ArticleThe American journal of pathology1986
No aggravation of the course of experimental glomerulonephritis in spontaneously hypertensive rats.
Article in The American journal of pathology, 1986. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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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.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- Vascular Hyperactivity in the Rat Renal Aorta Participates in the Association between Immune Complex-Mediated Glomerulonephritis and Systemic Hypertension.International journal of environmental research and public health · 2018Article
- Chronic glucocorticoid therapy amplifies glomerular injury in rats with renal ablation.The Journal of clinical investigation · 1987Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Functional and morphologic glomerular alterations induced by antiglomerular basement membrane (anti-GBM) nephritis were investigated in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto controls (WKY) for assessment of the role of systemic hypertension in immunologically mediated renal injury. Over a 6-week period serial measurements of systolic blood pressure (BP), serum creatinine (SCreat), creatinine clearance (CCreat), and urinary albumin excretion (UAlbV) were obtained with inulin clearances (CInulin) at the end of the study. Renal tissue was examined by light microscopy (LM), electron microscopy, immunofluorescence, flash 3H-thymidine autoradiography (AR), and staining for nonspecific esterase (NSE). Immunologic humoral response was evaluated by measurement of rat anti-rabbit IgG antibody production. At all time periods studied, SHR and WKY rats with anti-GBM nephritis demonstrated comparable elevations in SCreat and UAlb V as well as diminution of CCreat and CInulin as compared with non-nephritic control rats of each strain. In nephritic WKY rats mild hypertension developed, whereas in nephritic and control SHR rats marked elevations in BP developed. Morphologic injury as assessed by percent glomerular crescents and hypercellularity on LM, numbers of monocyte macrophages by NSE staining, immunofluorescence for IgG, C3, fibrinogen and Ia positivity, and numbers of glomerular 3H-thymidine-labeled cells by AR was notably comparable in both nephritic strains. Humoral antibody responses were also shown to be similar in all rats studied. These results demonstrate that the 5-week course of experimental anti-GBM nephritis is not exacerbated by systemic hypertension. Glomerular autoregulatory capacity may be important in determining the extent of immune-mediated renal injury.
Indexed as
Identifiers
3513602PMC1888211W1839592677What OpenQuestion holds
Registered trials
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.