| pubmed-article:19776779 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19776779 | lifeskim:mentions | umls-concept:C0549526 | lld:lifeskim |
| pubmed-article:19776779 | lifeskim:mentions | umls-concept:C0699748 | lld:lifeskim |
| pubmed-article:19776779 | lifeskim:mentions | umls-concept:C0680243 | lld:lifeskim |
| pubmed-article:19776779 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:19776779 | pubmed:dateCreated | 2009-9-24 | lld:pubmed |
| pubmed-article:19776779 | pubmed:abstractText | The two most common HIV-associated renal diseases, HIV-associated nephropathy and HIV immune-complex kidney disease, share the common pathologic finding of hyperplasia within the glomerulus. Podocyte injury is central to the pathogenesis of these diseases; however, the source of the proliferating glomerular epithelial cell remains a topic of debate. Parenchymal injury has been linked to direct infection of renal epithelial cells by HIV-1, although the mechanism of viral entry into this non-lymphoid compartment is unclear. Although transgenic rodent models have provided insight into viral proteins responsible for inducing renal disease, such models have substantial limitations. Rodent HIV-1 models, for instance, cannot replicate all features of immune activation, a process that could have an important role in the pathogenesis of the HIV-associated renal diseases. | lld:pubmed |
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