Experimental Myoglobinuric Acute Renal Failure: The Effect of Vitamin C

Üstündağ, Sedat; Yalçın, Ömer; Sen, Sayan; Cukur, Ziya; Ciftci, Senturk; Demirkan, Bora

doi:10.1080/08860220802212965

Cited by 26 publications

(21 citation statements)

References 43 publications

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“…In several studies, it has been demonstrated that ROS play an important role in the pathogenesis of myoglobinuric ARF, based on the findings that in rats with rhabdomyolysis, levels of MDA and F 2 isoprostanes in the kidney increase. [1,[3][4][5][6]21] Elevated renal MDA levels, as well as their relations with tubular cell necrosis and the urinary NAG/creatinine ratio in glycerol-administered rats, suggest that lipid peroxidation was an important contributing factor to the development of kidney damage in the present study. Also, we observed that lipid peroxidation, which was connected to functional, biochemical, and morphological renal impairment, was prevented by L-carnitine, implying this molecule's antioxidant effect.…”

Section: Discussionmentioning

confidence: 65%

“…[1,3] There is also increasing evidence indicating that reactive oxygen species (ROS) plays an important role in the pathogenesis of myoglobinuric ARF. [4][5][6] During renal vasoconstriction/hypoperfusion, ATP is degraded to hypoxanthine. When xanthine oxidase converts hypoxanthine to xanthine in the presence of molecular oxygen, superoxide radical (O 2 − ) is generated.…”

Section: Introductionmentioning

confidence: 99%

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L-Carnitine Ameliorates Glycerol-Induced Myoglobinuric Acute Renal Failure in Rats

et al. 2009

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Section: Discussionmentioning

confidence: 65%

Section: Introductionmentioning

confidence: 99%

L-Carnitine Ameliorates Glycerol-Induced Myoglobinuric Acute Renal Failure in Rats

et al. 2009

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“…Oxidative stress manifests as an accumulation of oxidized lipids, depletion of endogenous antioxidants, and activation of pro-inflammatory pathways. Variable reno-protective outcomes have been reported for different natural (5,15,23,58) and synthetic antioxidants (32,40) in animal models of RM. However, largescale therapeutic interventions with antioxidants in humans have not been reported.…”

Section: Discussionmentioning

confidence: 99%

Selenium Inhibits Renal Oxidation and Inflammation But Not Acute Kidney Injury in an Animal Model of Rhabdomyolysis

Shanu

Groebler

Kim

et al. 2013

Antioxidants & Redox Signaling

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Acute kidney injury (AKI) is a manifestation of rhabdomyolysis (RM). Extracellular myoglobin accumulating in the kidney after RM promotes oxidative damage, which is implicated in AKI. Aim: To test whether selenium (Se) supplementation diminishes AKI and improves renal function. Results: Dietary selenite increased Se in the renal cortex, as demonstrated by X-ray fluorescence microscopy. Experimental RM-stimulated AKI as judged by increased urinary protein/creatinine, clusterin, and kidney injury molecule-1 (KIM-1), decreased creatinine clearance (CCr), increased plasma urea, and damage to renal tubules. Concentrations of cholesterylester (hydro)peroxides and F 2 -isoprostanes increased in plasma and renal tissues after RM, while aortic and renal cyclic guanidine monophosphate (cGMP; marker of nitric oxide (NO) bioavailability) decreased. Renal superoxide dismutase-1, phospho-P65, TNFa gene, MCP-1 protein, and the 3-chloro-tyrosine/tyrosine ratio (Cl-Tyr/Tyr; marker of neutrophil activation) all increased after RM. Dietary Se significantly decreased renal lipid oxidation, phospho-P65, TNFa gene expression, MCP-1 and Cl-Tyr/Tyr, improved NO bioavailability in aorta but not in the renal microvasculature, and inhibited proteinuria. However, CCr, plasma urea and creatinine, urinary clusterin, and histopathological assessment of AKI remained unchanged. Except for the Se++ group, renal angiotensin-receptor-1/2 gene/protein expression increased after RM with parallel increases in MEK1/2 inhibitor-sensitive MAPkinase (ERK) activity. Innovation: We employed synchrotron radiation to identify Se distribution in kidneys, in addition to assessing reno-protection after RM. Conclusion: Se treatment has some potential as a therapeutic for AKI as it inhibits oxidative damage and inflammation and decreases proteinuria, albeit histopathological changes to the kidney and some plasma and urinary markers of AKI remain unaffected after RM. Antioxid Redox Signal. 18, 756-769.

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“…This may predispose to chronic ischemia of kidney. It has been proposed that successful regeneration of peritubular capillaries following injury is the key in preventing CKD [22] . Therefore, mobilization of Endothelial Progenitor Cells (EPCs) may be a promising new treatment approach that could enhance the repair of damaged vessel segments [26] .…”

Section: Discusionmentioning

confidence: 99%

“…These findings were in line with an earlier study [21] . PAS stain was done to assess brush border preservation which is a highly sensitive marker for monitoring survival of proximal tubular cells, site where IR induced injury is most intense [7] , affecting sodium and glucose reabsorption in these tubules [22] .…”

Section: Discusionmentioning

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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Experimental Myoglobinuric Acute Renal Failure: The Effect of Vitamin C

Cited by 26 publications

References 43 publications

L-Carnitine Ameliorates Glycerol-Induced Myoglobinuric Acute Renal Failure in Rats

L-Carnitine Ameliorates Glycerol-Induced Myoglobinuric Acute Renal Failure in Rats

Selenium Inhibits Renal Oxidation and Inflammation But Not Acute Kidney Injury in an Animal Model of Rhabdomyolysis

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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