Diabetic Nephropathy and Proximal Tubular Damage

Diabetic nephropathy (DN) is a major cause of uremia in developed societies. Inflammation is emerging as an important mechanism for its pathogenesis and progression. Herein, we review 4 recently described cellular receptors that have been shown to mediate diabetic interstitial kidney disease. Peroxi...

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Veröffentlicht in:Journal of renal nutrition 2015-03, Vol.25 (2), p.230-233
Hauptverfasser: Tang, Sydney C.W., MD, PhD, Yiu, Wai Han, PhD, Lin, Miao, MD, PhD, Lai, Kar Neng, MD, DSc
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Sprache:eng
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Zusammenfassung:Diabetic nephropathy (DN) is a major cause of uremia in developed societies. Inflammation is emerging as an important mechanism for its pathogenesis and progression. Herein, we review 4 recently described cellular receptors that have been shown to mediate diabetic interstitial kidney disease. Peroxisome proliferator-activated receptor-γ attenuates STAT-1 activation and has shown promise in renoprotection. Its clinical utility is limited mainly by fluid retention through upregulation of sodium–hydrogen exchanger-3 and aquaporin-1 channels in the proximal tubule. The bradykinin receptor 2 of the kallikrein–kinin system has been shown to mediate diabetic kidney injury and its blockade conferred renoprotective effects in animal models of DN. The related protease-activated receptor, especially receptor 4, has recently been shown to participate in DN. Further studies are required to confirm its role. Finally, the toll-like receptor, especially TLR4 and TLR2, has been verified in multiple models to be a significant sensor of and reactor to hyperglycemia and other diabetic substrates that orchestrate interstitial inflammation in DN.
ISSN:1051-2276
1532-8503
DOI:10.1053/j.jrn.2014.10.020