Internal Medicine University of Missouri School of Medicine Health Sciences Center, MA 436 Columbia, Missouri 65212 USA

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Cardiovascular Diabetology 2005, 4:4doi:10.1186/1475-2840-4-4


Published:	18 March 2005

Abstract

Background

Vascular calcification is associated with metabolic syndrome, diabetes, hypertension, atherosclerosis, chronic kidney disease, and end stage renal disease. Each of the above contributes to an accelerated and premature demise primarily due to cardiovascular disease. The above conditions are associated with multiple metabolic toxicities resulting in an increase in reactive oxygen species to the arterial vessel wall, which results in a response to injury wound healing (remodeling). The endothelium seems to be at the very center of these disease processes, acting as the first line of defense against these multiple metabolic toxicities and the first to encounter their damaging effects to the arterial vessel wall.

Results

The pathobiomolecular mechanisms of vascular calcification are presented in order to provide the clinician – researcher a database of knowledge to assist in the clinical management of these high-risk patients and examine newer therapies. Calciphylaxis is associated with medial arteriolar vascular calcification and results in ischemic subcutaneous necrosis with vulnerable skin ulcerations and high mortality. Recently, this clinical syndrome (once thought to be rare) is presenting with increasing frequency. Consequently, newer therapeutic modalities need to be explored. Intravenous sodium thiosulfate is currently used as an antidote for the treatment of cyanide poisioning and prevention of toxicities of cisplatin cancer therapies. It is used as a food and medicinal preservative and topically used as an antifungal medication.

Conclusion

A discussion of sodium thiosulfate's dual role as a potent antioxidant and chelator of calcium is presented in order to better understand its role as an emerging novel therapy for the clinical syndrome of calciphylaxis and its complications.