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Rheumatology 2006 45(Supplement 3):iii39-iii41; doi:10.1093/rheumatology/kel277
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© The Author 2006. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Endothelin in human autoimmune diseases with renal involvement

W. Neuhofer and D. Pittrow1

Department of Physiology and Medical Clinic Innenstadt, University of Munich, Munich and 1Institute for Clinical Pharmacology, Technical University of Dresden, Dresden, Germany.

Correspondence to: PD Dr Wolfgang Neuhofer, Department of Physiology, University of Munich, Pettenkoferstrasse 12, D-80336 Munich, Germany. E-mail: Wolfgang.Neuhofer{at}med.uni-muenchen.de

Endothelin (ET)-1 is a potent renal vasoconstrictor with pro-inflammatory, profibrotic and mitogenic potential. Animal studies support a pathogenetic contribution of ET-1 and its cognate receptors in several renal manifestations of autoimmune disorders. However, data in humans are limited. The present minireview thus summarizes the observations available in humans. Similar to animal models, ET-1 is overexpressed in glomerular and tubulointerstitial lesions, which is reflected by an increased urinary excretion of ET-1. Since antagonizing the ET system has beneficial effects in experimental models, this approach may be translated to the human kidney, thus counteracting vasoconstriction, inflammation and extracellular matrix deposition during the course of human autoimmune disease.


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