{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T15:02:30Z","timestamp":1784127750380,"version":"3.55.0"},"reference-count":25,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2014,12,23]],"date-time":"2014-12-23T00:00:00Z","timestamp":1419292800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Nephrology"],"published-print":{"date-parts":[[2015,1]]},"abstract":"Abstract<\/jats:title>Background<\/jats:title>In glomerulonephritis the final common pathway to end\u2010stage renal disease (ESRD)<\/jats:styled-content> is tubulo\u2010interstitial damage (TID<\/jats:styled-content>) whose main determinants are proteinuria and hypoxia consequent to haemodynamic and vascular alterations that reduce interstitial blood flow. Since oxygen tension is difficult to measure in human disease, arteriolar hyalinosis and arterial hypertension have been considered as possible surrogate markers of interstitial hypoxia.<\/jats:p><\/jats:sec>Methods<\/jats:title>The relationship between TID<\/jats:styled-content> and arteriolar hyalinosis and arterial hypertension was evaluated in 132 IgA<\/jats:styled-content> nephropathy (IgAN<\/jats:styled-content>) and 79 idiopathic membranous nephropathy (IMN<\/jats:styled-content>) patients. At biopsy tubulo\u2010interstitial damage and arteriolar hyalinosis score were semi\u2010quantitatively evaluated; urinary protein\/creatinine ratio (P<\/jats:styled-content>\/C<\/jats:styled-content>), fractional excretion (FE<\/jats:styled-content>) of \u03b11\u2010microglobulin, urinary \u03b2\u2010NAG<\/jats:styled-content>\/creatinine ratio (NAG<\/jats:styled-content>\/C<\/jats:styled-content>\/eGFR<\/jats:styled-content>) and urinary SDS\u2010PAGE<\/jats:styled-content> pattern were measured.<\/jats:p><\/jats:sec>Results<\/jats:title>In IgAN<\/jats:styled-content> arteriolar hyalinosis (AH<\/jats:styled-content>) score correlates with TID<\/jats:styled-content> score (P<\/jats:italic>\u2009<\u20090.0001), FE<\/jats:styled-content> \u03b11m (P<\/jats:italic>\u2009=\u20090.004) and NAG<\/jats:styled-content>\/C<\/jats:styled-content>\/eGFR<\/jats:styled-content> (P<\/jats:italic>\u2009=\u20090.001), but not with P<\/jats:styled-content>\/C<\/jats:styled-content> (P<\/jats:italic>\u2009=\u20090.10). Patients with or without AH<\/jats:styled-content> were different in terms of global glomerulosclerosis (GGS<\/jats:styled-content>: P<\/jats:italic>\u2009<\u20090.001), TID<\/jats:styled-content> score (P<\/jats:italic>\u2009<\u20090.001), FE<\/jats:styled-content> \u03b11m (P<\/jats:italic>\u2009=\u20090.015), NAG<\/jats:styled-content>\/C<\/jats:styled-content>\/eGFR<\/jats:styled-content> (P<\/jats:italic>\u2009=\u20090.002), but not of P<\/jats:styled-content>\/C<\/jats:styled-content> (P<\/jats:italic>\u2009=\u20090.19). In IMN AH<\/jats:styled-content> score correlates with TID<\/jats:styled-content> score (P<\/jats:italic>\u2009<\u20090.0001), FE\u03b11m (P<\/jats:italic>\u2009=\u20090.04), NAG<\/jats:styled-content>\/C<\/jats:styled-content>\/eGFR<\/jats:styled-content> (P<\/jats:italic>\u2009=\u20090.001), SDS\u2010PAGE<\/jats:styled-content> pattern (P<\/jats:italic>\u2009=\u20090.018), but not with P<\/jats:styled-content>\/C<\/jats:styled-content> (P<\/jats:italic>\u2009=\u20090.10). Patients with or without AH<\/jats:styled-content> were different in term of GGS<\/jats:styled-content>% (P<\/jats:italic>\u2009=\u20090.05), TID<\/jats:styled-content> score (P<\/jats:italic>\u2009=\u20090.001), FE<\/jats:styled-content> \u03b11m (P<\/jats:italic>\u2009=\u20090.039), NAG<\/jats:styled-content>\/C<\/jats:styled-content>\/eGFR<\/jats:styled-content> (P<\/jats:italic>\u2009=\u20090.001), SDS\u2010PAGE<\/jats:styled-content> pattern (P<\/jats:italic>\u2009=\u20090.02), but not of P<\/jats:styled-content>\/C<\/jats:styled-content> (P<\/jats:italic>\u2009=\u20090.065). Similar results for normal versus<\/jats:italic> high blood pressure.<\/jats:p><\/jats:sec>Conclusions<\/jats:title>Arteriolar hyalinosis and arterial hypertension, associated with TID<\/jats:styled-content> and GGS<\/jats:styled-content>, factors that reduce interstitial capillary bed and blood flow, may be considered as reliable surrogate markers of hypoxia and co\u2010determinants of TID<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/nep.12339","type":"journal-article","created":{"date-parts":[[2014,9,17]],"date-time":"2014-09-17T07:42:10Z","timestamp":1410939730000},"page":"11-17","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["Arteriolar hyalinosis and arterial hypertension as possible surrogate markers of reduced interstitial blood flow and hypoxia in glomerulonephritis"],"prefix":"10.1111","volume":"20","author":[{"given":"Claudio","family":"Bazzi","sequence":"first","affiliation":[{"name":"D'Amico Foundation for Renal Disease Research Milan Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gilda","family":"Stivali","sequence":"additional","affiliation":[{"name":"Baxter S.p.A. 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