scholarly journals Corrigendum to “Protective effects of cortex fraxini coumarines against oxonate-induced hyperuricemia and renal dysfunction in mice” [Eur. J. Pharmacol. 666 (2011) 196–204]

2022 ◽  
pp. 174740
Author(s):  
Jian-Mei Li ◽  
Xian Zhang ◽  
Xing Wang ◽  
Yong-Chang Xie ◽  
Ling-Dong Kong
Keyword(s):  
Renal Dysfunction ◽  
Protective Effects

scholarly journals Comprehensive Comparisons among Inotropic Agents on Mortality and Risk of Renal Dysfunction in Patients Who Underwent Cardiac Surgery: A Network Meta-Analysis of Randomized Controlled Trials

2021 ◽  
Vol 10 (5) ◽  
pp. 1032
Author(s):  
Wei-Cheng Chen ◽  
Meng-Hsuan Lin ◽  
Chieh-Lung Chen ◽  
Ying-Chieh Chen ◽  
Chih-Yu Chen ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Randomized Controlled Trials ◽  
Renal Dysfunction ◽  
Systolic Function ◽  
Meta Analysis ◽  
Treatment Strategies ◽  
Controlled Trials ◽  
Protective Effects ◽  
Renal Protection ◽  
Randomized Controlled

Several kinds of inotropes have been used in critically ill patients to improve hemodynamics and renal dysfunction after cardiac surgery; however, the treatment strategies for reducing mortality and increasing renal protection in patients who underwent cardiac surgery remain controversial. Therefore, we performed a comprehensive network meta-analysis to overcome the lack of head-to-head comparisons. A systematic database was searched up to 31 December 2020, for randomized controlled trials that compared different inotropes on mortality outcomes and renal protective effects after cardiac surgery. A total of 29 trials were included and a frequentist network meta-analysis was performed. Inconsistency analyses, publication bias, and subgroup analyses were also conducted. Compared with placebo, use of levosimendan significantly decreased the risks of mortality (odds ratio (OR): 0.74; 95% confidence interval (CI): 0.56–0.97) and risk of acute renal injury (OR: 0.61; 95% CI: 0.45–0.82), especially in low systolic function patients. Use of levosimendan also ranked the best treatment based on the P-score (90.1%), followed by placebo (64.5%), milrinone (49.6%), dopamine (49.5%), dobutamine (29.1%), and fenoldopam (17.0%). Taking all the available data into consideration, levosimendan was a safe renal-protective choice for the treatment of patients undergoing cardiac surgery, especially for those with low systolic function.

Oestrogen protects against ischaemic acute renal failure in rats by suppressing renal endothelin-1 overproduction

2002 ◽  
Vol 103 (s2002) ◽  
pp. 434S-437S ◽  
Author(s):  
Masanori TAKAOKA ◽  
Mikihiro YUBA ◽  
Toshihide FUJII ◽  
Mamoru OHKITA ◽  
Yasuo MATSUMURA
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Renal Dysfunction ◽  
Tissue Injury ◽  
Male Rats ◽  
Left Renal Artery ◽  
Protective Effects ◽  
Endothelin 1 ◽  
Ischaemia Reperfusion

We investigated whether the treatment with 17β-oestradiol has renal protective effects in male rats with ischaemic acute renal failure (ARF). We also examined if the effect of 17β-oestradiol is accompanied by suppression of enhanced endothelin-1 production in postischaemic kidneys. Ischaemic ARF was induced by clamping the left renal artery and vein for 45min followed by reperfusion, 2 weeks after contralateral nephrectomy. Renal function parameters such as blood urea nitrogen, plasma creatinine and creatinine clearance were measured to test the effectiveness of the steroid hormone. Renal function in ARF rats markedly decreased 24h after reperfusion. The ischaemia/reperfusion-induced renal dysfunction was dose-dependently improved by pretreatment with 17β-oestradiol (20 or 100µg/kg, intravenously). Histopathological examination of the kidney of untreated ARF rats revealed severe lesions, such as tubular necrosis, proteinaceous casts in tubuli and medullary congestion, all of which were markedly improved by the higher dose of 17β-oestradiol. In addition, endothelin-1 content in the kidney after the ischaemia/reperfusion increased significantly by approx. 2-fold over sham-operated rats, and this elevation was dose-dependently suppressed by the 17β-oestradiol treatment. These results suggest that oestrogen exhibits protective effects against renal dysfunction and tissue injury induced by ischaemia/reperfusion, possibly through the suppression of endothelin-1 overproduction in postischaemic kidneys.

scholarly journals P2X7 receptor inhibition protects against ischemic acute kidney injury in mice

2015 ◽  
Vol 308 (6) ◽  
pp. C463-C472 ◽  
Author(s):  
Yanli Yan ◽  
Jianwen Bai ◽  
Xiaoxu Zhou ◽  
Jinhua Tang ◽  
Chunming Jiang ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Dysfunction ◽  
P2x7 Receptor ◽  
Renal Tubule ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Tubular Damage ◽  
Protective Effects ◽  
Proinflammatory Response ◽  
Hypertensive Nephropathy

Activation of the purinergic P2X7 receptor (P2X7R) has been associated with the development of experimental nephritis and diabetic and hypertensive nephropathy. However, its role in acute kidney injury (AKI) remains unknown. In this study, we examined the effects of P2X7R inhibition in a murine model of ischemia-reperfusion (I/R)-induced AKI using A438079, a selective inhibitor of P2X7R. At 24 h after I/R, mice developed renal dysfunction and renal tubular damage, which was accompanied by elevated expression of P2X7R. Early administration of A438079 immediately or 6 h after the onset of reperfusion protected against renal dysfunction and attenuated kidney damage whereas delayed administration of A438079 at 24 h after restoration of perfusion had no protective effects. The protective actions of A438079 were associated with inhibition of renal tubule injury and cell death and suppression of renal expression of monocyte chemotactic protein-1 and regulated upon expression normal T cell expressed and secreted (RANTES). Moreover, I/R injury led to an increase in phosphorylation (activation) of extracellular signal-regulated kinases 1/2 in the kidney; treatment with A438079 diminished this response. Collectively, these results indicate that early P2X7R inhibition is effective against renal tubule injury and proinflammatory response after I/R injury and suggest that targeting P2X7R may be a promising therapeutic strategy for treatment of AKI.

Role of recombinant human erythropoietin against mitomycin C-induced cardiac, hepatic and renal dysfunction in Wistar rats

2014 ◽  
Vol 34 (5) ◽  
pp. 468-478 ◽  
Author(s):  
K Rjiba-Touati ◽  
I Ayed-Boussema ◽  
A Belarbia ◽  
M Mokni ◽  
A Achour ◽  
...  
Keyword(s):  
Body Weight ◽  
Renal Dysfunction ◽  
Mitomycin C ◽  
Recombinant Human Erythropoietin ◽  
Wistar Rats ◽  
Protective Effects ◽  
Normal Tissues ◽  
Human Erythropoietin ◽  
Male Wistar Rats ◽  
Glutamyl Transferase

Mitomycin C (MMC) is one of the most effective chemotherapeutic drugs. However, the dose of MMC is greatly limited by its toxicity in normal tissues. Recombinant human erythropoietin (rhEPO), an erythropoietic hormone, has also been shown to exert tissue protective effects. The purpose of this study was to explore the protective effect of rhEPO against MMC-induced heart, liver, and renal dysfunction. Adult male Wistar rats were divided into six groups (with six animals each), namely control, rhEPO alone group, MMC alone group, and rhEPO + MMC group (pre-, co-, and posttreatment conditions). The results showed that MMC induced a marked cardiac, renal, and liver failure characterized by a significant decrease in body weight, organs weight, and organs ratio and a significant increase in creatinine, blood urea nitrogen, alanine aminotransferase, aspartate aminotransferase, γ-glutamyl transferase, and conjugated and total bilirubin levels in serum. Histological examination showed that MMC caused liver alterations. rhEPO treatment restored body weight, organs weight, and organs ratio as well as serum biochemical parameters and histological damage caused by MMC exposure.

scholarly journals Cardio-renal protective effects of SGLT2 inhibitors in patients with type 2 diabetes mellitus and severely impaired renal function

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
M Kanai ◽  
K Kimura ◽  
H Motoki ◽  
S Suzuki ◽  
T Okano ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Renal Dysfunction ◽  
Impaired Renal Function ◽  
Sglt2 Inhibitors ◽  
Protective Effects ◽  
Primary Endpoints ◽  
Group A ◽  
Severe Renal Dysfunction ◽  
Group B

Abstract Background Prognostic impact of Sodium-Glucose Cotransporter 2 (SGLT2) inhibitors on cardiovascular and renal outcome was unknown in patients with type-2 diabetes mellitus (DM) and severely impaired renal function. Methods From July 2015 to December 2020, patients with type-2 DM who were taken SGLT2 inhibitors for more than six months were retrospectively screened. Patients with estimated glomerular filtration rate (eGFR) over 60ml/min/1.73m2 were excluded. We divided those patients into two groups by eGFR; less than 45ml/min/1,73m2 were group A and 46–60ml/min/m2 were group B. Randomly selected patients with DM not taking SGLT2 inhibitors and having severe renal dysfunction: eGFR less than 45ml/min/m2 (Group C) were set as controls. The primary outcome was a composite of cardiovascular/renal death, initiation of dialysis, doubling of the serum creatine level, decline in the eGFR more than 30%, nonfatal myocardial infraction, nonfatal stroke, and hospitalization for heart failure. Results Totally 418 patients were enrolled. Median age was 71 years (group A, n=106), 64 years (group B, n=115), and 77 years (group C, n=201) (p<0.001). After median 24 months follow-up, primary endpoints were observed 24.5% in group A, 4.3% in group B, 36.8% in group C (p<0.001). In Kaplan-Meier analysis, significantly lower incidence of primary endpoints were observed in SGLT2 groups (group A and B) than controls (p<0.001, Figure 1). In patients with severe renal dysfunction, taking SGLT2 inhibitors tended to decrease future renal event (Figure 2). The incidence of SGLT2 related adverse events was not different between 2 groups (A and B). Conclusions Even in patients with severe renal dysfunction, SGLT2 inhibitors would have cardio-renal protective effects without drug-related adverse effects. FUNDunding Acknowledgement Type of funding sources: None.

scholarly journals Nitrooleic Acid Protects against Cisplatin Nephropathy: Role of COX-2/mPGES-1/PGE2Cascade

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Haiping Wang ◽  
Zhanjun Jia ◽  
Jing Sun ◽  
Liang Xu ◽  
Bing Zhao ◽  
...  
Keyword(s):  
Renal Dysfunction ◽  
Kidney Injury ◽  
Histological Change ◽  
Peroxisome Proliferator ◽  
Mrna Levels ◽  
Protective Effects ◽  
Plasma Urea ◽  
Lipid Product ◽  
Cox 2 ◽  
Peroxisome Proliferator Activated Receptors

Nitrooleic acid (OA-NO2) is an endogenous lipid product which has novel signaling properties, particularly the activation of peroxisome proliferator-activated receptors. The current study aimed to evaluate the protective effects of OA-NO2against cisplatin-induced kidney injury in mice. Mice were pretreated with OA-NO2for 48 h before cisplatin administration, and the cisplatin-caused nephrotoxicity was evaluated. After the cisplatin treatment (72 h), the vehicle-treated mice displayed renal dysfunction, as evidenced by the elevated plasma urea and creatinine, which was consistent with the histological damage, such as tubular necrosis, dilation, protein cast, and desquamation of epithelial cells. In contrast, the severity of the renal dysfunction and histological change were reduced in the OA-NO2pretreated mice. The renal COX-2 and mPGES-1 mRNAs and their respective proteins expression, together with the renal PGE2amounts, were induced by the cisplatin treatment, but their initiation was reduced by OA-NO2. Moreover, the circulating TNF-α, renal TNF-α, IL-1β, MCP-1, ICAM-1, and VACAM-1 mRNA levels were higher in the cisplatin-treated mice, compared with the controls, but they were attenuated in the OA-NO2pretreatment group. In summary, the pretreatment with OA-NO2remarkably ameliorated the cisplatin-induced kidney injury in mice, possibly via the inhibition of the inflammatory response, associated with the COX-2/mPGES-1/PGE2cascade.

scholarly journals Melatonin and alpha lipoic acid restore electrolytes and kidney morphology of lopinavir/ritonavir-treated rats

2019 ◽  
Vol 9 (1) ◽  
pp. e06-e06 ◽  
Author(s):  
Elias Adikwu ◽  
Nelson Brambaifa ◽  
Wolfe Atuboyedia Obianime
Keyword(s):  
Renal Dysfunction ◽  
Lipoic Acid ◽  
Total Protein ◽  
Morphological Changes ◽  
Albino Rats ◽  
Protective Effects ◽  
Alpha Lipoic Acid ◽  
Serum Electrolytes ◽  
Kidney Morphology ◽  
Dose Dependent

Introduction: Lopinavir/ritonavir (LPV/r) may cause renal dysfunction such as electrolyte and acid base disorders and alteration in kidney morphology. Drug–induced renal dysfunction can occur through multiple mechanisms including oxidative stress and inflammation. Objectives: The current study aimed at evaluating the protective effects of melatonin (MT) and alpha lipoic acid (ALA) against serum electrolytes and kidney histology of LPV/r-treated rats. Adult albino rats were randomized into six groups (A to F). Rats in the control groups were treated orally with normal saline and 1% ethanol as placebo and solvent control for 90 days respectively. Rats in the experimental groups were pre-treated orally with 10 mg/kg of MT, 10 mg/kg of ALA, and MT+ ALA daily before treatment with 22.9/5.71, 45.6/11.4 94 and 91.4/22.9 mg/kg/d of LPV/r for 90 days respectively. Materials and Methods: At the end of treatment, rats were euthanized. Blood samples were collected and serum samples were extracted and evaluated for electrolytes, total protein, and albumin. Additionally, kidneys were excised via dissection and evaluated for morphological changes. Results: Significant (P<0.001) decreases in serum sodium, potassium, chloride, bicarbonate, total protein and albumin in a dose-dependent fashion were obtained in LPV/r-treated rats when compared to control. Dose-dependent kidney morphological changes characterised by tubular necroses were obtained in LPV/r-treated rats. The observations in LPV/r-treated rats were significantly reversed in MT (P<0.01), ALA (P<0.01) and MT+ALA (P<0.001) pre-treated rats when compared to LPV/r-treated rats. Conclusion: MT and ALA can serve as adjuvant therapies for LPV/r-associated alterations in serum electrolytes and kidney histology.

Protective effects of cortex fraxini coumarines against oxonate-induced hyperuricemia and renal dysfunction in mice

2011 ◽  
Vol 666 (1-3) ◽  
pp. 196-204 ◽  
Author(s):  
Jian-Mei Li ◽  
Xian Zhang ◽  
Xing Wang ◽  
Yong-Chang Xie ◽  
Ling-Dong Kong
Keyword(s):  
Renal Dysfunction ◽  
Protective Effects

scholarly journals Protective Effects of Bee Venom against Endotoxemia-Related Acute Kidney Injury in Mice

Biology ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 154 ◽  
Author(s):  
Jung-Yeon Kim ◽  
Sun-Jae Lee ◽  
Young-In Maeng ◽  
Jaechan Leem ◽  
Kwan-Kyu Park
Keyword(s):  
Acute Kidney Injury ◽  
Renal Dysfunction ◽  
Cell Apoptosis ◽  
Immune Cell ◽  
Medical Condition ◽  
Kidney Injury ◽  
Tubular Cell ◽  
Bee Venom ◽  
Protective Effects ◽  
Structural Injury

Sepsis-associated acute kidney injury (AKI) is a leading cause of death in hospitalized patients worldwide. Despite decades of effort, there is no effective treatment for preventing the serious medical condition. Bee venom has long been used to treat a variety of inflammatory diseases. However, whether bee venom has protective effects against lipopolysaccharide (LPS)-induced AKI has not been explored. The aim of this study was to evaluate the effects of bee venom on LPS-induced AKI. The administration of bee venom alleviated renal dysfunction and structural injury in LPS-treated mice. Increased renal levels of tubular injury markers after LPS treatment were also suppressed by bee venom. Mechanistically, bee venom significantly reduced plasma and tissue levels of inflammatory cytokines and immune cell infiltration into damaged kidneys. In addition, mice treated with bee venom exhibited reduced renal expression of lipid peroxidation markers after LPS injection. Moreover, bee venom attenuated tubular cell apoptosis in the kidneys of LPS-treated mice. In conclusion, these results suggest that bee venom attenuates LPS-induced renal dysfunction and structural injury via the suppression of inflammation, oxidative stress, and tubular cell apoptosis, and might be a useful therapeutic option for preventing endotoxemia-related AKI.

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