2013
DOI: 10.1159/000355537
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Perspective on Rhabdomyolysis-Induced Acute Kidney Injury and New Treatment Options

Abstract: Aim: The purpose of this study was to assess the role of caspase-dependent apoptosis, caspase 1, calpain 1, inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) and the protective effect of grape seed proanthocyanidin extract (GSPE) in the development of rhabdomyolysis-induced acute kidney injury (AKI). Materials and Methods: Twenty-one rats were divided into 3 groups - control, rhabdomyolysis and rhabdomyolysis + GSPE. Rhabdomyolysis was induced in the rhabdomyolysis and rhabdom… Show more

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Cited by 12 publications
(12 citation statements)
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References 22 publications
(45 reference statements)
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“…17,18 This is in accordance with the present study which showed significant decline in the renal functions (increase in serum urea, serum creatinine and BUN) in ARF model groups when compared to the normal control groups. Moreover, Xing et al and Liu et al reported similar results.…”
Section: Discussionsupporting
confidence: 92%
“…17,18 This is in accordance with the present study which showed significant decline in the renal functions (increase in serum urea, serum creatinine and BUN) in ARF model groups when compared to the normal control groups. Moreover, Xing et al and Liu et al reported similar results.…”
Section: Discussionsupporting
confidence: 92%
“…18 Moreover, iNOS-mediated NO production correlates with apoptosis and necrosis in the kidney in a NO level-dependent manner. 35,36 In our study, an inappropriately high level of iNOS-derived NO release might be related to renal tubular damage and subsequent AKI soon after rhabdomyolysis.…”
Section: Discussionmentioning
confidence: 56%
“…In ischaemia‐induced AKI, lipid peroxidation injury originates from iNOS via ONOO − formation, which promotes tissue injury in a lipid peroxidation‐dependent manner . Moreover, iNOS‐mediated NO production correlates with apoptosis and necrosis in the kidney in a NO level‐dependent manner . In our study, an inappropriately high level of iNOS‐derived NO release might be related to renal tubular damage and subsequent AKI soon after rhabdomyolysis.…”
Section: Discussionmentioning
confidence: 57%
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“…Previous reports have demonstrated that the mechanisms of rhabdomyolysis-induced AKI are caused by myoglobin flowing out of the destroyed muscle tissue and binding with Tamm-Horsfall protein in the renal tubule to form a cast that increases consumption of NO, vasoconstriction, and reactive oxygen species production, resulting in apoptosis and tubular cell damage. 5,25,26 Although it is considered that the main mechanism of renoprotective effect of ALA is a reduction of oxidative stress and inhibition of apoptosis, it is also notable that ALA reduces cast formation in tubule in our experiment. A recent report suggested that the apoptosis inhibitor of macrophage (AIM) accumulates on cell debris within the kidney proximal tubules during AKI and binds to the kidney injury molecule (KIM)-1, which is expressed in injured tubular epithelial cells.…”
Section: Discussionmentioning
confidence: 57%