Endotheliopathy: A continuum of hemolytic uremic syndrome due to mitomycin therapy

James A. Groff, Mark Kozak, John P. Boehmer, Trudy M. Demko, Jonathan R. Diamond

Research output: Contribution to journalArticlepeer-review

20 Scopus citations


Hemolytic uremic syndrome (HUS) is a rare, often fatal complication of mitomycin C therapy. It is generally accepted that HUS is, in part, caused by endothelial cell dysfunction. Endothelial cells modulate blood flow, blood pressure, and myointimal proliferation. Endothelial cells synthesize and release products that modulate vascular tone and regulate vascular smooth muscle cell growth. We describe a patient who developed HUS secondary to mitomycin C, resulting in end-stage renal disease and necessitating chronic hemodialysis. Over several months, the patient subsequently developed multisystem organ failure involving the heart, liver, and intestine that was associated with angiographically documented small, distal vessel occlusive disease and ultrasonographically identified coronary artery intimal hyperplasia. We propose that a diffuse ongoing endothelial cell dysfunction (ie, endotheliopathy) is the putative mechanism for this patient's clinical course. TO our knowledge, this continuum of HUS presenting as a multisystem, progressive disorder has not been previously reported.

Original languageEnglish (US)
Pages (from-to)280-284
Number of pages5
JournalAmerican Journal of Kidney Diseases
Issue number2
StatePublished - Feb 1997

All Science Journal Classification (ASJC) codes

  • Nephrology


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