{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,23]],"date-time":"2026-04-23T23:27:52Z","timestamp":1776986872248,"version":"3.51.4"},"reference-count":46,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2005,10,6]],"date-time":"2005-10-06T00:00:00Z","timestamp":1128556800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["pathsocjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Pathology"],"published-print":{"date-parts":[[2005,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Proteinuria is associated with macrophage\u2010dependent interstitial fibrosis (IF). Osteopontin (OPN), a macrophage chemoattractant, may be involved in the transition of proteinuria to IF but protective properties have also been reported. To elucidate whether OPN may be involved in the proteinuria\u2010induced cascade of tubulointerstitial damage, renal expression of OPN was studied during the development of proteinuria\u2010induced renal damage and during anti\u2010proteinuric intervention with ACE inhibition (ACEi). First, the temporal relationships between proteinuria, interstitial OPN induction, and IF in adriamycin nephrosis (AN), a model of chronic proteinuria\u2010induced renal damage, were studied. Second, the effect of anti\u2010proteinuric treatment on OPN expression was investigated. The time course of OPN induction and markers of renal damage was studied in rats with unilateral AN at 6\u2010week intervals until week 30. In a second study, a renal biopsy was taken 6 weeks after induction of bilateral AN; subsequently, rats were treated with ACEi until termination (week 12). In unilateral AN, proteinuria developed gradually and stabilized at week 10. In proteinuric kidneys, OPN expression was induced from week 12 onwards. Simultaneously, a progressive increase in interstitial macrophages, \u03b1\u2010smooth muscle actin (\u03b1\u2010SMA), collagen type III, and focal glomerulosclerosis (FGS) was observed. In bilateral AN, ACEi reduced proteinuria and OPN protein and stabilized fibrosis. In untreated animals,\n                    <jats:italic>OPN<\/jats:italic>\n                    mRNA increased, with stable OPN protein and fibrosis and increased FGS. Thus, in AN, development of proteinuria is followed by up\u2010regulation of OPN along with markers of renal damage. The up\u2010regulation of OPN is reversible by anti\u2010proteinuric treatment without a corresponding reduction in fibrosis. Whereas these data are consistent with a role for OPN in the cascade of transition from proteinuria to fibrosis, intervention with ACEi showed that reduction of OPN does not attenuate established fibrosis. Copyright \u00a9 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.\n                  <\/jats:p>","DOI":"10.1002\/path.1856","type":"journal-article","created":{"date-parts":[[2005,10,6]],"date-time":"2005-10-06T10:46:47Z","timestamp":1128595607000},"page":"483-492","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Modulation of osteopontin in proteinuria\u2010induced renal interstitial fibrosis"],"prefix":"10.1002","volume":"207","author":[{"given":"Andrea B","family":"Kramer","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sharon D","family":"Ricardo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Darren J","family":"Kelly","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Femke","family":"Waanders","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Harry","family":"van Goor","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gerjan","family":"Navis","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,10,6]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199811123392007"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00874.x"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1042\/cs0900393"},{"issue":"1","key":"e_1_2_6_5_2","first-page":"47","article-title":"Prognostic value of the short\u2010term antiproteinuric response to ACE inhibition for prediction of GFR decline in patients with nondiabetic renal disease","volume":"4","author":"Wapstra FH","year":"1996","journal-title":"Exp Nephrol"},{"key":"e_1_2_6_6_2","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V104804"},{"key":"e_1_2_6_7_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00941.x"},{"key":"e_1_2_6_8_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00905.x"},{"key":"e_1_2_6_9_2","doi-asserted-by":"crossref","first-page":"409","DOI":"10.1111\/j.1399-0012.1998.tb00990.x","article-title":"Antiproteinuric efficacy of fosinopril after renal transplantation","volume":"12","author":"Lufft V","year":"1998","journal-title":"Clin Transplant"},{"key":"e_1_2_6_10_2","first-page":"115","article-title":"Long\u2010term prognosis of focal sclerosing glomerulonephritis. 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