{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T20:17:25Z","timestamp":1761164245523,"version":"build-2065373602"},"reference-count":30,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2005,6,15]],"date-time":"2005-06-15T00:00:00Z","timestamp":1118793600000},"content-version":"vor","delay-in-days":6771,"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":[[1986,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Fixed anionic charges in the mammalian glomerulus, on both the basement membrane and the eptihelial cell foot processes, are believed to form an important part of the glomerular filtration barrier. There is good evidence that their loss causes proteinuria. The charges can be visualized ultrastructurally using cationic dyes, but the requirement of these techniques for perfusion or immersion of fresh tissue has largely confined such studies to experimental models.<\/jats:p>\n                  <jats:p>We have extended the widely used polyethyleneimine technique, to study the charge of glomerular basement membranes in human tissue reprocessed out of paraffin blocks up to 10 years old. We studied selected cases of glomerular disease, where the diagnosis was not in any doubt. In the majority of diseases studied, a continuous charge layer persisted despite severe abnormalities of the basement membrane. Two exceptions were found. In amyloidosis, accumulation of fibrils was associated with a considerable decrease or loss of stainable basement membrane charge. In S.L.E., numerous small defects in the charge layer were noted.<\/jats:p>\n                  <jats:p>The persistence of charge is contrary to reported findings in several animal models of glomerular disease, including puromycin nephrosis, Heymann nephritis and streptozotocin diabetes. Although this method is not subject to precise quantitative analysis, we conclude that in the majority of cases, proteinuria in man is not caused by an extensive loss of glomerular basement membrane anionic charge.<\/jats:p>","DOI":"10.1002\/path.1711500406","type":"journal-article","created":{"date-parts":[[2005,6,22]],"date-time":"2005-06-22T10:44:47Z","timestamp":1119437087000},"page":"267-278","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Basement membrane charge in human glomerular disease"],"prefix":"10.1002","volume":"150","author":[{"given":"Peter N.","family":"Furness","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David R.","family":"Turner","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Roger E.","family":"Cotton","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,6,15]]},"reference":[{"key":"e_1_2_1_2_2","first-page":"7","article-title":"Biophysiology of glomerular filtration and proteinuria","volume":"51","author":"Kanwar YS","year":"1984","journal-title":"Lab Invest"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1984.2"},{"key":"e_1_2_1_4_2","first-page":"177","article-title":"Removal of sulfated (heparan sulfate) or nonsulfated (sialic acid) glycosaminoglycans results increased permeability of the glomerular basement membrane to 125I\u2010bovine serum albumin","volume":"47","author":"Rosenzweig LJ","year":"1982","journal-title":"Lab Invest"},{"key":"e_1_2_1_5_2","first-page":"505","article-title":"Loss of anionic sites from the glomerular basement membrane in aminonucleoside nephrosis","volume":"39","author":"Caulfield JP","year":"1978","journal-title":"Lab Invest"},{"key":"e_1_2_1_6_2","first-page":"649","article-title":"Glomerular polyanion; alteration in aminonucleoside nephrosis","volume":"23","author":"Michael AF","year":"1970","journal-title":"Lab Invest"},{"key":"e_1_2_1_7_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF02890171"},{"key":"e_1_2_1_8_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF02890122"},{"key":"e_1_2_1_9_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00495634"},{"key":"e_1_2_1_10_2","first-page":"477","article-title":"Glomerular sialic acid and proteinuria in human renal disease","volume":"28","author":"Blau EB","year":"1973","journal-title":"Lab Invest"},{"key":"e_1_2_1_11_2","first-page":"99","article-title":"Ultrastructural assessment by colloidal iron of the distribution and localization of anionic sites in human glomerulonephritides","volume":"102","author":"Hirsch HZ","year":"1981","journal-title":"Am J Pathol"},{"key":"e_1_2_1_12_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.76.3.1303"},{"key":"e_1_2_1_13_2","doi-asserted-by":"publisher","DOI":"10.1177\/26.8.690407"},{"key":"e_1_2_1_14_2","first-page":"503","article-title":"Alteration in the distribution of alcian blue staining fibrillar anionic sites in the glomerular basement membrane in aminonucleoside nephrosis","volume":"40","author":"Caufield JP","year":"1979","journal-title":"Lab Invest"},{"key":"e_1_2_1_15_2","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.81.1.137"},{"key":"e_1_2_1_16_2","first-page":"375","article-title":"Detachment of endothelium and epithelium from glomerular basement membrane produced by perfusion with neuraminidase","volume":"42","author":"Kanwar YS","year":"1980","journal-title":"Lab Invest"},{"key":"e_1_2_1_17_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198310273091701"},{"key":"e_1_2_1_18_2","first-page":"474","article-title":"Glomerular anonic site distribution in nonproteinuric rats. A computer assisted morphometric analysis","volume":"121","author":"Pilia PA","year":"1985","journal-title":"Am J Pathol"},{"key":"e_1_2_1_19_2","first-page":"547","article-title":"Glomerular permeability. 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