Artemisinin attenuates tubulointerstitial inflammation and fibrosis via the NF‐κB/NLRP3 pathway in rats with 5/6 subtotal nephrectomy

2018 ◽  
Vol 120 (3) ◽  
pp. 4291-4300 ◽  
Author(s):  
Yi Wen ◽  
Ming‐Ming Pan ◽  
Lin‐Li Lv ◽  
Tao‐Tao Tang ◽  
Le‐Ting Zhou ◽  
...  
Keyword(s):  
Subtotal Nephrectomy ◽  
Tubulointerstitial Inflammation

ACE INHIBITION ATTENUATES RENAL PDGF GENE EXPRESSION AND CELL PROLIFERATION IN SUBTOTAL NEPHRECTOMY

Nephrology ◽  
2000 ◽  
Vol 5 (3) ◽  
pp. A104-A104
Author(s):  
Jandeleit‐Dahm K ◽  
Wu Ll ◽  
Johnson Rj ◽  
Cox Aj ◽  
Kelly Dj ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Ace Inhibition ◽  
Subtotal Nephrectomy

The extent of tubulointerstitial inflammation is an independent predictor of renal survival in lupus nephritis

2021 ◽  
Author(s):  
Manuel Ferreira Gomes ◽  
Claudia Mardones ◽  
Marc Xipell ◽  
Miquel Blasco ◽  
Manel Solé ◽  
...  
Keyword(s):  
Lupus Nephritis ◽  
Independent Predictor ◽  
Renal Survival ◽  
Tubulointerstitial Inflammation

scholarly journals CD36 promotes NLRP3 inflammasome activation via the mtROS pathway in renal tubular epithelial cells of diabetic kidneys

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Yanjuan Hou ◽  
Qian Wang ◽  
Baosheng Han ◽  
Yiliang Chen ◽  
Xi Qiao ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
High Glucose ◽  
Inflammasome Activation ◽  
Ros Production ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Nlrp3 Inflammasome Activation ◽  
Ampk Activity ◽  
Renal Tubular ◽  
Tubulointerstitial Inflammation

AbstractTubulointerstitial inflammation plays a key role in the pathogenesis of diabetic nephropathy (DN). Interleukin-1β (IL-1β) is the key proinflammatory cytokine associated with tubulointerstitial inflammation. The NLRP3 inflammasome regulates IL-1β activation and secretion. Reactive oxygen species (ROS) represents the main mediator of NLRP3 inflammasome activation. We previously reported that CD36, a class B scavenger receptor, mediates ROS production in DN. Here, we determined whether CD36 is involved in NLRP3 inflammasome activation and explored the underlying mechanisms. We observed that high glucose induced-NLRP3 inflammasome activation mediate IL-1β secretion, caspase-1 activation, and apoptosis in HK-2 cells. In addition, the levels of CD36, NLRP3, and IL-1β expression (protein and mRNA) were all significantly increased under high glucose conditions. CD36 knockdown resulted in decreased NLRP3 activation and IL-1β secretion. CD36 knockdown or the addition of MitoTempo significantly inhibited ROS production in HK-2 cells. CD36 overexpression enhanced NLRP3 activation, which was reduced by MitoTempo. High glucose levels induced a change in the metabolism of HK-2 cells from fatty acid oxidation (FAO) to glycolysis, which promoted mitochondrial ROS (mtROS) production after 72 h. CD36 knockdown increased the level of AMP-activated protein kinase (AMPK) activity and mitochondrial FAO, which was accompanied by the inhibition of NLRP3 and IL-1β. The in vivo experimental results indicate that an inhibition of CD36 could protect diabetic db/db mice from tubulointerstitial inflammation and tubular epithelial cell apoptosis. CD36 mediates mtROS production and NLRP3 inflammasome activation in db/db mice. CD36 inhibition upregulated the level of FAO-related enzymes and AMPK activity in db/db mice. These results suggest that NLRP3 inflammasome activation is mediated by CD36 in renal tubular epithelial cells in DN, which suppresses mitochondrial FAO and stimulates mtROS production.

scholarly journals POS0722 HISTOPATHOLOGICAL ANALYSIS OF LUPUS NEPHRITIS INCORPORATING BANFF CRITERIA EMPHASIZES THE IMPORTANCE OF TUBULOINTERSTITIAL CHANGES FOR CREATININE AND PROTEINURIA AT 12 MONTHS AFTER RENAL BIOPSY

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 611.1-611
Author(s):  
M. Plüß ◽  
S. Hakroush ◽  
N. Niebusch ◽  
B. Tampe ◽  
P. Korsten
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Nephritis ◽  
Lupus Erythematosus ◽  
Interstitial Fibrosis ◽  
Laboratory Data ◽  
Histopathological Analysis ◽  
Systemic Lupus ◽  
Long Term Outcome ◽  
Banff Classification ◽  
Tubulointerstitial Inflammation

Background:Lupus nephritis (LN) occurs in about 30-60% of patients with systemic lupus erythematosus (SLE). LN is associated with increased mortality. Currently, the diagnosis relies on histopathologic characteristics according to the ISN/RPS classification (1). This classification relies heavily on glomerular changes and may not accurately reflect all changes occurring in LN. For the description of transplanted kidney, the BANFF classification has been established which, in addition to glomerular changes, also incorporates tubular pathologies (2).Objectives:With the present study, we aim to describe histopathologic changes according to the BANFF classification in a single-center cohort of LN patients.Methods:We retrospectively recorded epidemiological, clinical and laboratory data of 58 patients with LN over a ten-year period. Histopathologic diagnoses according to ISN/RPS classification or the former WHO classification were also documented. We then re-analyzed representative kidney samples according to the BANFF classification and performed Spearman rank correlation for BANFF findings and creatinine at biopsy and 12 months as well as proteinuria at biopsy and at 12 months.Results:We analyzed 58 patients with LN. 9 were male, 49 were female. Median age was 38 (15-78) years. According to ISN/RPS, 3 had class I LN, 6 had class II, 14 had class III, 16 had class IV, 6 had class V, and 0 had class VI. Median eGFR at biopsy was 60 ml/min/1.73m2 (13-137). According to the BANFF classification, tubulointerstitial inflammation (ti) was associated with creatinine at 12 months. Proteinuria at 12 months was associated with interstitial fibrosis (ci) (Figure 1).Conclusion:In LN, the current ISN/RPS classification puts emphasis on glomerular changes. Nevertheless, for the long-term outcome, tubulointerstitial changes (tubulointerstitial inflammation and interstitial fibrosis) may at least be as important as glomerular changes. These findings have to be corroborated in larger cohorts with prespecified renal endpoints.References:[1]Weening et al. The classification of glomerulonephritis in systemic lupus erythematosus revisited. JASN 2004.[2]Jeong HY. Diagnosis of renal transplant rejection: Banff classification and beyond. Kidney Res Clin Pract 2020.Disclosure of Interests:Marlene Plüß: None declared, Samy Hakroush: None declared, Noah Niebusch: None declared, Björn Tampe: None declared, PETER KORSTEN Speakers bureau: Abbvie, Pfizer, Chugai, Sanofi, Boehringer-Ingelheim, GSK, Novartis, Consultant of: Abbvie, Pfizer, Chugai, Sanofi, Boehringer-Ingelheim, GSK, Novartis, Lilly, Gilead, Grant/research support from: GSK

scholarly journals Temporal serum creatinine increase and exacerbation of tubulointerstitial inflammation during the first two months in resolving polyomavirus BK nephropathy

Nephrology ◽  
2015 ◽  
Vol 20 ◽  
pp. 45-50 ◽  
Author(s):  
Kosuke Masutani ◽  
Akihiro Tsuchimoto ◽  
Yuta Matsukuma ◽  
Kei Kurihara ◽  
Takehiro Nishiki ◽  
...  
Keyword(s):  
Serum Creatinine ◽  
Polyomavirus Bk ◽  
Tubulointerstitial Inflammation

scholarly journals Comparative proteomic analysis of rat aorta in a subtotal nephrectomy model

PROTEOMICS ◽  
2010 ◽  
Vol 10 (13) ◽  
pp. 2429-2443 ◽  
Author(s):  
Yao-Ping Lin ◽  
Meng - Erh Hsu ◽  
Yi-Ying Chiou ◽  
Hung-Yi Hsu ◽  
Hiao-Chien Tsai ◽  
...  
Keyword(s):  
Proteomic Analysis ◽  
Rat Aorta ◽  
Comparative Proteomic Analysis ◽  
Subtotal Nephrectomy

Renal Blood Flow After Subtotal Nephrectomy

1937 ◽  
Vol 36 (2) ◽  
pp. 196-198 ◽  
Author(s):  
W. Dock ◽  
D. A. Rytand
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Subtotal Nephrectomy
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