NDT Advance Access originally published online on July 22, 2006
Nephrology Dialysis Transplantation 2006 21(10):2690-2694; doi:10.1093/ndt/gfl369
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
The protean face of sarcoidosis revisited
Medical Faculty of the Charité, Franz Volhard Clinic and Department of Pathology, HELIOS Klinikum-Berlin, Germany
Correspondence and offprint requests to: Ralph Kettritz, MD, Franz Volhard Clinic, Wiltbergstrasse 50, 13122 Berlin, FRG. Email: kettritz@charite.de
Keywords: glomerulopathy; granulomatosis; hypocomplementaemia; interstitial nephritis; immunotactoid; kidney; sarcoidosis
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| Introduction |
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Sarcoidosis is a multisystem disorder characterized by non-caseating, epithelioid granulomas. Sarcoidosis predominantly affects the lungs; however, almost every organ can be involved including the kidneys. In fact, the absense of pulmonary findings by no means excludes sarcoidosis. The aetiology of the disease is still not fully elucidated. On the one hand, we have strong evidence from various sources suggesting that increased macrophage and CD4 helper T-cell activity results in accelerated inflammation. This extensive local response ultimately causes the granuloma formation. On the other hand, sarcoidosis patients show suppressed immune responses to in vivo and in vitro antigen challenges, such as tuberculin. The latter state of affairs is in stark contrast to the accelarated inflammation hypothesis and suggests an anergic state. Anergy is believed to be responsible for the increased risk of sarcoidosis patients to aquire opportunistic infections and cancer.
Interesting new findings from affected patients show that expanded CD4+CD25bright
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