Evidence map›Paper›PMID 7593622›Full record

ArticleThe Journal of clinical investigation1995

Tubulointerstitial injury induced in rats by a monoclonal antibody that inhibits function of a membrane inhibitor of complement.

A Nomura, K Nishikawa, Y Yuzawa, H Okada, N Okada, B P Morgan, S J Piddlesden, M Nadai, T Hasegawa, S Matsuo

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.8field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Endotoxemia alters tight junction gene and protein expression in the kidney.American journal of physiology. Renal physiology · 2012
    Article
  11. Article
  12. Dynamic control of the complement system by modulated expression of regulatory proteins.Laboratory investigation; a journal of technical methods and pathology · 2011
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Complement regulation during pregnancy.Immunologic research · 2005
    Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

A NomuraThird Department of Internal Medicine, Nagoya University School of Medicine, Japan.
K Nishikawa
Y Yuzawa
H Okada
N Okada
B P Morgan
S J Piddlesden
M Nadai
T Hasegawa
S Matsuo
Nagoya University Hospital · JPNagoya City University · JPUniversity of Wales · GBNagoya University · JP

Funding

Wellcome Trust
6 · The paper itself

Abstract

The kidney widely expresses membrane-associated complement regulatory proteins (membrane inhibitors of complement). The aim of this work was to evaluate the roles of these molecules in rat kidneys in vivo. To suppress functions of rat membrane inhibitors of complement, two mAbs, 512 and 6D1, were used. 5I2 and 6D1 inhibit functions of membrane inhibitors of complement at C3 level (rat Crry/p65) and C8/9 level (rat CD59), respectively. F(ab')2 fragment of 5I2 or 6D1 was perfused in the left kidneys, and perfusate was discarded from the renal vein. After perfusion, the left kidneys were connected to systemic circulation. In rats perfused with 5I2, mouse IgG was found in glomeruli, peritubular capillaries, vascular bundles, and tubules 15 min after recirculation. Binding of C3 and C5b-9 was evident in these areas. 1 d after perfusion with 5I2, cast formation, dilatation of tubular lumen, and tubular cell degeneration were observed. At day 4 through day 7, significant mononuclear cell infiltration and proximal tubule damage were observed. These changes were completely prevented by complement depletion. Rats perfused with 6D1 showed the binding of mouse IgG in the similar areas as 5I2, but C3 or C5b-9 deposition was not observed. Rats perfused with 6D1 or vehicle only did not show any pathology in the left kidneys. These results suggest that rat Crry/p65 plays protective roles against spontaneously occurring indiscriminate attack to tubulointerstitial tissues by autologous complement and that rat Crry/p65 is one of the important factors to maintain normal integrity of the kidney in rats.

Indexed as

AnimalsAntibodies, MonoclonalComplement C3Complement Inactivator ProteinsFemaleImmunoglobulin GKidneyKidney TubulesMicePerfusionRatsRats, WistarAntibodies, MonoclonalComplement C3Complement Inactivator ProteinsImmunoglobulin G

Identifiers

PMID7593622
PMCPMC185886
OpenAlexW2005328294

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.