| pubmed-article:21252520 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21252520 | lifeskim:mentions | umls-concept:C0017662 | lld:lifeskim |
| pubmed-article:21252520 | lifeskim:mentions | umls-concept:C0268743 | lld:lifeskim |
| pubmed-article:21252520 | lifeskim:mentions | umls-concept:C0332257 | lld:lifeskim |
| pubmed-article:21252520 | lifeskim:mentions | umls-concept:C0086272 | lld:lifeskim |
| pubmed-article:21252520 | pubmed:dateCreated | 2011-1-21 | lld:pubmed |
| pubmed-article:21252520 | pubmed:abstractText | Membranoproliferative glomerulonephritis (MPGN) is characterised by mesangial expansion and hypercellularity and capillary wall thickening with capillary wall and mesangial deposits of immunoglobulin and/or complement. Two main forms are described in humans: MPGN type I with subendothelial and mesangial electron-dense deposits on electron microscopy, and MPGN type II, or dense deposit disease, with electron dense transformation of the glomerular capillary wall. Spontaneous MPGN type I has been described in dogs and sheep in association with C3 deficiency. Induced models of MPGN type I have been described in mice with cryoglobulinaemia. Glomerulonephritis resembling MPGN type II has occurred spontaneously in pigs that have a genetic deficiency of the complement control protein factor H. The animals develop capillary wall deposits of C3 before birth. Mice have been genetically engineered with a deficiency of factor H and similarly develop glomerular capillary wall C3 with MPGN. This model has been used to study both pathogenesis and therapeutic interventions. In particular, MPGN associated with factor H deficiency is absolutely dependent on both the ability to activate C3 and on the ability of factor I to cleave C3b. There is an important role for C5 activation in the development of glomerular inflammation in this model. Factor H dysfunction is associated with an increased susceptibility to complement-activating nephrotoxic insults and in these scenarios C5 activation appears to play a major role in mediating glomerular injury. | lld:pubmed |
| pubmed-article:21252520 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21252520 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21252520 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:21252520 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21252520 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21252520 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21252520 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21252520 | pubmed:issn | 1662-2782 | lld:pubmed |
| pubmed-article:21252520 | pubmed:author | pubmed-author:PickeringMatt... | lld:pubmed |
| pubmed-article:21252520 | pubmed:author | pubmed-author:CookTerenceT | lld:pubmed |
| pubmed-article:21252520 | pubmed:author | pubmed-author:VernonKatheri... | lld:pubmed |
| pubmed-article:21252520 | pubmed:copyrightInfo | Copyright © 2011 S. Karger AG, Basel. | lld:pubmed |
| pubmed-article:21252520 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21252520 | pubmed:volume | 169 | lld:pubmed |
| pubmed-article:21252520 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21252520 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21252520 | pubmed:pagination | 198-210 | lld:pubmed |
| pubmed-article:21252520 | pubmed:meshHeading | pubmed-meshheading:21252520... | lld:pubmed |
| pubmed-article:21252520 | pubmed:meshHeading | pubmed-meshheading:21252520... | lld:pubmed |
| pubmed-article:21252520 | pubmed:meshHeading | pubmed-meshheading:21252520... | lld:pubmed |
| pubmed-article:21252520 | pubmed:meshHeading | pubmed-meshheading:21252520... | lld:pubmed |
| pubmed-article:21252520 | pubmed:meshHeading | pubmed-meshheading:21252520... | lld:pubmed |
| pubmed-article:21252520 | pubmed:meshHeading | pubmed-meshheading:21252520... | lld:pubmed |
| pubmed-article:21252520 | pubmed:meshHeading | pubmed-meshheading:21252520... | lld:pubmed |
| pubmed-article:21252520 | pubmed:meshHeading | pubmed-meshheading:21252520... | lld:pubmed |
| pubmed-article:21252520 | pubmed:meshHeading | pubmed-meshheading:21252520... | lld:pubmed |
| pubmed-article:21252520 | pubmed:meshHeading | pubmed-meshheading:21252520... | lld:pubmed |
| pubmed-article:21252520 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21252520 | pubmed:articleTitle | Experimental models of membranoproliferative glomerulonephritis, including dense deposit disease. | lld:pubmed |
| pubmed-article:21252520 | pubmed:affiliation | Centre for Complement and Inflammation Research, Department of Medicine, Imperial College, London, UK. | lld:pubmed |
| pubmed-article:21252520 | pubmed:publicationType | Journal Article | lld:pubmed |
