scholarly journals The Efficacy of Cinnamon Extract ( Cinnamomum burmannii ) on Reducing Staging Acute Kidney Injury in Ischemia Reperfusion (IR) Model

2020 ◽  
Vol 5 (1) ◽  
pp. 178-181
Author(s):  
Evi Lusiana ◽  
Nia Savitri Tamzil ◽  
Desi Oktarina
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Filtration Rate ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Sham Operation ◽  
Cinnamon Extract ◽  
Model Method ◽  
Before And After ◽  
Cinnamomum Burmannii

A B S T R A C TIntroduction. Acute kidney injury (AKI) is defined as sudden decline in theglomerular filtration rate, resulting in the retention of nitrogenous wastes, such asurea and creatinine in plasma. Cinnamomum burmannii is known as a anti-inflammatory renoprotective agent, although the precise mechanism is not wellunderstood. This study aimed to elucidate the effectiveness of Cinnamomumburmannii extract in decreasing creatinine level of acute kidney injury Ischemiareperfusion (IR) model. Method. We performed Ischemia reperfusion (IR) in maleWistar rat to induce acute kidney injury. The rat (n=30) were divided into six groups:IR, 1 group treated with methylprednisolone as a control (IR+M), 3 groups treatedwith different oral Cinnamomum burmannii extract doses (50mg/kg (IR+EKM1),100mg/kg (IR+EKM2), and 200 mg/kg (IR+EKM3), and a Sham operation (SO)group. AKI stage reduction based on serum creatinine levels, before and aftermodeling, before and after the cinnamon extract intervention. Creatinine levels werequntified by spectrophotometry and analyzed by SPSS. Result. Cinnamomumburmannii extract lowers creatinine levels; significant (P <0.05). 200 mg / kgbb isthe effective dose of lowering creatinine levels in the IR model. Conclusion.Cinnamomum burmannii extract reduced serum creatinine levels associated withdecreased acute renal staging in the IR model.

scholarly journals Efficacy of cinnamon (Cinnamomum burmannii) extract to decrease serum creatinine in acute kidney injury induced male wistar rats

2019 ◽  
Vol 3 (4) ◽  
pp. 29-38
Author(s):  
Evi Lusiana ◽  
Nia Savitri Tamzil ◽  
Desi Oktarina
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Wistar Rats ◽  
Kidney Injury ◽  
Control Group ◽  
Control Group Design ◽  
Cinnamon Extract ◽  
White Rats ◽  
Male Wistar Rats ◽  
Cinnamomum Burmannii

Background Kidney vital function as a regulator of blood volume and chemical composition to excrete solute and water selectively. Acute kidney injury (AKI) is a sudden decline in kidney function which is temporary, is marked by an increase in serum creatinine levels and decreased urine output. Objective This study aims to determine the effectiveness of cinnamon extract in acute kidney injury induced male wistar rats. Method An experimental in vivo with pre-post control group design was conducted in twenty-five wistar strain white rats that were divided into 5 treatment groups that received methylprednisolone as a positive control, aquades, and different dose of cinnamon extracts (50 mg/kgBW, 100 mg/kgBW, and 200 mg/kgBW). The rat model of acute kidney injury was prepared by the method of unilateral ureteral obstruction (UUO). The effectiveness of cinnamon extract was carried out by creatinine levels checked using ELISA and analyzed by ANOVA. Results The extract of cinnamon can lower serum creatinine levels were significantly (p <0.05). A dose of 100mg / KgBW is an effective dose in AKI compare to methylprednisolone. Conclusion Extract of cinnamon (Cinnamomum burmannii) corrected creatinine levels of acute kidney injury induced male wistar rats.   Keywords: Acute kidney injury, cinnamon extract, creatinine    

scholarly journals THE STUDY OF RENOPROTECTIVE PROPERTIES OF ERYTROPOETIN DERIVATIVES ON THE KIDNEY ISCHEMIA-REPERFUSION MODEL

2018 ◽  
Vol 25 (6) ◽  
pp. 73-77 ◽  
Author(s):  
V. V. Elagin ◽  
D. A. Kostina ◽  
O. I. Bratchikov ◽  
M. V. Pokrovsky ◽  
T. G. Pokrovskaya
Keyword(s):  
Acute Kidney Injury ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Fractional Sodium Excretion ◽  
Male Wistar Rats ◽  
Microcirculatory Disorders

Aim.The research was designed to study the renoprotective properties of erythropoietin derivatives on the kidney ischemiareperfusion experimental model.Materials and methods.The renoprotective properties of asialo erythropoietin (0.4 μg/kg and 2.4 μg/kg 30 minutes before the induction of ischemia) and carbamylated darbepoetin (50 μg/kg 24 hours before the ischemic stimulus) were studied in comparison with erythropoietin and darbepoetin in a series of experiments on male Wistar rats on a 40-minute bilateral model of renal ischemia-reperfusion. The renoprotective properties were evaluated by the results of biochemical markers of acute kidney injury, the dynamics of glomerular filtration rate and fractional sodium excretion, as well as the severity of microcirculatory disorders.Results.It was found that the prophylactic use of asialo erythropoietin (dose-dependent) and carbamylated darbepoetin leads to a decrease in the serum concentration of markers of acute renal damage, an increase in the glomerular filtration rate, a decrease in fractional sodium excretion, and a decrease in microcirculatory disorders.Conclusion.Asialo erythropoietin and carbamylated darbepoetin have the pronounced renoprotective properties and are the promising agents for the prevention and treatment of acute kidney injury.

scholarly journals Is Tubular Dysfunction a Risk Factor for AKI?

Nephron ◽  
2020 ◽  
Vol 144 (12) ◽  
pp. 680-682
Author(s):  
Alexander L. Bullen ◽  
Joachim H. Ix
Keyword(s):  
Acute Kidney Injury ◽  
Risk Factor ◽  
Filtration Rate ◽  
Estimated Glomerular Filtration Rate ◽  
Function Versus ◽  
Clinical Care ◽  
Kidney Injury ◽  
Tubular Dysfunction ◽  
Routine Clinical Care ◽  
Before And After

Tubular functions are critical for homeostasis maintenance. However, tubular function markers are not typically assessed in routine clinical care. Recent research by our group has revealed that tubular dysfunction at baseline is a risk factor for subsequent acute kidney injury (AKI), independent of estimated glomerular filtration rate and albuminuria. Here, we describe the underlying hypotheses and biological insights and contrast the changes in tubule function versus injury both before and after an AKI episode.

scholarly journals New mouse model of chronic kidney disease transitioned from ischemic acute kidney injury

2019 ◽  
Vol 317 (2) ◽  
pp. F286-F295 ◽  
Author(s):  
Jin Wei ◽  
Jie Zhang ◽  
Lei Wang ◽  
Shan Jiang ◽  
Liying Fu ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Reperfusion Injury ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury

Acute kidney injury (AKI) significantly increases the risk of development of chronic kidney disease (CKD), which is closely associated with the severity of AKI. However, the underlying mechanisms for the AKI to CKD transition remain unclear. Several animal models with AKI to CKD transition have been generated and widely used in research; however, none of them exhibit the typical changes in glomerular filtration rate or plasma creatinine, the hallmarks of CKD. In the present study, we developed a novel model with a typical phenotype of AKI to CKD transition in C57BL/6 mice. In this model, life-threatening ischemia-reperfusion injury was performed in one kidney, whereas the contralateral kidney was kept intact to maintain animal survival; then, after 2 wk of recovery, when the renal function of the injured kidney restored above the survival threshold, the contralateral intact kidney was removed. Animals of this two-stage unilateral ischemia-reperfusion injury model with pedicle clamping of 21 and 24 min exhibited an incomplete recovery from AKI and subsequent progression of CKD with characteristics of a progressive decline in glomerular filtration rate, increase in plasma creatinine, worsening of proteinuria, and deleterious histopathological changes, including interstitial fibrosis and glomerulosclerosis. In conclusion, a new model of the AKI to CKD transition was generated in C57BL/6 mice.

Netrin-1 and kidney injury. II. Netrin-1 is an early biomarker of acute kidney injury

2008 ◽  
Vol 294 (4) ◽  
pp. F731-F738 ◽  
Author(s):  
W. Brian Reeves ◽  
Osun Kwon ◽  
Ganesan Ramesh
Keyword(s):  
Acute Kidney Injury ◽  
Folic Acid ◽  
Serum Creatinine ◽  
Renal Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Peak Level ◽  
Urine Samples ◽  
Mortality And Morbidity ◽  
Early Biomarker

Acute kidney injury is an important complication in hospitalized patients often diagnosed late and associated with high mortality and morbidity. Although biomarkers for nephrotoxicity are available, they often lack sensitivity and specificity for detecting tubular injury. Netrin-1 is a laminin-like molecule highly expressed in many organs including kidney. To determine the value of netrin-1 as a biomarker of renal injury, we analyzed its urinary excretion following ischemia-reperfusion-, cisplatin-, folic acid-, and endotoxin-induced renal injury in mice. Urinary netrin-1 levels increased markedly within 3 h of ischemia-reperfusion (40 ± 14-fold, P < 0.01 vs. baseline), reached a peak level at 6 h, and decreased thereafter, returning to near baseline by 72 h. Serum creatinine significantly increased only after 24 h of reperfusion. Similarly, in cisplatin-, folic acid-, and lipopolysaccharide-treated mice, urine netrin-1 excretion increased as early as 1 h and reached a peak level at 6 h after injection. However, serum creatinine was raised significantly after 6, 24, and 72 h after folic acid, lipopolysaccharide, and cisplatin administration, respectively. NGAL excretion in folic acid- and lipopolysaccharide-treated mice urine samples could only be detected by 24 h after drug administration. Furthermore, urinary netrin-1 excretion increased dramatically in 13 acute renal failure patients, whereas none was detected in 6 healthy volunteer urine samples. Immunohistochemical localization showed that netrin-1 is highly expressed in tubular epithelial cells in transplanted human kidney. We conclude that urinary netrin-1 is a promising early biomarker of renal injury.

scholarly journals Global miRNA expression is temporally correlated with acute kidney injury in mice

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e1729 ◽  
Author(s):  
Rui Cui ◽  
Jia Xu ◽  
Xiao Chen ◽  
Wenliang Zhu
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Mirna Expression ◽  
Ischemia Reperfusion Injury ◽  
Dominant Role ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Current Evidence ◽  
Tubulointerstitial Injury ◽  
Pathological Development

MicroRNAs (miRNAs) are negative regulators of gene expression and protein abundance. Current evidence shows an association of miRNAs with acute kidney injury (AKI) leading to substantially increased morbidity and mortality. Here, we investigated whether miRNAs are inductive regulators responsible for the pathological development of AKI. Microarray analysis was used to detect temporal changes in global miRNA expression within 48 h after AKI in mice. Results indicated that global miRNA expression gradually increased over 24 h from ischemia reperfusion injury after 24 h, and then decreased from 24 h to 48 h. A similar trend was observed for the index of tubulointerstitial injury and the level of serum creatinine, and there was a significant correlation between the level of total miRNA expression and the level of serum creatinine (p< 0.05). This expression-phenotype correlation was validated by quantitative reverse transcription PCR on individual miRNAs, including miR-18a, -134, -182, -210 and -214. Increased global miRNA expression may lead to widespread translational repression and reduced cellular activity. Furthermore, significant inflammatory cytokine release and peritubular capillary loss were observed, suggesting that the initiation of systematic destruction programs was due to AKI. Our findings provide new understanding of the dominant role of miRNAs in promoting the pathological development of AKI.

Abstract 15477: Endothelial Cells Overexpressing Interleukin-8 Receptors are Renoprotective in Rats With Acute Kidney Injury

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Fadi G Hage ◽  
Dongqi Xing ◽  
Samantha Giordano ◽  
Yuanyuan Guo ◽  
Suzanne Oparil ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Endothelial Cells ◽  
Serum Creatinine ◽  
Ischemia Reperfusion ◽  
Femoral Vein ◽  
Kidney Injury ◽  
Capillary Density ◽  
Interleukin 8 ◽  
Left Renal Artery ◽  
Sprague Dawley

Introduction: In ischemia-reperfusion acute kidney injury (AKI) interleukin-8 (IL8) attracts neutrophils to the site of injury. Neutrophils interact with the damaged endothelium triggering the pro-inflammatory response that prolongs the underperfused state of the kidney and exacerbates injury. Hypothesis: We tested the hypothesis that intravenous transfusion of rat aortic endothelial cells (ECs) transduced with IL8 receptors (IL8RA/RB-ECs) ameliorates renal dysfunction and promotes structural recovery of the kidney post AKI. Methods and Results: Male Sprague-Dawley rats were subjected to sham surgery or AKI by clamping the left renal artery for 45 min and removing the right kidney. At time of reperfusion, 1.5x10 6 IL8RA/RB-ECs, ECs with empty adenoviral vector (AdNull-ECs), or vehicle were infused in the femoral vein. At 24 hrs after AKI, serum creatinine increased ~ 10 fold in the vehicle-treated group and then decreased towards baseline. IL8RA/RB-ECs but not AdNull-ECs significantly blunted the rise in serum creatinine (Fig) and decreased the local expression in the kidney and the circulating levels of inflammatory mediators at 24 hrs after AKI. At 6 wks after AKI, vehicle-treated rats had significant albuminuria compared to sham controls and EC treatment decreased albuminuria by ~65% (Fig). Stained kidney sections at 6 wks after AKI showed that vehicle-treated rats had increased interstitial collagen and decreased capillary density compared to sham controls. IL-8RA/RB-ECs were more effective at reducing interstitial collagen staining than AdNull-ECs. IL8RA/RB-ECs but not AdNull-ECs increased capillary density compared to vehicle (Fig). Conclusions: Following ischemia-reperfusion AKI, ECs equipped with IL8 receptors are attracted to the site of injury in order to inhibit inflammation, accelerate tissue repair, and preserve renal function. Our innovative cell-based strategy holds promise for improving outcomes after AKI.

MO066GASDERMIND MUTATION IS PROTECTIVE AGAINST RENAL ISCHEMIA REPERFUSION INJURY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Natasha Rogers ◽  
Jennifer Li ◽  
Stephen Alexander
Keyword(s):  
Bone Marrow ◽  
Acute Kidney Injury ◽  
Cell Death ◽  
Serum Creatinine ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Chimeric Mice ◽  
Wild Type ◽  
Donor Bone Marrow

Abstract Background and Aims Ischemia reperfusion injury (IRI) is an important contributor to acute kidney injury (AKI) and manifests as delayed graft function following kidney transplantation. Limiting the damage of IRI has implications on graft outcomes and has driven further exploration of the underlying pathophysiology. We hypothesize that pyroptosis, a pro-inflammatory form of cell death, has an important role in IRI and AKI. The pyroptosis pathway converges to the cleavage and release of N-terminal of the Gasdermin-D protein, leading to pore formation in the cell membrane and cell death. We examined the effects of Gasdermin-D mutation on inflammation in acute kidney injury. Method Male C57BL/6 mice were exposed to ethyl-N-nitrosourea mutagenesis, leading to a loss-of-function, single nucleotide polymorphism (isoleucine to asparagine mutation, I105N) in the Gasdermin-D gene. Age- and gender-matched littermate control wild-type, heterozygous and homozygous Gasdermin-DI105N mice were subjected to bilateral renal IRI (36°C, 22mins) and sacrificed 24-hours post-reperfusion for analysis of renal function, histology and biomolecular phenotyping. To delineate if the GasderminD mutation in renal parenchymal or hematopoietic cells were key drivers of IRI, we generated chimeric mice with whole body irradiation and infusion of syngeneic donor bone marrow. Following 8 weeks of engraftment, bilateral renal IRI was performed with analysis at 24 h reperfusion. Results Homozygote and heterozygote Gasdermin-DI105N mice were protected from renal IRI in a gene dose-dependent manner when compared to wild-type, with lower mean serum creatinine (15.7, 48.1 and 85.5µmol/L respectively, p&lt;0.001), less histological tubular injury and cell death (1.8, 3.6 and 5.1 TUNEL+ cells/hpf, p&lt;0.01) and significantly decreased expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, RANTES). Homozygote GasderminDI105N chimeric mice (reconstituted with wild-type donor bone marrow) were more susceptible to IRI, and serum creatinine was similar to that of wild-type chimeric control mice, indicating that hematopoietic cells rather than parenchymal cells, are likely predominant drivers of injury. Similarly, adoptive transfer of CpG-activated CD11c+ dendritic cells into homozygous Gasdermin-DI105N mice augmented renal injury compared to GpC-treated cells. Conclusion GasderminDI105N mice were protected from IRI and demonstrates the importance of the pyroptosis pathway on acute kidney injury. Manipulation of GasderminD is potentially an attractive target to mitigate inflammation and cellular death following injury.

Keratinocyte-derived chemokine is an early biomarker of ischemic acute kidney injury

2006 ◽  
Vol 290 (5) ◽  
pp. F1187-F1193 ◽  
Author(s):  
Roshni R. Molls ◽  
Vladimir Savransky ◽  
Manchang Liu ◽  
Shannon Bevans ◽  
Tulsi Mehta ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Graft Function ◽  
Kidney Injury ◽  
Deceased Donor ◽  
Kidney Transplants ◽  
Donor Kidney ◽  
Deceased Donor Kidney

Renal ischemia-reperfusion injury (IRI) is the leading cause of acute kidney injury [AKI; acute renal failure (ARF)] in native kidneys and delayed graft function in deceased donor kidney transplants. Serum creatinine rises late after renal IRI, which results in delayed diagnosis. There is an important need to identify novel biomarkers for early diagnosis and prognosis in renal IRI. Given the inflammatory pathophysiology of renal IRI, we used a protein array to measure 18 cytokines and chemokines in a mouse model of renal IRI at 3, 24, and 72 h postischemia. A rise in renal keratinocyte-derived chemokine (KC) was the earliest and most consistent compared with other molecules, with 3-h postischemia values being 9- and 13-fold greater than sham and normal animals, respectively. Histological changes were evident within 1 h of IRI but serum creatinine only increased 24 h after IRI. With the use of an ELISA, KC levels in serum and urine were highest 3 h postischemia, well before a significant rise in serum creatinine. The human analog of KC, Gro-α, was markedly elevated in urine from humans who received deceased donor kidney transplants that required dialysis, compared with deceased donor kidney recipients with good graft function and live donor recipients with minimal ischemia. Measurement of KC and its human analog, Gro-α, could serve as a useful new biomarker for ischemic ARF.

Sign in / Sign up

Export Citation Format

Share Document