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Article: A relationship between proteinuria and acute tubulointerstitial disease in rats with experimental nephrotic syndrome

TitleA relationship between proteinuria and acute tubulointerstitial disease in rats with experimental nephrotic syndrome
Authors
Issue Date1991
Citation
American Journal of Pathology, 1991, v. 138, n. 5, p. 1111-1123 How to Cite?
AbstractThe relationship between tubulointerstitial nephritis and proteinuria was characterized in experimental nephrosis in rats. In one group, proteinuria induced by aminonucleoside of puromycin (PAN) was reduced by using an 8% protein diet and adding the angiotensin I-converting enzyme (ACE) inhibitor enalapril to the drinking water. Two control groups were injected with saline and PAN, respectively, and fed a 27% protein diet. The first group had significantly reduced albuminuria and a definite attenuation of tubular cell injury. There was a strong positive correlation between the number of interstitial macrophages and albuminuria. The beneficial effect was reproduced by dietary-protein restriction alone, whereas ACE inhibition alone had an insignificant effect on the degree of proteinuria. Depletion of circulating T lymphocytes in one group of nephrotic rats eliminated interstitial lymphocytes but did not affect interstitial macrophage influx. Inhibition of the in situ proliferation of resident interstitial macrophages by unilateral kidney irradiation failed to change the intensity of the macrophage infiltration. Treatment of rats with sodium maleate produced proximal tubular cell toxicity but interstitial inflammation did not develop, suggesting that the latter is not a nonspecific response to tubular injury. These studies demonstrate a strong relationship between tubulointerstitial nephritis and the severity of proteinuria in experimental nephrosis.
Persistent Identifierhttp://hdl.handle.net/10722/205686
ISSN
2015 Impact Factor: 4.206
2015 SCImago Journal Rankings: 2.653
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorEddy, AA-
dc.contributor.authorMcCulloch, L-
dc.contributor.authorLiu, E-
dc.contributor.authorAdams, J-
dc.date.accessioned2014-10-06T08:02:12Z-
dc.date.available2014-10-06T08:02:12Z-
dc.date.issued1991-
dc.identifier.citationAmerican Journal of Pathology, 1991, v. 138, n. 5, p. 1111-1123-
dc.identifier.issn0002-9440-
dc.identifier.urihttp://hdl.handle.net/10722/205686-
dc.description.abstractThe relationship between tubulointerstitial nephritis and proteinuria was characterized in experimental nephrosis in rats. In one group, proteinuria induced by aminonucleoside of puromycin (PAN) was reduced by using an 8% protein diet and adding the angiotensin I-converting enzyme (ACE) inhibitor enalapril to the drinking water. Two control groups were injected with saline and PAN, respectively, and fed a 27% protein diet. The first group had significantly reduced albuminuria and a definite attenuation of tubular cell injury. There was a strong positive correlation between the number of interstitial macrophages and albuminuria. The beneficial effect was reproduced by dietary-protein restriction alone, whereas ACE inhibition alone had an insignificant effect on the degree of proteinuria. Depletion of circulating T lymphocytes in one group of nephrotic rats eliminated interstitial lymphocytes but did not affect interstitial macrophage influx. Inhibition of the in situ proliferation of resident interstitial macrophages by unilateral kidney irradiation failed to change the intensity of the macrophage infiltration. Treatment of rats with sodium maleate produced proximal tubular cell toxicity but interstitial inflammation did not develop, suggesting that the latter is not a nonspecific response to tubular injury. These studies demonstrate a strong relationship between tubulointerstitial nephritis and the severity of proteinuria in experimental nephrosis.-
dc.languageeng-
dc.relation.ispartofAmerican Journal of Pathology-
dc.titleA relationship between proteinuria and acute tubulointerstitial disease in rats with experimental nephrotic syndrome-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid2024704-
dc.identifier.scopuseid_2-s2.0-0025910792-
dc.identifier.volume138-
dc.identifier.issue5-
dc.identifier.spage1111-
dc.identifier.epage1123-
dc.identifier.isiWOS:A1991FK71700008-

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