Advances in understanding ischemic acute kidney injury

Munshi, Raj; Hsu, Christine; Himmelfarb, Jonathan

doi:10.1186/1741-7015-9-11

Cited by 130 publications

(100 citation statements)

References 45 publications

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“…Several drugs have been showed to protect ischemic organs against I/R damage. 7,8 Trimetazidine or (1-2(2,3,4-trimeoxibenzyl)-piperazine) (TMZ), is used as an anti-anginal agent, selectively inhibits long-chain 3-ketoacyl coenzyme A thiolase (the last enzyme involved in b-oxidation) activity. 9 Its anti-ischemic effects on the kidney have been experimentally assessed in various models including cell culture 10 isolated and perfused kidneys 11 and in vivo.…”

Section: Introductionmentioning

confidence: 99%

Effects of trimetazidine on the Akt/eNOS signaling pathway and oxidative stress in anin vivorat model of renal ischemia-reperfusion

et al. 2014

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Renal ischemia reperfusion (I/R) injury, which occurs during renal surgery or transplantation, is the major cause of acute renal failure. Trimetazidine (TMZ), an anti-ischemic drug, protects kidney against the deleterious effects of I/R. However its protective mechanism remains unclear. The aim of this study is to examine the relevance of Akt, endothelial nitric oxide synthase (eNOS), and hypoxia inducible factor-1a (HIF-1a) on TMZ induced protection of kidneys against I/R injury. Wistar rats were subjected to 60 min of warm renal ischemia followed by 120 min of reperfusion, or to intraperitoneal injection of TMZ (3 mg/kg) 30 min before ischemia. In sham operated group renal pedicles were only dissected. Compared to I/R, TMZ treatment decreased lactate dehydrogenase (845 ± 13 vs. 1028 ± 30 U/L). In addition, creatinine clearance and sodium reabsorption rates reached 105 ± 12 versus 31 ± 11 mL/min/g kidney weight and 95 ± 1 versus 68 ± 5%, respectively. Besides, we noted a decrease in malondialdehyde concentration (0.33 ± 0.01 vs. 0.59 ± 0.03 nmol/mg of protein) and an increase in glutathione concentration (2.6 ± 0.2 vs. 0.93 ± 0.16 mg GSH/mg of protein), glutathione peroxidase (95 ± 4 vs. 61 ± 3 mg GSH/min/mg of protein), and superoxide dismutase (25 ± 3 vs. 11 ± 2 U/mg of protein) and catalase (91 ± 12 vs. 38 ± 9 mmol/min/mg of protein) activities. Parallely, we noted a significant increase in p-Akt, eNOS, nitrite and nitrate (18 ± 2 vs. 8 ± 0.1 pomL/mg of protein), HIF-1a (333 ± 48 vs. 177 ± 14 mg/mg of protein) and heme oxygenase-1 (HO-1) levels regarding I/R. TMZ treatment improves renal tolerance to warm I/R. Such protection implicates an activation of Akt/eNOS signaling pathway, HIF-1a stabilization and HO-1 activation.

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Section: Introductionmentioning

confidence: 99%

Effects of trimetazidine on the Akt/eNOS signaling pathway and oxidative stress in anin vivorat model of renal ischemia-reperfusion

et al. 2014

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“…Although the return of blood flow to ischemic tissue may result in the recovery of Mahmoudi A et al 68 normal function, paradoxically, the tissue may also be injured during the process of reperfusion (16). In accordance to reperfusion pathophysiology, several interventions have been proposed to reduce the extent of renal injuries.…”

mentioning

confidence: 99%

Postconditioning is protective in renal reperfusion injury only in male rats. A gender difference study

Mahmoudi¹,

Kadkhodaee²,

Golab³

et al. 2015

Acta Physiologica Hungarica

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Purpose:We investigated the impact of sex on the protective effect of postconditioning (POC), a series of brief ischemia-reperfusion (IR) cycles at the reperfusion onset, as a recently described novel approach to attenuate renal IR injury. In this study, the left renal pedicles of uni-nephrectomized male and female rats were clamped for 45 minutes followed by 24 hours of reperfusion as IR groups. Uni-nephrectomized, sham-operated male and female rats served as control groups. Ischemic postconditioning was performed using 4 cycles of 10 seconds IR of renal pedicle at the end of the ischemia. Twenty-four hours later, BUN (blood urea nitrogen), plasma creatinine (Cr), and renal histological changes, as well as kidney levels of MDA (malondialdehyde) and SOD (superoxide dismutase) as oxidative stress markers were evaluated to detect the protective effect of POC against IR injury in rats. Results: Induction of IR resulted in significant reduction in renal function, demonstrated by increase in plasma Cr and BUN, histological changes and oxidative stress in both genders. Application of POC afforded significant protection against these injuries in male rats, namely decreased levels of BUN and Cr, histological improvements and less oxidative damages. However, there were no significant differences in the above-mentioned parameters in female rats. Conclusion: While POC is shown to be beneficial against renal IR injury in male rats, it did not show any protective effect in female rats.

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“…It has been also accompanied with increased length of hospital stay and adjusted ratios of 4.1 for hospital mortality and 2.0 for discharge [1] . Attacks of hypotension or surgical clamping of renal arteries are the major causes of acute tubular necrosis of kidney which is responsible for the majority of cases of AKI affecting renal functions [2] .…”

Section: Introductionmentioning

confidence: 99%

Role of Erythropoietin Induced Stem Cell Mobilization in the Repairing of Acute Kidney Injury Following Ischemia Reperfusion in Albino Rats: A Histological Study

Nada

Ahmed

Farag

et al. 2017

Journal of Medical Histology

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Background: The incidence of acute kidney injury (AKI), the new term for acute renal failure, has increased in recent years. Ischemia-reperfusion (IR) is one of the main causes of AKI. Erythropoietin (EPO) is a complex molecule, which regulates red blood cell production in the bone marrow. Recent studies provide evidence of potential therapeutic effect of EPO on AKI. Aim of the Work: Investigate the role of EPO in mobilization of bone marrow derived stem cells and its role in repairing AKI. Materials and Methods:This study included 32 adult male albino rats, divided into three groups; control, non-treated IR and EPO treated group. AKI was done by induction of IR via clamping both renal pedicles for 40 minutes and EPO 5000 U|kg was injected in treated group once intraperitoneally immediately after IR. Rats were sacrificed 48 hours and 1 week after intervention, then renal sections were stained with hematoxylin & eosin, PAS and immunohistochemically for CD34. Results: Erythropoietin improved the impaired kidney manifestations occurred by IR including increasing the reduced urea and creatinine levels, improved histological architecture of kidney. Also, increasing CD34 immunopositive hematopoietic and endothelial progenitor stem cells. Conclusion: This work concluded that administration of EPO at time of renal IR resulted in enhanced mobilization of stem cells resulting in structural recovery and improved functions.

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Advances in understanding ischemic acute kidney injury

Cited by 130 publications

References 45 publications

Effects of trimetazidine on the Akt/eNOS signaling pathway and oxidative stress in anin vivorat model of renal ischemia-reperfusion

Effects of trimetazidine on the Akt/eNOS signaling pathway and oxidative stress in anin vivorat model of renal ischemia-reperfusion

Postconditioning is protective in renal reperfusion injury only in male rats. A gender difference study

Role of Erythropoietin Induced Stem Cell Mobilization in the Repairing of Acute Kidney Injury Following Ischemia Reperfusion in Albino Rats: A Histological Study

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