scholarly journals Sepsis-induced acute kidney injury: kidney protection effects by antioxidants

2018 ◽  
Vol 71 (4) ◽  
pp. 1921-1927 ◽  
Author(s):  
Carolina Ferreira Vasco ◽  
Mirian Watanabe ◽  
Cassiane Dezoti da Fonseca ◽  
Maria de Fátima Fernandes Vattimo
Keyword(s):  
Blood Pressure ◽  
Acute Kidney Injury ◽  
Creatinine Clearance ◽  
Experimental Model ◽  
Kidney Function ◽  
Cecal Ligation ◽  
Kidney Injury ◽  
Cecal Ligation And Puncture ◽  
Antioxidant Action ◽  
Average Blood Pressure

ABSTRACT Objective: To evaluate the antioxidant action of N-acetylcysteine and diosmin-hesperidin in an experimental model of sepsis-induced acute kidney injury in rats. Methods: The study used 20 Wistar adult male rats divided into the following groups: control (laparotomy with no induction of abdominal sepsis), sepsis (experimental model of sepsis with cecal ligation and puncture), N-acetylcysteine + sepsis and diosmin-hesperidin + sepsis. The evaluation contemplated physiological parameters (temperature, glycemia, and average blood pressure), kidney function (creatinine clearance), oxidative stress (urinary peroxides) and kidney histology. Results: The animals submitted to cecal ligation and puncture (sepsis) presented lower body temperature, lower average blood pressure, reduced creatinine clearance and increased urinary hydrogen peroxide levels. Treatment with diosmin-hesperidin improved kidney function and led to a reduction in the excretion of oxidative metabolites. Conclusion: The present study highlighted the protective antioxidant action of diosmin-hesperidin in the experimental model of sepsis-induced acute kidney injury.

Platycodin D Ameliorates Acute Kidney Injury in Septic Rats by Regulating Mitogen Activated Protein Kinase Pathway

2020 ◽  
Vol 19 (3) ◽  
pp. 270-276
Author(s):  
Jianying Wang ◽  
Xiaoting Yu
Keyword(s):  
Acute Kidney Injury ◽  
Protein Kinase ◽  
Protective Effect ◽  
Cecal Ligation ◽  
Kidney Injury ◽  
B Cell Lymphoma ◽  
Mitogen Activated Protein Kinase ◽  
Cecal Ligation And Puncture ◽  
Platycodin D ◽  
Mitogen Activated Protein

Acute kidney injury is a severe complication of sepsis. We have shown a protective effect of Platycodin D on sepsis induced acute kidney injury in an animal model that employs cecal ligation and puncture. Cecal ligation and puncture induced a series of degenerative changes in kidney, such as edema, hyperemia, and expansion in glomerular capillary, and inflammatory cells infiltration that were attenuated by Platycodin D. Also, rise in proinflammatory cytokine levels in septic rats was blunted by Platycodin D. Furthermore, Platycodin D administration reduced rise in serum levels of kidney injury markers-blood urea nitrogen and serum creatinine-in septic rats. Moreover, Platycodin D administration also suppressed the cell apoptosis in kidney that was associated with enhanced B-cell lymphoma 2 protein and reduced cleaved cysteine-aspartic protease-3 and BCL2-associated X protein. Lastly, Platycodin D administration attenuated sepsis-induced increase of phospho (p)-extracellular signal-regulated kinase, p-c-Jun NH2-terminal kinase, and p-p38. In conclusion, Platycodin D demonstrated protective effect against sepsis induced acute kidney injury through inactivation of mitogen activated protein kinase pathways, thus providing promising therapeutic strategy for the treatment of sepsis.

scholarly journals Intravenous Arginine Administration Downregulates NLRP3 Inflammasome Activity and Attenuates Acute Kidney Injury in Mice with Polymicrobial Sepsis

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Sharon Angela Tanuseputero ◽  
Ming-Tsan Lin ◽  
Sung-Ling Yeh ◽  
Chiu-Li Yeh
Keyword(s):  
Acute Kidney Injury ◽  
Protein Expression ◽  
Kidney Function ◽  
Nlrp3 Inflammasome ◽  
Cecal Ligation ◽  
Kidney Injury ◽  
Major Complication ◽  
Receptor Protein ◽  
No Production ◽  
Inflammasome Activity

Acute kidney injury (AKI) is a major complication of sepsis. Nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasomes are multiprotein complexes that mediate septic AKI. L-arginine (Arg) is a conditionally essential amino acid in catabolic conditions and a substrate for nitric oxide (NO) production; however, its use in sepsis is controversial. This study investigated the effect of intravenous Arg supplementation on modulating NLRP3 inflammasome activity in relation to septic AKI. Mice were divided into normal control (NC), sham, sepsis saline (SS), and sepsis Arg (SA) groups. In order to investigate the role of NO, L-N6-(1-iminoethyl)-lysine hydrochloride (L-NIL), an inducible NO synthase inhibitor, was administered to the sepsis groups. Sepsis was induced using cecal ligation and puncture (CLP). The SS and SA groups received saline or Arg via tail vein 1 h after CLP. Mice were sacrificed at 6, 12, and 24 h after sepsis. The results showed that compared to the NC group, septic mice had higher plasma kidney function parameters and lower Arg levels. Also, renal NLRP3 inflammasome protein expression and tubular injury score increased. After Arg treatment, plasma Arg and NO levels increased, kidney function improved, and expressions of renal NLRP3 inflammasome-related proteins were downregulated. Changes in plasma NO and renal NLRP3 inflammasome-related protein expression were abrogated when L-NIL was given to the Arg sepsis groups. Arg plus L-NIL administration also attenuated kidney injury after CLP. The findings suggest that intravenous Arg supplementation immediately after sepsis restores plasma Arg levels and is beneficial for attenuating septic AKI, partly via NO-mediated NLRP3 inflammasome inhibition.

MO389PREDICTORS OF COMMUNITY-ACQUIRED ACUTE KIDNEY INJURY IN PATIENTS WITH ACUTE CARDIAC DISEASES

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Marina Efremovtseva ◽  
Svetlana Avdoshina ◽  
Maria Markova ◽  
Zhanna Kobalava
Keyword(s):  
Blood Pressure ◽  
Risk Assessment ◽  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Hospital Mortality ◽  
Kidney Function ◽  
Kidney Injury ◽  
Assessment Scale ◽  
Cardiac Diseases ◽  
L 14

Abstract Background and Aims Acute kidney injury (AKI) is a common and serious problem associated with poor prognosis. The aim of the study was to reveal the prevalence and predictors of community-acquired AKI in patients with acute cardiac diseases. Method 566 patients (278 with acute decompensated heart failure (ADHF), 288 with non-ST-elevation acute coronary syndrome (NSTE-ACS), 46% male, 71±11 years (M±SD), smokers 26%, arterial hypertension 91%, previous myocardial infarction (MI) 45%, diabetes mellitus (DM) 28%, atrial fibrillation 35%, chronic kidney disease (CKD) 46%, previous hospitalization with ADHF 36%, ejection fraction (EF) <35% 15%, blood pressure (BP) 142±30/83±16 mmHg) were examined. AKI was diagnosed according 2012 KDIGO Guidelines. Community-acquired AKI was identified in patients with elevated serum creatinine levels on admission, which decreased during hospitalization. Results: Incidence of AKI in all patients, patients with ADHF and NSTE-ACS was 40, 43.5 and 37.2%. In-hospital mortality in patients with AKI was higher than in those with stable kidney function (14.9 vs 3.6%, p<0.001). Community-acquired AKI was present in 18% of patients (20.5 and 15.6% in ADHF and NSTE-ACS respectively), in-hospital mortality was 16.7% (10.5 and 24.4% respectively). The risk assessment scale for community-acquired AKI was developed based on independent predictors of AKI, using binary logistic regression and ROC analysis (AUC 0.860, 95% CI 0.821-0.898). Independent variables included in the model, and the corresponding points (pts) are listed below: clinical and demographic characteristics (male gender - 6 pts, alcohol abuse - 7 pts, DM - 1 pt), present on admission (MI - 5 pts, AHF/ADHF - 9 pts, systolic BP <120 - 10 pts, <110 - 15 pts, <90 mmHg - 27 pts; state of kidney function on admission: serum creatinine >98 and >128 mkmol/L - 14 and 22 pts, GFRCKD-EPI <45 and <15 ml/min/1.73 m2 - 7 and 14 pts; glucose level >7 mmol/L - 4 pts), outpatient intake of ACE inhibitors - 4 pts, absence of spironolactone in outpatient therapy - 1 pt. Diagnostically significant risk score for predicting AKI was >30 pts, the risk prediction model showed sensitivity 89%, specificity 66%. Conclusion Community-acquired AKI is common in patients in acute cardiovascular events, is associated with high mortality, and often is underdiagnosed. Usage of risk assessment scale in clinical practice may help to detect patients with high-risk of AKI on admission. Baseline kidney function and blood pressure level are main predictors of AKI in patients admitted with acute cardiac diseases.

scholarly journals Influence of autophagy on acute kidney injury in a murine cecal ligation and puncture sepsis model

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Satoshi Sunahara ◽  
Eizo Watanabe ◽  
Masahiko Hatano ◽  
Paul E. Swanson ◽  
Takehiko Oami ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cecal Ligation ◽  
Kidney Injury ◽  
Cecal Ligation And Puncture ◽  
Sepsis Model

scholarly journals Mesenchymal Stem Cells Protect Against Sepsis-associated Acute Kidney Injury by Inducing Gal-9/Tim-3 to Remodel Immune Homeostasis

2021 ◽  
Author(s):  
congjuan luo ◽  
Feng Luo ◽  
Lin Che ◽  
Hui Zhang ◽  
Long Zhao ◽  
...  
Keyword(s):  
Stem Cells ◽  
Acute Kidney Injury ◽  
Group Treatment ◽  
Th17 Cells ◽  
Cecal Ligation ◽  
Kidney Injury ◽  
Immune Homeostasis ◽  
Cecal Ligation And Puncture ◽  
Specific Mechanism ◽  
Nitrogen Levels

Abstract Objective: The aim of the present study was to investigate the specific mechanism by which MSCs protect against SA-AKI.Methods: Male C57BL/6 mice underwent cecal ligation and puncture operation to induce sepsis and then received either normal IgG or MSCs (1* 106 cells intravenously) plus Gal-9 or soluble-Tim-3 3h after surgery. Results: After cecal ligation and puncture operation, injection with Gal-9 or MSCs plus Gal-9 had a higher survival rate than the IgG treatment group. Treatment with MSCs plus Gal-9 decreased serum creatinine and blood urea nitrogen levels and improved recovery of tubular function. Reduce the levels of IL-17, RORγt and induce the expression of IL-10 and FOXP3. Additionly, remodel the balance of TH17/Treg. However, when used soluble Tim-3 to block the Gal-9/Tim-3 pathway, the septic mice developed badly kidney injury and exhibited a higher mortality. Treatment with MSCs plus soluble Tim-3 blunted the therapeutic effect of MSCs, and inhibited the induction of Tregs and suppressed the inhibition of the differentiation to Th17 cells.Conclusion: Treatment with MSCs significantly reversed the TH1/TH2 balance. And the important mechanism for MSCs protection against SA-AKI maybe through the Gal-9/Tim-3 pathway.

scholarly journals Mouse Models of Acute Kidney Injury

2021 ◽  
Author(s):  
Navjot Pabla ◽  
Yogesh Scindia ◽  
Joseph Gigliotti ◽  
Amandeep Bajwa
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Mouse Models ◽  
Poor Prognosis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cecal Ligation ◽  
Kidney Injury ◽  
Cecal Ligation And Puncture ◽  
High Degree

Acute Kidney Injury (AKI) is a poor prognosis in hospitalized patients that is associated with high degree of mortality. AKI is also a major risk factor for development of chronic kidney disease. Despite these serious complications associated with AKI there has not been a great amount of progress made over the last half-century. Here we have outlined and provided details on variety of mouse models of AKI. Some of the mouse models of AKI are renal pedicle clamping (ischemia reperfusion injury), Cisplatin induced nephrotoxicity, sepsis (LPS, cecal slurry, and cecal ligation and puncture), folic acid, and rhabdomyolysis. In this chapter we describe in detail the protocols that are used in our laboratories.

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