2012
DOI: 10.5812/nephropathol.7512
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Inhibition of gentamicin–induced renal tubular cell necrosis

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Cited by 31 publications
(20 citation statements)
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“…However, gentamicin‐induced nephrotoxicity put a serious limitation on its use. In some cases, the drug must be discontinued because of the severity of this side effect …”
Section: Introductionmentioning
confidence: 99%
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“…However, gentamicin‐induced nephrotoxicity put a serious limitation on its use. In some cases, the drug must be discontinued because of the severity of this side effect …”
Section: Introductionmentioning
confidence: 99%
“…RAS is essentially responsible for the pathogenic progression of kidney injury, because angiotensin II is likely to be a powerful inducer of reactive oxygen species (ROS) and alterations of oxidant‐antioxidant status in renal and cardiovascular diseases . It is postulated that gentamicin‐induced nephrotoxicity is greatly related to the generation of ROS in the kidney . These ROS provoke cellular damage and necrosis by means of lipid peroxidation and protein alteration .…”
Section: Introductionmentioning
confidence: 99%
“…The etiologies of renal failure were diabetic nephropathy, hypertension, various glomerular diseases, autosomal dominant poly cystic kidney disease(ADPKD) and also urinary tract infections [32][33][34][35][36][37][38].According to the severity of secondary hyperparathyroidism, each patient was treated with oral active vitamin D3 (Rocaltrol), calcium carbonate, and Rena-Gel capsules at various doses. According to the severity of anemia, patients were treated with IV iron therapy Iron Source (venofer) at various doses after each dialysis session .All patients were under treatments of 6 mg folic acid daily, oral vitamin B-complex tablet daily and also 2000 U IV Eprex (recombinant human erythropoietin (rHuEPO) were given to each patient after each dialysis session routinely [39][40][41]. Exclusion criteria were active or chronic infection.…”
Section: Methodsmentioning
confidence: 99%
“…8 More recently, we also observed that estrogen abolishes the protective effect of erythropoietin against CIN in ovariectomized rats, 9 whereas nephroprotective effects of erythropoietin were also detected in our previous study. [10][11][12] Hence, it is well documented that there is a gender difference in CIN in the rat model. It is documented that some cases of chronic kidney diseases are gender related too.…”
mentioning
confidence: 99%