Kidney - Fibrosis
comment:Renal (interstitial) fibrosis is associated with previous or ongoing injury to the renal parenchyma,such as that associated with chronic interstitial inflammation. The amount of fibrosis dependson the inciting condition, the amount of damage to the renal parenchyma, and the chronicity of the lesion. Fibrosis results from a complex interaction involving cytokines released by inflammatory cells, thedebatable influence of tubule epithelial-mesenchyme transition, and decreased removal of collagen due to inhibition of collagenolytic enzymes. Fibrosis appears as a slightly fibrillar, eosinophilic material in the interstitium ( Figure 1 and Figure 2 ). Fibrosis may result in progressive atrophy of the nephron in affected areas and/or dilation of renal tubules and Bowman’s space.
recommendation:If fibrosis is a primary change or is present with little or no inflammation, then it should be diagnosed and given a severity grade. When fibrosis is secondary to another process, such as inflammation, and both are present concurrently, the pathologist should use his or her judgment in deciding whether or not the fibrosis is prominent enough to warrant a separate diagnosis.
related links:Kidney - Infarct
Kidney - Inflammation
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Eddy AA. 1996. Molecular insights into renal interstitial fibrosis. J Am Soc Nephrol 7:2495-2508. Abstract: http://www.ncbi.nlm.nih.gov/pubmed/8989727
Frazier KS, Dube P, Paredes A, Styer E. 2000. Connective tissue growth factor expression in the rat remnant kidney model and association with tubular epithelial cells undergoing transdifferentiation. Vet Pathol 37:328-335. Full Text: http://vet.sagepub.com/content/37/4/328.full.pdf
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Yang J, Liu Y. 2001. Dissection of key events in tubular epithelial to myofibroblast transition and its implications in renal interstitial fibrosis. Am J Pathol 159:1465-1475. Full Text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1850509/
Web page last updated on: October 28, 2014