Abstract
The pathogenesis of renal interstitial fibrosis leading eventually to renal failure is highly debatable. Whereas the so-called tubular hypothesis, involving an increased tubular uptake of potentially toxic substances that induce a variety of cytokines, growth factors, and profibrogenic factors, is based to a large extent on cell-culture studies, the glomerular hypothesis is based mainly on careful morphological observations. Unraveling the pathways appears to be extremely complex, but in vivo studies appear to offer the most reliable results.
Cite
CITATION STYLE
Christensen, E. I., & Verroust, P. J. (2008). Interstitial fibrosis: Tubular hypothesis versus glomerular hypothesis. Kidney International. Nature Publishing Group. https://doi.org/10.1038/ki.2008.421
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