ArticleWorld journal of nephrology2016
C5b-9 does not mediate tubulointerstitial injury in experimental acute glomerular disease characterized by selective proteinuria.
Article in World journal of nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- The lipid-podocyte axis: emerging clues in membranous nephropathy pathogenesis.Frontiers in medicine · 2026Review
- Alternative pathway-mediated tubular complement activation in human proteinuric kidney diseases: a proof-of-concept study.Clinical kidney journal · 2025Article
- Crosstalk between glomeruli and tubules.Nature reviews. Nephrology · 2025Review
- Apical tubular complement activation and the loss of kidney function in proteinuric kidney diseases.Clinical kidney journal · 2024Review
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1 author at 1 institution in 1 country.
Funding
Abstract
aimTo determine whether complement membrane attack complex (C5b-9) has a pathogenic role in tubulointerstitial injury in a renal disease model characterized by acute highly selective proteinuria.
methodsProtein-overload nephropathy (PON) was induced in adult female Piebald-Viral-Glaxo rats with or without complement C6 deficiency (C6(-) and C6(+)) by daily intraperitoneal injections of bovine serum albumin (BSA, 2 g/d), and examined on days 2, 4 and 8.
resultsGroups with PON developed equivalent levels of heavy proteinuria within 24 h of BSA injection. In C6(+) rats with PON, the tubulointerstitial expression of C5b-9 was increased and localized predominantly to the basolateral surface of tubular epithelial cells (TECs), whereas it was undetectable in C6(-) animals. TEC proliferation (as assessed by the number of BrdU+ cells) increased by more than 50-fold in PON, peaking on day 2 and declining on days 4 to 8. There was a trend for a reduction in the number of BrdU+ TECs on day 4 in the C6(-) PON group (P = 0.10 compared to C6(+)) but not at any other time-point. Kidney enlargement, TEC apoptosis (TUNEL(+) cells) and markers of tubular injury (tubule dilatation, loss of TEC height, protein cast formation) were not altered by C6 deficiency in PON. Interstitial monocyte (ED-1+ cell) accumulation was partially reduced in C6(-) animals with PON on day 4 (P = 0.01) but there was no change in myofibroblast accumulation.
conclusionThese data suggest that C5b-9 does not mediate tubulointerstitial injury in acute glomerular diseases characterized by selective proteinuria.
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