BACKGROUND: Advanced glycation endproducts (AGEs) are believed to mediate long-term complications in diabetes mellitus. In this context we studied the expression of the receptor for AGEs (RAGE) in the kidney of patients with a variety of different renal diseases. METHODS: RAGE was detected by immunocytochemistry in renal biopsies. We compared the staining for RAGE in nine patients with diabetic nephropathy, 20 with inflammatory and/or immune complex and 10 with non-inflammatory renal diseases. Normal renal tissue from seven patients with tumour nephrectomies served as controls. RESULTS: In controls the only cells expressing RAGE constitutively were interstitial cells and vascular smooth muscle cells (6/7), while distal tubular cells were rarely positive (1/7). Endothelial cells of arteries/arterioles, glomerular endothelial cells, podocytes, and capsular epithelial cells were consistently negative. In diabetic nephropathy, inflammatory and/or immune complex, and non-inflammatory renal diseases, all cell types mentioned above became positive for RAGE. Whilst the distribution of RAGE in the tissue was quite similar, staining intensity in inflammatory and/or immune complex diseases was higher than in diabetic nephropathy. CONCLUSION: RAGE induction in the kidney is not specific for diabetic nephropathy and occurs in other types of renal diseases as well.
BACKGROUND: Advanced glycation endproducts (AGEs) are believed to mediate long-term complications in diabetes mellitus. In this context we studied the expression of the receptor for AGEs (RAGE) in the kidney of patients with a variety of different renal diseases. METHODS:RAGE was detected by immunocytochemistry in renal biopsies. We compared the staining for RAGE in nine patients with diabetic nephropathy, 20 with inflammatory and/or immune complex and 10 with non-inflammatory renal diseases. Normal renal tissue from seven patients with tumour nephrectomies served as controls. RESULTS: In controls the only cells expressing RAGE constitutively were interstitial cells and vascular smooth muscle cells (6/7), while distal tubular cells were rarely positive (1/7). Endothelial cells of arteries/arterioles, glomerular endothelial cells, podocytes, and capsular epithelial cells were consistently negative. In diabetic nephropathy, inflammatory and/or immune complex, and non-inflammatory renal diseases, all cell types mentioned above became positive for RAGE. Whilst the distribution of RAGE in the tissue was quite similar, staining intensity in inflammatory and/or immune complex diseases was higher than in diabetic nephropathy. CONCLUSION:RAGE induction in the kidney is not specific for diabetic nephropathy and occurs in other types of renal diseases as well.
Authors: Birgit Liliensiek; Markus A Weigand; Angelika Bierhaus; Werner Nicklas; Michael Kasper; Stefan Hofer; Jens Plachky; Herman-Josef Gröne; Florian C Kurschus; Ann Marie Schmidt; Shi Du Yan; Eike Martin; Erwin Schleicher; David M Stern; G ünterJ Hämmerling G; Peter P Nawroth; Bernd Arnold Journal: J Clin Invest Date: 2004-06 Impact factor: 14.808
Authors: Angelika Bierhaus; Per M Humpert; Michael Morcos; Thoralf Wendt; Triantafyllos Chavakis; Bernd Arnold; David M Stern; Peter P Nawroth Journal: J Mol Med (Berl) Date: 2005-08-24 Impact factor: 4.599
Authors: M D Oldfield; L A Bach; J M Forbes; D Nikolic-Paterson; A McRobert; V Thallas; R C Atkins; T Osicka; G Jerums; M E Cooper Journal: J Clin Invest Date: 2001-12 Impact factor: 14.808
Authors: Y Yamamoto; I Kato; T Doi; H Yonekura; S Ohashi; M Takeuchi; T Watanabe; S Yamagishi; S Sakurai; S Takasawa; H Okamoto; H Yamamoto Journal: J Clin Invest Date: 2001-07 Impact factor: 14.808