Abstract:
BACKGROUND:Primary collapsing glomerulopathy recurs postransplant, raising the possibility of circulating factors implicated in the pathogenesis of the disease. METHODS:To determine the presence of circulating factors in collapsing glomerulopathy patients, we tested serum from those patients in an in vivo assay. Eleven groups of rats received serum from collapsing glomerulopathy patients, idiopathic focal segmental glomerulosclerosis (FSGS) or healthy subjects in its native form, isolated IgG, or serum without IgG. The presence of proteinuria and creatinine clearance were determined. Histopathologic analysis included light, immunofluorescence, and electron microscopy. RESULTS:Collapsing glomerulopathy rats developed proteinuria while rats injected with serum from FSGS and healthy subjects did not. Rats injected with serum of collapsing glomerulopathy in its native form developed marked proteinuria (99.2 +/- 42 mg/24 hours at day 5, P= 0.0001, compared to the baseline), and decreased in creatinine clearance. Rats receiving isolated IgG or serum without IgG from collapsing glomerulopathy developed mild proteinuria (46.5 +/- 8.4 mg/24 hours and 30.9 +/- 11 mg/24 hours, respectively, at day 5 (P= 0.0001). Glomerular tuft retraction and podocyte damage were seen only in collapsing glomerulapthy rats. No abnormalities were found in rats injected with serum from FSGS or healthy subjects. CONCLUSION:Circulating factors in the serum of collapsing glomerulopathy patients produce podocyte damage, whereas such factors are not present in noncollapsing FSGS. IgG eluates from collapsing glomerulopathy produce proteinuria when injected into the rat. Such factors remain in the circulation when serum of patients is adsorbed into protein A, raising the possibility that there are more than one circulating factor present in patients with collapsing glomerulopathy.
journal_name
Kidney Intjournal_title
Kidney internationalauthors
Avila-Casado Mdel C,Perez-Torres I,Auron A,Soto V,Fortoul TI,Herrera-Acosta Jdoi
10.1111/j.1523-1755.2004.00715.xsubject
Has Abstractpub_date
2004-07-01 00:00:00pages
133-43issue
1eissn
0085-2538issn
1523-1755pii
S0085-2538(15)50014-8journal_volume
66pub_type
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journal_title:Kidney international
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journal_title:Kidney international
pub_type: 杂志文章
doi:10.1038/ki.1996.363
更新日期:1996-08-01 00:00:00
abstract::During the heterologous phase of experimental anti-glomerular basement membrane (anti-GBM) nephritis, leukocyte influx peaks within hours, whereas albuminuria occurs within 1 day. In the subsequent autologous phase, endogenous anti-GBM IgG develops and albuminuria persists. Heparan sulfate (HS) proteoglycans like synd...
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pub_type: 杂志文章,多中心研究
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pub_type: 杂志文章
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更新日期:1983-04-01 00:00:00
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pub_type: 杂志文章
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pub_type: 杂志文章,评审
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pub_type: 杂志文章
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更新日期:1980-04-01 00:00:00
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