Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/133925
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dc.titleRenal tubular antiproteinase (alpha-1-antitrypsin and alpha-1-antichymotrypsin) response in tubulo-interstitial damage
dc.contributor.authorKhan, T.N.
dc.contributor.authorSinniah, R.
dc.date.accessioned2016-12-20T08:41:33Z
dc.date.available2016-12-20T08:41:33Z
dc.date.issued1993
dc.identifier.citationKhan, T.N., Sinniah, R. (1993). Renal tubular antiproteinase (alpha-1-antitrypsin and alpha-1-antichymotrypsin) response in tubulo-interstitial damage. Nephron 65 (2) : 232-239. ScholarBank@NUS Repository.
dc.identifier.issn00282766
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/133925
dc.description.abstractWe studied the role of proteinase inhibitors (Pls) α1-antitrypsin and α-antichymotrypsin in relation to lysozyme (LZM), and membrane attack complex (C5b-9) in renal tubular damage by immunohistochemical techniques. Fifty-five cases, including 45 patients with glomerular diseases, and 10 controls were studied. The patients were divided into two groups; one with tubulo-interstitial lesions (TILs; 30 cases), and the other without (15 cases). Significant antiproteinase response was observed in the proximal tubules in both disease groups, indicating that they were subjected to proteolytc attack. This response correlated with proteinuria and occurred in tubules which showed protein reabsorption as demonstrated by the presence of LZM staining in consecutive serial sections. Increased deposition of membrane attack complex (C5b-9) was observed in the disease group with TILs, indicating direct damage to cell membranes. C5b-9 may also generate oxygen species, potent inhibitors of Pls, which allow the proteases to cause tubular damage.
dc.subjectα1-antichymotrypsin
dc.subjectα1-antitrypsin
dc.subjectLysozyme
dc.subjectProteases
dc.subjectProteinase inhibitors
dc.subjectTubulo-interstitial damage
dc.typeArticle
dc.contributor.departmentPATHOLOGY
dc.description.sourcetitleNephron
dc.description.volume65
dc.description.issue2
dc.description.page232-239
dc.description.codenNPRNA
dc.identifier.isiutNOT_IN_WOS
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