scholarly journals Xianling Gubao Capsule Prevents Cadmium-Induced Kidney Injury

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Jian Huang ◽  
Xiao-tong Ma ◽  
Duo-duo Xu ◽  
Bao-jin Yao ◽  
Da-qing Zhao ◽  
...  
Keyword(s):  
Oral Administration ◽  
Kidney Injury ◽  
Bone Diseases ◽  
Control Group ◽  
National Medical ◽  
Fluorescence Quantitative Pcr ◽  
Cadmium Poisoning ◽  
Injury Model ◽  
Renal Tubular ◽  
The Impact

Xianling Gubao Capsule (XGC), a kind of capsule preparation of Chinese herbal officially approved for sale by the National Medical Products Administration (NMPA), has the effect of tonifying kidney and strengthening bones. Although the impact of XGC in treating bone diseases has been widely studied, the effect of XGC in kidney injury is unknown yet. The kidney injury model is established by intraperitoneal injection with cadmium chloride (CdCl2). Before model establishment, each XGC group was pregavaged with XGC for 10 d. After 10 d, CdCl2 was injected intraperitoneally into the model group and each XGC group, each XGC group continued to be gavaged with XGC for 4 weeks, and the control group was gavaged with equal doses of distilled water once daily. The level of serum urea nitrogen (BUN) and serum creatinine (Cr) is evaluated by kit. The effect of XGC on protecting kidney injury in mice with kidney injury is analyzed by histopathology (HE stain), immunohistochemistry (IHC), and real-time fluorescence quantitative PCR (RT-qPCR). The results show that CdCl2 significantly increases the level BUN and Cr in serum and results in remarkable pathological changes in the nephron, including tubule edema, congestion, and necrosis. While oral administration of XGC can significantly decrease BUN and Cr in serum and prevent and protect the kidney from the above injuries. In addition, the protein expression of p-mTOR was remarkably reduced, and the ratio of LC3II/LC3I protein and mRNA was significantly increased in mice with oral administration of XGC. Our findings suggest that XGC can prevent and protect kidney injury by improving the state of renal tubular hyperemia and necrosis and reduce the level of BUN and Cr in cadmium poisoning mice.

scholarly journals Effect of alpha-lipoic acid on antioxidant gene expression and kidney injury in alloxan-induced diabetic rats

2018 ◽  
Vol 8 (1) ◽  
pp. 6-6 ◽  
Author(s):  
Parisa Jamor ◽  
Hassan Ahmadvand ◽  
Hesam Ashoory ◽  
Esmaeel Babaeenezhad
Keyword(s):  
Gene Expression ◽  
Lipoic Acid ◽  
Kidney Injury ◽  
Diabetic Rats ◽  
Pcr Analysis ◽  
Control Group ◽  
Diabetic Patients ◽  
Alpha Lipoic Acid ◽  
The Impact ◽  
Gpx Activity

Background: Myeloperoxidase (MPO) is involved in the initiation, progression, and complications of atherosclerosis in diabetic patients. Objectives: In the current study, the impact of alpha-lipoic acid (LA), a natural antioxidant and a cofactor in the enzyme complexes on MPO, catalase (CAT) and glutathione peroxidase (GPx) activity, glutathione (GSH) and malondialdehyde (MDA) level, histopathology of kidney and expression of antioxidant enzymes, superoxide dismutase (SOD), GPx and CAT which are involved in the detoxification of reactive oxygen species (ROS), was evaluated in alloxan-induced diabetic rats. Materials and Methods: In this study, 30 male Rattus norvegicus rats randomly divided into three groups; control (C), non-treated diabetic (NTD), and LA-treated diabetics (LATD) was induced by alloxan monohydrate (100mg/kg; subcutaneous [SC]). Then treatment was performed with alphaLA (100 mg/kg intraperitoneal (i.p) daily to 6 weeks). Blood sample of animals collected to measure levels of MPO, CAT and GPx activity GSH and MDA. Kidney paraffin sections were prepared to estimate histological studies and to measure quantitative gene expression SOD, GPX and CAT in kidney. Results: Induction of diabetes led to a significant increase in MPO and MDA, reduced GSH level and GPx and CAT activities (P < 0.05). However, treatment with alpha-LA led to a significant elevation in GPx, CAT and GSH levels with a reduction in MPO activities and MDA levels (P < 0.05). Furthermore, the real-time reverse transcriptase-polymerase chain reaction (RT-PCR) analysis results showed increased expressions of GPx, CAT and SOD enzyme in the treatment group compared with the diabetic control group. Histopathological lesions such as increased glomerular volume and lymphocyte infiltration were attenuated in the alpha-LA treated group. Conclusions: Our findings indicated that alpha-LA supplementation is effective in preventing complications induced by oxidative stress and atherosclerosis in diabetic rats.

Multimodal Analgesia and Decreased Opioid Use in Adult Trauma Patients

2020 ◽  
Vol 86 (8) ◽  
pp. 950-954
Author(s):  
Andrew L. Drahos ◽  
Anthony M. Scott ◽  
Tracy J. Johns ◽  
Dennis W. Ashley
Keyword(s):  
Acute Kidney Injury ◽  
Management Strategies ◽  
Kidney Injury ◽  
Multimodal Analgesia ◽  
The United States ◽  
Control Group ◽  
Trauma Patients ◽  
Opioid Use ◽  
Trauma Service ◽  
The Impact

Background There is an opioid epidemic in the United States. With the increased concern of over-prescribing opioids, physicians are seeking alternative pain management strategies. The purpose of this study is to review the impact of instituting a multimodal analgesia (MMA) guideline on decreasing opioid use in trauma patients at a Level 1 trauma center. Methods In 2017, an MMA guideline was developed and included anti-inflammatories, muscle relaxants, neuropathic agents, and local analgesics in addition to opioids. Staff were educated and the guideline was implemented. A retrospective review of medications prescribed to patients admitted from 2016 through 2018 was performed. Patients admitted in 2016 served as the control group (before MMA). In 2018, all patients received multimodal pain therapy as standard practice, and served as the comparison group. Results A total of 10 340 patients were admitted to the trauma service from 2016 through 2018. There were 3013 and 3249 patients for review in 2016 and 2018, respectively. Total morphine milligram equivalents were 2 402 329 and 1 975 935 in 2016 and 2018, respectively, a 17.7% decrease ( P < .001). Concurrently, there was a statistically significant increase in the use of multimodal pain medications. A secondary endpoint was studied to evaluate for changes in acute kidney injury; there was not a statistically significant increase (0.56% versus 0.68%, P = .55). Discussion Implementation of an MMA guideline significantly reduced opioid use in trauma patients. The use of nonopioid MMA medications increased without an increased incidence of acute kidney injury.

scholarly journals Renal tubular injury exacerbated by vasohibin-1 deficiency in a murine cisplatin-induced acute kidney injury model

2019 ◽  
Vol 317 (2) ◽  
pp. F264-F274 ◽  
Author(s):  
Satoshi Tanimura ◽  
Katsuyuki Tanabe ◽  
Hiromasa Miyake ◽  
Kana Masuda ◽  
Keigo Tsushida ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Endothelial Cells ◽  
Kidney Injury ◽  
Protective Effects ◽  
Tubular Injury ◽  
Injury Model ◽  
Peritubular Capillaries ◽  
Renal Tubular ◽  
And Function ◽  
Hospital Acquired

Acute kidney injury (AKI) is frequently encountered in clinical practice, particularly secondarily to cardiovascular surgery and administration of nephrotoxic agents, and is increasingly recognized for initiating a transition to chronic kidney disease. Clarifying the pathogenesis of AKI could facilitate the development of novel preventive strategies, because the occurrence of hospital-acquired AKI is often anticipated. Vasohibin-1 (VASH1) was initially identified as an antiangiogenic factor derived from endothelial cells. VASH1 expression in endothelial cells has subsequently been reported to enhance cellular stress tolerance. Considering the importance of maintaining peritubular capillaries in preventing the progression of AKI, the present study aimed to examine whether VASH1 deletion is involved in the pathogenesis of cisplatin-induced AKI. For this, we injected male C57BL/6J wild-type (WT) and VASH1 heterozygous knockout (VASH1+/−) mice intraperitoneally with either 20 mg/kg cisplatin or vehicle solution. Seventy-two hours after cisplatin injection, increased serum creatinine concentrations and renal tubular injury accompanied by apoptosis and oxidative stress were more prominent in VASH1+/− mice than in WT mice. Cisplatin-induced peritubular capillary loss was also accelerated by VASH1 deficiency. Moreover, the increased expression of ICAM-1 in the peritubular capillaries of cisplatin-treated VASH1+/− mice was associated with a more marked infiltration of macrophages into the kidney. Taken together, VASH1 expression could have protective effects on cisplatin-induced AKI probably by maintaining the number and function of peritubular capillaries.

scholarly journals Assessment of Urinary Kidney Injury Molecule-1 as an Indicator of Early Renal Insult in Children with Cystic Fibrosis

2020 ◽  
Vol 8 (B) ◽  
pp. 262-267
Author(s):  
Walaa Shahin ◽  
Ahmed Bader ◽  
Rawdah Ahmed ◽  
Mona Alattar ◽  
Mona Alfalaki ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Urine Analysis ◽  
Kidney Injury ◽  
Fractional Excretion ◽  
Control Group ◽  
Renal Ultrasound ◽  
Fractional Excretion Of Sodium ◽  
Beta 2 ◽  
Renal Tubular ◽  
Kidney Injury Molecule 1

BACKGROUND: The risk of acute kidney injury in cystic fibrosis (CF) patients is due to renal tubular affection by CFTR gene. AIM: Our study aimed at early detection of renal impairment in CF patients, to enable careful monitoring and adjustment of nephrotoxic medications. METHODS: Fifty patients with CF were enrolled in our study; they were age- and sex-matched to 40 healthy control children. All subjects were screened by urine analysis, measurements of kidney function tests, fractional excretion of sodium, β2-microglobulin (beta-2-M) excretion, and renal ultrasound examination. Urinary kidney injury molecule-1 (KIM-1) was assayed using ELISA technique. RESULTS: Both urinary beta-2-M and KIM-1 concentrations were significantly higher in CF patients compared to the control group (p < 0.001). The duration of the disease was significantly positively correlated with the urinary beta-2-M and KIM-1 levels (r = 0.6 and 0.7, respectively; p < 0.01). CONCLUSIONS: Our results showed that urinary KIM-1 can be considered as a sensitive early indicator of acute renal injury.

Adult Zebrafish Model for Screening Drug-Induced Kidney Injury

2020 ◽  
Vol 174 (2) ◽  
pp. 241-253 ◽  
Author(s):  
Yuki Kato ◽  
Yutaka Tonomura ◽  
Hiroyuki Hanafusa ◽  
Kyohei Nishimura ◽  
Tamio Fukushima ◽  
...  
Keyword(s):  
Predictive Value ◽  
Safety Issue ◽  
Kidney Injury ◽  
Pathological Examination ◽  
Control Group ◽  
Adult Zebrafish ◽  
Drug Induced ◽  
Zebrafish Model ◽  
Renal Tubular

Abstract Drug-induced kidney injury is a serious safety issue in drug development. In this study, we evaluated the usefulness of adult zebrafish as a small in vivo system for detecting drug-induced kidney injury. We first investigated the effects of typical nephrotoxicants, gentamicin and doxorubicin, on adult zebrafish. We found that gentamicin induced renal tubular necrosis with increased lysosome and myeloid bodies, and doxorubicin caused foot process fusion of glomerular podocytes. These findings were similar to those seen in mammals, suggesting a common pathogenesis. Second, to further evaluate the performance of the model in detecting drug-induced kidney injury, adult zebrafish were treated with 28 nephrotoxicants or 14 nonnephrotoxicants for up to 4 days, euthanized 24 h after the final treatment, and examined histopathologically. Sixteen of the 28 nephrotoxicants and none of the 14 nonnephrotoxicants caused drug-induced kidney injury in zebrafish (sensitivity, 57%; specificity, 100%; positive predictive value, 100%; negative predictive value, 54%). Finally, we explored genomic biomarker candidates using kidneys isolated from gentamicin- and cisplatin-treated zebrafish using microarray analysis and identified 3 candidate genes, egr1, atf3, and fos based on increased expression levels and biological implications. The expression of these genes was upregulated dose dependently in cisplatin-treated groups and was &gt; 25-fold higher in gentamicin-treated than in the control group. In conclusion, these results suggest that the adult zebrafish has (1) similar nephrotoxic response to those of mammals, (2) considerable feasibility as an experimental model for toxicity studies, and (3) applicability to pathological examination and genomic biomarker evaluation in drug-induced kidney injury.

Inhibition of TRAF1 protects renal tubular epithelial cells against hypoxia/reoxygenation injury

2021 ◽  
Keyword(s):  
Cell Viability ◽  
Western Blotting ◽  
Mtt Assay ◽  
Cell Apoptosis ◽  
Mapk Pathway ◽  
Kidney Injury ◽  
Control Group ◽  
Injury Model ◽  
Hk2 Cells ◽  
Hypoxia Reoxygenation

Background and objective: This study aimed to explore the expression of TRAF1 in vitro kidney injury model, and the function mechanism of TRAF1 in the model growth and apoptosis. Methods: After transfecting HK2 cells with short hair RNA (shRNA), shTRAF1 gene silencing model was established. The cells were divided into shRNA group and shNC group. For kidney injury model, we used hypoxia/reoxygenation to establish H/R cell lines. MTT assay was used to determine cell viability. PI/FITC staining was used to determine cell apoptosis. The genes expressions were determined by RT-qPCR and western blotting, respectively. The concentration of MDA, SOD, iNOS and LDH was determined by ELISA. Results: The results of RT-qPCR and western blotting assay revealed that TRAF1 upregulated expression in AKI model cells. The results of MTT assay revealed that shRNA group exhibited significantly higher cell viability and lower cell apoptosis compared with the control group in H/R HK2 cells. In addition, TRAF1 downregulated expression inhibits oxidative stress response in H/R treated HK2 cell. Mechanically, TRAF1 deficiency protects HK2 cell via inhibiting p38-MAPK pathway. Conclusions: Our study suggests that TRAF1 could be a target in kidney injury treatment.

scholarly journals The Downregulation of Placental Lumican Promotes the Progression of Preeclampsia

2021 ◽  
Author(s):  
Chao Liu ◽  
Yulian Hu ◽  
Zhongying Wang ◽  
Hua Pan ◽  
Yan Ren ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Line ◽  
Control Group ◽  
Trophoblast Cells ◽  
Human Trophoblast ◽  
P53 Expression ◽  
Fluorescence Quantitative Pcr ◽  
And Migration ◽  
Negative Controls ◽  
The Impact

AbstractMultiple pieces of evidence illustrate that impaired trophoblast function results in preeclampsia (PE), and migration/invasion of human trophoblast cells is stringently regulated by extracellular matrix (ECM) components. Many studies have indicated abnormal expressions of placental ECM components are associated with preeclampsia. However, the change and influence of lumican, a vital member of extracellular matrix (ECM) molecules, on trophoblast cells during preeclampsia remain unclear. This study examines the possibility that the roles of lumican in trophoblast cells contribute to PE. To address this issue, the expression of lumican in human placental tissues was observed using immunohistochemistry, fluorescence quantitative PCR, and Western blot technology. After the HTR-8/SVneo cell line was transfected with pcDNA3.1-human lumican, pGPU6-human lumican shRNA, and their negative controls, the impact of lumican on the HTR-8/SVneo cell line was investigated. Lumican was expressed in human placental tissues. Compared with the control group, its expression was significantly lower in PE placentas. Lumican downregulation inhibited cell proliferation significantly and reduced Bcl-2 expression, but increased P53 expression. These results indicate that the downregulation of placental lumican may drive PE development via promoting the downregulation of Bcl-2 expression and upregulation of P53.

scholarly journals A review of Covid-19 and acute kidney injury: from pathophysiology to clinical results

2021 ◽  
Author(s):  
Inah Maria D. Pecly ◽  
Rafael B. Azevedo ◽  
Elizabeth S. Muxfeldt ◽  
Bruna G. Botelho ◽  
Gabriela G. Albuquerque ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Organ Dysfunction ◽  
Kidney Injury ◽  
Clinical Results ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Renal Tubular Cells ◽  
Kidney Involvement ◽  
Renal Tubular ◽  
The Impact

Abstract Acute kidney injury (AKI) in hospitalized patients with COVID-19 is associated with higher mortality and a worse prognosis. Nevertheless, most patients with COVID-19 have mild symptoms, and about 5% can develop more severe symptoms and involve hypovolemia and multiple organ dysfunction syndrome. In a pathophysiological perspective, severe SARS-CoV-2 infection is characterized by numerous dependent pathways triggered by hypercytokinemia, especially IL-6 and TNF-alpha, leading to systemic inflammation, hypercoagulability, and multiple organ dysfunction. Systemic endotheliitis and direct viral tropism to proximal renal tubular cells and podocytes are important pathophysiological mechanisms leading to kidney injury in patients with more critical infection, with a clinical presentation ranging from proteinuria and/or glomerular hematuria to fulminant AKI requiring renal replacement therapies. Glomerulonephritis, rhabdomyolysis, and nephrotoxic drugs are also associated with kidney damage in patients with COVID-19. Thus, AKI and proteinuria are independent risk factors for mortality in patients with SARS-CoV-2 infection. We provide a comprehensive review of the literature emphasizing the impact of acute kidney involvement in the evolutive prognosis and mortality of patients with COVID-19.

scholarly journals Evaluation of Ceftolozane/Tazobactam, Ceftazidime/Avibactam and Meropenem/Vaborbactam Against Multidrug-Resistant (MDR) Pseudomonas

2021 ◽  
Vol 1 (S1) ◽  
pp. s69-s70
Author(s):  
Haider Shamsulddin ◽  
Jeffrey Lin ◽  
Julie Ribes ◽  
Thein Myint
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Patient Outcomes ◽  
Kidney Injury ◽  
Multidrug Resistant ◽  
New Combination ◽  
Control Group ◽  
Retrospective Case ◽  
University Of Kentucky ◽  
Combination Antibiotics ◽  
The Impact

Background: Data on the patient outcomes for newer β-lactam–β-lactamase inhibitor (BLBI) drugs compared to carbapenem-containing combination antibiotics for multidrug-resistant (MDR)–Pseudomonas aeruginosa infections are limited. Methods: This retrospective, case–control observational study was based on chart review of the patients managed at the University of Kentucky. Results: In total, 143 patients with MDRO Pseudomonas aeruginosa infections were identified and divided into 2 groups: 1 group received newer BLBI combinations with or without aminoglycosides or polymyxins, for at least 72 hours, and the control group received carbapenem containing combination antibiotics or other antibiotics. Baseline characteristics and patient outcomes are shown in Table 1. Discussion: The newer BLBI combinations group consisted of 60.8% MDR Pseudomonas bacteremia, whereas the control group had 68.4% of MDR Pseudomonas respiratory cultures. Overall, the use of newer BLBI combinations such as ceftazidime/avibactam, ceftolozane/tazobactam, and meropenem/vaborbactam was associated with lower rates of acute kidney injury (AKI), shorter LOS, and lower mortality rates compared to the control group, and these differences were statistically significant. Because the 2 populations of patient differed significantly based on the site of infection (sepsis vs pneumonia), the data were reanalyzed to evaluate the impact of therapy on the occurrence of AKI, LOS, and mortality based on the site of infection. Only those patients with sepsis who received the newer combination drugs had significantly better rates of AKI, lower LOS, and had lower rates of mortality. The 2 treatment arms were not statistically different when comparing patients with pneumonia. Additionally, the use of these new combination therapies did not make a difference regarding readmission rates or duration of bacteremia for the patients included in the study.Funding: NoDisclosures: None

scholarly journals Impact of Ciprofloxacin With Autophagy on Acute Kidney Injury

2021 ◽  
Author(s):  
Woo Yeong Park ◽  
Sun-Ha Lim ◽  
Yaerim Kim ◽  
Jin Hyuk Paek ◽  
Kyubok Jin ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Caspase 3 ◽  
Kidney Injury ◽  
Underlying Mechanism ◽  
Beclin 1 ◽  
Control Group ◽  
Renal Tubules ◽  
Tubular Injury ◽  
Renal Tubular Cells ◽  
Renal Tubular

Abstract Renal tubular injury caused by oxidative stress and inflammation results in acute kidney injury. Recent research reported that antibiotics may restore deteriorated renal tubules, but the underlying mechanism remains unclear. Therefore, we investigated the efficacy and mechanism of action of antibiotics against renal tubular injury. We screened ciprofloxacin, ceftizoxime, minocycline, and netilmicin and selected ciprofloxacin to examine further because of its low toxicity towards renal tubular cells. We evaluated the effect of ciprofloxacin on cell survival by analyzing apoptosis and autophagy. TUNEL assay results showed that the ciprofloxacin group had less apoptotic cells than the control group. The ratio of cleaved caspase 3 to caspase 3, the final effector in the apoptosis process, was decreased, but the ratio of Bax to Bcl-2 located upstream of caspase 3 was not decreased in the ciprofloxacin group. Therefore, apoptosis inhibition does not occur via Bax/Bcl-2. Conversely, the levels of phosphorylated Bcl-2, and Beclin-1, an autophagy marker, were increased, and that of caspase-3 was decreased in the ciprofloxacin group. This indicates that ciprofloxacin enhanced autophagy, increasing the amount of free Beclin-1 via phosphorylated Bcl-2, and inhibited caspase activity. Therefore, ciprofloxacin might increase renal cell viability through the autophagy activation in acute kidney injury.

Sign in / Sign up

Export Citation Format

Share Document