scholarly journals Overview of sepsis associated acute kidney injury: literature review

2021 ◽  
Author(s):  
Mona Al-Shahrani ◽  
Sarah Khalil Soofy ◽  
Mouaz Abdullah Mohammad ◽  
Ibrahim Yahya Alfalahi ◽  
Ali Alhussain Alhazmi ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Animal Studies ◽  
Kidney Injury ◽  
Hemodynamic Instability ◽  
Renal Tissue ◽  
Shock State ◽  
Inflammatory State ◽  
Hospital Stays ◽  
Better Than ◽  
Significant Factors

The incidence of acute kidney injury has been estimated to be around a fifth of the adult patients during their hospital stays. Sepsis is estimated to be the commonest cause for AKI development in critically-ill patients; contributing to the pathology in 20-50% of the cases. We reviewed some aspects of sepsis-associated AKI. Among the risk factors that may contribute to the development of AKI, age, sex, and the presence of comorbidities as diabetes, heart, and liver diseases were reported as significant factors associated with the development of the condition. The pathophysiology of sepsis-induced AKI is still unclear; however, some authors said that it may be related to the hypoperfusion of the renal tissue and subsequently induced ischemia. This theory was supported by animal studies; however, other investigations on humans reported no association between the two events. On the other hand, we believe that sepsis-induced AKI is probably due to the associated severe inflammatory state and hemodynamic instability are the main accusants. The management of this condition requires early diagnosis and early intervention by managing sepsis. Moreover, vasopressors as epinephrines have proved efficient in managing the shock state, even better than renal replacement therapy.

scholarly journals Endothelial progenitor cells-derived exosomal microRNA-21-5p alleviates sepsis-induced acute kidney injury by inhibiting RUNX1 expression

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Yue Zhang ◽  
Hongdong Huang ◽  
Wenhu Liu ◽  
Sha Liu ◽  
Xue Yan Wang ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Cecal Ligation ◽  
Kidney Injury ◽  
Renal Tissue ◽  
Endothelial Glycocalyx ◽  
Endothelial Progenitor ◽  
Marker Proteins ◽  
Related Transcription Factor

AbstractThe role of microRNA-21-5p (miR-21-5p) in sepsis-induced acute kidney injury (AKI) has been seldom discussed. Therefore, the objective of this present study was to investigate the mechanism of endothelial progenitor cells-derived exosomes (EPCs-exos) in sepsis-induced AKI via miR-21-5p/runt-related transcription factor 1 (RUNX1) axis. miR-21-5p was downregulated and RUNX1 was upregulated in the kidney of cecal ligation and puncture (CLP) rats, and miR-21-5p targeted RUNX1. Elevation of miR-21-5p improved renal function and renal tissue pathological damage, attenuated serum inflammatory response, as well as reduced apoptosis and oxidative stress response in renal tissues, and regulated endothelial glycocalyx damage marker proteins syndecan-1 and heparanase-1 in CLP rats. Overexpression of RUNX1 abolished the impacts of elevated miR-21-5p in CLP rats. Also, EPCs-exos upregulated miR-21-5p expression, and functioned similar to elevation of miR-21-5p for CLP rats. Downregulating miR-21-5p partially reversed the effects of EPCs-exos on sepsis-induced AKI. Collectively, our study suggests that EPCs release miR-21-5p-containing exosomes to alleviate sepsis-induced AKI through RUNX1 silencing.

scholarly journals DNA demethylase Tet2 suppresses cisplatin-induced acute kidney injury

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yinwu Bao ◽  
Mengqiu Bai ◽  
Huanhuan Zhu ◽  
Yuan Yuan ◽  
Ying Wang ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Signaling Pathway ◽  
Cell Injury ◽  
Inflammatory Responses ◽  
Kidney Injury ◽  
Renal Tissue ◽  
Clinical Samples ◽  
Mice Model ◽  
Expression Levels ◽  
Ppar Signaling

AbstractDemethylase Tet2 plays a vital role in the immune response. Acute kidney injury (AKI) initiation and maintenance phases are marked by inflammatory responses and leukocyte recruitment in endothelial and tubular cell injury processes. However, the role of Tet2 in AKI is poorly defined. Our study determined the degree of renal tissue damage associated with Tet2 gene expression levels in a cisplatin-induced AKI mice model. Tet2-knockout (KO) mice with cisplatin treatment experienced severe tubular necrosis and dilatation, inflammation, and AKI markers’ expression levels than the wild-type mice. In addition, the administration of Tet2 plasmid protected Tet2-KO mice from cisplatin-induced nephrotoxicity, but not Tet2-catalytic-dead mutant. Tet2 KO was associated with a change in metabolic pathways like retinol, arachidonic acid, linolenic acid metabolism, and PPAR signaling pathway in the cisplatin-induced mice model. Tet2 expression is also downregulated in other AKI mice models and clinical samples. Thus, our results indicate that Tet2 has a renal protective effect during AKI by regulating metabolic and inflammatory responses through the PPAR signaling pathway.

scholarly journals Conservatism strikes back: later is better than earlier dialysis for acute kidney injury

2016 ◽  
Vol 8 (9) ◽  
pp. 2415-2419
Author(s):  
Dana Bielopolski ◽  
Kamyar Kalantar-Zadeh
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Better Than

scholarly journals Gene Microarray Integrated with High-Throughput Proteomics for the Discovery of Transthyretin in Rhabdomyolysis-Induced Acute Kidney Injury

2017 ◽  
Vol 43 (4) ◽  
pp. 1673-1688 ◽  
Author(s):  
Ou Li ◽  
Xiaodong Geng ◽  
Qian Ma ◽  
Weiwei Wang ◽  
Ran Liu ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Western Blotting ◽  
Kidney Injury ◽  
Physical Exertion ◽  
Renal Tissue ◽  
Gene Microarray ◽  
Absolute Quantitation ◽  
Gene And Protein Expression ◽  
Isobaric Tagging

Background/Aims: Rhabdomyolysis, one of the leading causes of acute kidney injury (AKI), develops after trauma, drug toxicity, infections, burns, and physical exertion. The aim of this study was to investigate differences in gene and protein expression to elucidate the pathogenesis of rhabdomyolysis (RM)-induced AKI. Methods: In this study, we used glycerol induced renal injury as a model of RM-induced AKI. Affymetrix U133 plus 2.0 microarrays were used to perform gene microarray analysis. Isobaric tagging with related and absolute quantitation (iTRAQ) labeling mass spectrometry (MS) was applied to screen and identify differentially expressed proteins between RM-induced AKI and normal murine renal tissue. Verification experiments included immunohistochemistry (IHC), real-time PCR, Western blotting, and the measurement of ATP and ROS production. HK-2 cells were incubated in vitro with ferrous myoglobin and pcDNA-TTR, followed by assays to detect cell proliferation, ROS and apoptosis. Results: According to gene microarray and iTRAQ-MS analysis, we screened 17 common elements. After multiple analyses, we selected transthyretin (TTR) as our focus and investigated TTR in the kidney. Verification experiments with IHC confirmed differential expression levels of TTR proteins. Furthermore, Western blotting showed a stepwise decrease in TTR in AKI renal tissues. Cell-based experiments showed that overexpression of TTR could improve HK-2 cell viability and inhibit apoptosis. TTR reduced apoptosis by decreasing the accumulation of reactive oxygen species (ROS). Conclusion: This study reports a possible mechanism for RM-induced AKI and suggests that reductions in TTR could increase the generation of ROS and induce apoptosis. TTR may be a potentially valuable target for RM-induced AKI.

MO343SERUM RESPONSE FACTOR, A NOVEL EARLY DIAGNOSTIC BIOMARKER OF ACUTE KIDNEY INJURY

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Long Zhao ◽  
Yan Xu
Keyword(s):  
Acute Kidney Injury ◽  
Serum Response Factor ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Diagnostic Value ◽  
Renal Tissue ◽  
Response Factor ◽  
Diagnostic Biomarker ◽  
Renal Tubular ◽  
Early Diagnostic

Abstract Background and Aims Studies have shown that serum response factor (SRF) is increased in chronic kidney injury, such as diabetic nephropathy, hyperuricemic nephropathy and renal cell carcinoma. The objective is to explore the early diagnostic value of SRF in acute kidney injury (AKI). Method AKI-related microarray data were analyzed, and the expression and location of SRF were investigated in the early phase of AKI. Results Bioinformatics results demonstrated that SRF was dramatically elevated 2-4 h after ischemia/reperfusion (I/R) in mouse renal tissue. In I/R rats, SRF was mostly expressed and located in renal tubular epithelial cells (TECs). SRF started to increase at 1 h, peaked at 3-9 h and started to decrease at 12 h after I/R. The areas under the ROC curve of renal SRF mRNA, renal SRF protein, urinary SRF, serum SRF and serum creatinine (Scr) were 87.9%, 83.0%, 81.3%, 78.8%, 68.8%, respectively. Conclusion SRF is remarkably upregulated in early (before 24 h) AKI and can replace Scr as a potential new early diagnostic biomarker of AKI.

scholarly journals Enteral Baicalin, a Flavone Glycoside, Reduces Indicators of Cardiac Surgery-Associated Acute Kidney Injury in Rats

2018 ◽  
Vol 9 (1) ◽  
pp. 31-40 ◽  
Author(s):  
Jing Shi ◽  
Guofeng Wu ◽  
Xiaohua Zou ◽  
Ke Jiang
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Cardiac Surgery ◽  
Kidney Injury ◽  
Renal Tissue ◽  
Myeloperoxidase Activity ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Injury Index ◽  
Sprague Dawley Rats

Background/Aims: Cardiac surgery-associated acute kidney injury (CSA-AKI) is one of the most common postoperative complications in intensive care medicine. Baicalin has been shown to have anti-inflammatory and antioxidant roles in various disorders. We aimed to test the protective effects of baicalin on CSA-AKI using a rat model. Methods: Sprague-Dawley rats underwent 75 min of cardiopulmonary bypass (CPB) with 45 min of cardioplegic arrest (CA) to establish the AKI model. Baicalin was administered at different doses intragastrically 1 h before CPB. The control and treated rats were subjected to the evaluation of different kidney injury index and inflammation biomarkers. Results: Baicalin significantly attenuated CPB/CA-induced AKI in rats, as evidenced by the lower levels of serum creatinine, serum NGAL, and Kim1. Baicalin remarkably inhibited oxidative stress, reflected in the decreased malondialdehyde and myeloperoxidase activity, and enhanced superoxide dismutase activity and glutathione in renal tissue. Baicalin suppressed the expression of IL-18 and iNOS, and activated the Nrf2/HO-1 pathway. Conclusion: Our data indicated that baicalin mediated CPB/CA-induced AKI by decreasing the oxidative stress and inflammation in the renal tissues, and that baicalin possesses the potential to be developed as a therapeutic tool in clinical use for CSA-AKI.

scholarly journals Acute Kidney Injury in ADPKD Patients with Pneumonia

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Carlos Franco Palacios ◽  
Mira T. Keddis ◽  
Dingxin Qin ◽  
Ladan Zand ◽  
Guangxi Li ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Autosomal Dominant ◽  
Kidney Injury ◽  
Polycystic Kidney ◽  
X Ray ◽  
Lower Baseline ◽  
Acute Pneumonia ◽  
Chest X Ray ◽  
Hospital Stays ◽  
Autosomal Dominant Polycystic Kidney

Background. In animal models, polycystic kidneys are susceptible to acute kidney injury (AKI). We examined the occurrence of AKI in a cohort of autosomal dominant polycystic kidney disease (ADPKD) and non-ADPKD patients with acute pneumonia.Design. All ADPKD patients admitted to Mayo Clinic Rochester for pneumonia from January 1990 to April 2010 were examined. Sixty-three patients had lobar infiltration and consolidation on chest X-ray. After excluding patients on dialysis, with organ transplantation, and on chronic immunosuppression, 24 remaining ADPKD patients were enrolled. Twenty-three of the 24 were matched with 92 (1 : 4 ratio) non-ADPKD pneumonia patients based on their baseline eGFR. AKI was defined as serum creatinine elevation ≥0.3 mg/dL.Results. Sixteen of the 23 ADPKD patients (69.6%) and 36 of the 92 (39.1%) non-ADPKD patients developed AKI,P=0.008. In both groups, those who developed AKI had a lower baseline eGFR (41.1±5.00versus58.7±11.8in ADPKD and40.2±3.65versus51.8±2.24 mL/min/1.73 m2in the non-ADPKD group), more intensive care unit admissions, and longer hospital stays. AKI was associated with a reduced survival in both groups.Conclusions. Patients with ADPKD admitted for acute pneumonia had more frequent episodes of AKI than non-ADPKD patients with comparable kidney function.

scholarly journals Comparison of In-Hospital Outcomes Between Patients With or Without Acute Kidney Injury Developed After Hospitalization Following Acute Coronary Syndrome

2020 ◽  
Vol 16 (1) ◽  
pp. 3-10
Author(s):  
Md Sajjad Safi ◽  
Msi Tipu Chowdhury ◽  
Tanjima Parvin ◽  
Khurshed Ahmed ◽  
Md Ashraf Uddin Sultana ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Cardiogenic Shock ◽  
Hospital Stay ◽  
Kidney Injury ◽  
Duration Of Hospital Stay ◽  
Group A ◽  
Hospital Stays ◽  
Group B

Background: Acute Kidney Injury (AKI), a common complication of acute coronary syndromes (ACS), is associated with higher mortality and longer hospital stays. ACS patients with renal impairment during hospitalization are associated with adverse in-hospital outcomes in the form of heart failure, cardiogenic shock, arrhythmia, dialysis requirement and mortality. Objective: To compare the in-hospital adverse outcomesof patients with ACS with or without AKI. Materials and Methods: This prospective comparative study was conducted in the Department of Cardiology, BSMMU, Dhaka, during the period of August 2017 to July 2018. A total of 70 eligible patients were included in this study of which 35 patients were included in group A (ACS with AKI) and 35 patients were included in group B (ACS without AKI). AKI was diagnosed, on the basis of increased serum creatinine level 0.3mg/dL from baseline within 48 hours after hospitalization. They were subjected to electrocardiography, blood test for serum creatinine (on admission, 12 hours, 48 hours and at the time of discharge), lipid profile, 2-D echocardiography along with serum troponin, CK MB and electrolytes. Results: It was observed that mean age was 58.0±8.5 years in group A and 55.6±12.3 years in group B. Heart failure was more common in group A than in Group B (74.3% vs 34.2% p=0.001 respectively) and arrhythmia was more common in group A than in Group B (100% vs 74.2% respectively). 7(20%) patients of group A required dialysis. The mean duration of hospital stay was significantly higher in Group A than in the Group B (9.4±2.3 vs 7.2±0.6; p=0.001) days. Multiple logistic regression analysis revealed that heart failure, cardiogenic shock, duration of hospital stay were found to be the independently significant predictors of outcome of the patients with AKI with odds ratio being 5.53 (p=0.001), 4.353 (p=0.001) and 6.92 (p=0.001) Conclusion: This study shows that, heart failure, cardiogenic shock, arrhythmia, dialysis requirement, were more common in the patients with AKI (group A) than in the patients without AKI (group B). The duration of hospital stays were longer in patients with AKI (group A) than in the patients without AKI (group B). Therefore, an important research target is the identification of high-risk patients with ACS experiencing AKI, thereby appropriate medication and follow-up should be implemented. University Heart Journal Vol. 16, No. 1, Jan 2020; 3-10

Drug-Induced Kidney Disease Associated With Selected Antibiotics

2020 ◽  
Vol 35 (5) ◽  
pp. 225-229
Author(s):  
Alexia S. Alvarez ◽  
Oluseyi Oyerinde ◽  
Justin P. Reinert
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Older People ◽  
Hospital Costs ◽  
Kidney Injury ◽  
Clear Understanding ◽  
First Line ◽  
Drug Induced ◽  
Improved Outcomes ◽  
Hospital Stays

Structural and functional degeneration of the kidneys occur as the human body ages, making oler people especially susceptible to the consequences of acute kidney injury. Furthermore, the use of nephrotoxic agents, combined with the increased incidence of acute kidney injury and likelihood of an intensive-care unit admission, makes geriatric patients prone to develop drug-induced kidney disease. Vancomycin is routinely used as the first-line treatment for methicillin-resistant Staphylococcus aureus, but is known to be nephrotoxic; studies have shown that an early switch from vancomycin to alternatives does not necessarily prevent renal insult. Therefore, we aim to discuss the mechanisms of drug-induced kidney disease with regard to vancomycin, daptomycin, and ceftaroline and to provide insight as to their safety profiles with regard to older people. A clear understanding of this topic will aid clinicians in selecting drug therapy and may lead to shortened hospital stays, lower hospital costs, and improved outcomes of critically ill older people.

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