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Nephrol Dial Transplant (1999) 14: 2800-2803
© 1999 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

The role of Chlamydia in coronary heart disease—fact or fiction?

Thomas Quaschning and Christoph Wanner

Department of Cardiovascular Research, University of Zürich, Zürich, Switzerland and Division of Nephrology, University Hospital, University of Würzburg, Würzburg, Germany

Correspondence and offprint requests to: Thomas Quaschning, Department of Cardiovascular Research, Institute of Physiology, Winterthurer Str. 193, CH-8053Zürich, Switzerland.

Introduction

Atherosclerosis is an inflammatory disease. A number of traditional and non-traditional risk factors related to atherogenesis have been identified. Much of the attributable risk remains unexplained, however, the complex aetiology of atherosclerosis has not yet been entirely dissected. Pathologically, atherosclerosis involves injury, inflammation, infiltration, degeneration, and thrombosis [1]. In patients at risk a role for the local inflammatory response in plaques as well as systemic inflammation has been recognized and documented [2]. Several authors raised the possibility that infectious agents directly or indirectly trigger the cascade of biological and biochemical reactions leading to inflammation, atherosclerosis, and vascular thrombotic events [3].

A group of infective agents called Chlamydia has given pathologists a series of surprises. Once known mainly for causing illness in parrots, they turned out to be responsible for several sexually transmitted diseases. Distinct from . . . [Full Text of this Article]

Where is the link between atherosclerosis and C. pneumoniae?

Does histopathology support serology?

Which mechanisms could be pathophysiologically relevant?

What can we learn from therapeutic studies?

How can causality be proved?

Is there a link in the renal patient?

Conclusions

References


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