Effects of Gentamicin, Lipopolysaccharide, and Contrast Media on Immortalized Proximal Tubular Cells

Cunha, Maria Adelaide; Schor, Nestor

doi:10.1081/jdi-120015662

Cited by 13 publications

(3 citation statements)

References 8 publications

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“…Additionally, the present study revealed marked significant increase in urinary KIM-1 in gentamicin treated group as compared to control group. These results agreed with the study of Cunha and Schor (2002) who illustrated that, in the dose-response study, urinary KIM-1 and kidney KIM-1/Havcr1 mRNA expression are very sensitive to the renal injury produced by gentamicin. These results may be explained by the fact that gentamicin accumulates in the epithelial cells of renal proximal tubules, leading to structural changes and functional impairments of the plasma membrane, mitochondria, and lysosome (Ali, 1995).…”

Section: Discussionsupporting

confidence: 92%

The possible protective effects of saccharum officinarum l. (sugar cane) juice co-supplementation on gentamicin induced acute renal toxicity in adult albino rats

Hussein

EL-Shafey

2019

IJPT

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Gentamicin (GM) is an effective and probably the most commonly used aminoglycosides antibiotic, however the risk of causing nephrotoxicity limits its use. In the present study, the possible protective effects of Saccharum officinarum L. (sugar cane juice) on gentamicin induced acute oxidative renal injury in experimental rats were investigated. Twenty adult albino rats were randomly allocated into four groups (5 rats in each) and treated once daily for a period of 7 days as follows; group A being the negative control and was injected intraperitoneal with normal saline, group B (sugar cane juice treated group) was given sugar cane juice orally at a dose of 15 ml/kg/day, group C (GM treated group) and group D (sugar cane juice + GM treated group) were the experimental groups and were injected intraperitoneal with (80 mg/kg/day GM) & (sugar cane juice 15 ml/kg/day orally + 80 mg/kg/day GM intraperitoneal) respectively. By the end of the experiment, the biochemical kidney functions tests (urinary cystatin C and kidney injury molecule-1, blood urea and creatinine) were investigated. Also, oxidative stress parameters (malondialdehyde [MDA] level, superoxide dismutase [SOD] & glutathione peroxidase [GPX] enzymatic activity) in renal tissue were evaluated. Histopathological examinations of kidney were done to assess the degree of renal protection induced by sugarcane juice, Gentamicin treated rats showed; marked significant rise in the biochemical kidney functions tests and lipid peroxidation (MDA) parameter in renal tissues, along with significant reduction in renal tissue antioxidant enzymatic activity of both SOD & GPX. However, co-administration of sugar cane juice in group D leading to marked reduction in previous biochemical markers and MDA levels together with significant elevated renal SOD &GPX enzymatic activity which nearly tend to return to normal values. The histopathological examination of groups A and B showed normal kidney structure which was deranged in group C (GM treated), whereas group D showed significant recovery in histological structures. Gentamicin induced acute renal injury and oxidative damage. Co-administration of sugar cane juice may reduce this damage by improving antioxidant defense and tissue integrity in experimental albino rats.

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Section: Discussionsupporting

confidence: 92%

The possible protective effects of saccharum officinarum l. (sugar cane) juice co-supplementation on gentamicin induced acute renal toxicity in adult albino rats

Hussein

EL-Shafey

2019

IJPT

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“…Experimental animal studies performed in vivo and in vitro have suggested that iodinated contrast drugs can induce caspase-mediated apoptosis of tubular epithelial cells 57. Activation of shock proteins and concurrent inhibition of cytoprotective enzymes and prostaglandins may also cause contrast drug-induced apoptosis 70,71…”

Section: Contrast-induced Acute Kidney Injurymentioning

confidence: 99%

Update on the renal toxicity of iodinated contrast drugs used in clinical medicine

Andreucci¹,

Faga²,

Serra

et al. 2017

DHPS

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An important side effect of diagnostic contrast drugs is contrast-induced acute kidney injury (CI-AKI; a sudden decrease in renal function) occurring 48–72 hours after injection of a contrast drug that cannot be attributed to other causes. Its existence has recently been challenged, because of some retrospective studies in which the incidence of AKI was not different between subjects who received a contrast drug and those who did not, even using propensity score matching to prevent selection bias. For some authors, only patients with estimated glomerular filtration rate <30 mL/min/1.73 m2 are at significant risk of CI-AKI. Most agree that when renal function is normal, there is no CI-AKI risk. Many experimental studies, however, are in favor of the existence of CI-AKI. Contrast drugs have been shown to cause the following changes: renal vasoconstriction, resulting in a rise in intrarenal resistance (decrease in renal blood flow and glomerular filtration rate and medullary hypoxia); epithelial vacuolization and dilatation and necrosis of proximal tubules; potentiation of angiotensin II effects, reducing nitric oxide (NO) and causing direct constriction of descending vasa recta, leading to formation of reactive oxygen species in isolated descending vasa recta of rats microperfused with a solution of iodixanol; increasing active sodium reabsorption in the thick ascending limbs of Henle’s loop (increasing O2 demand and consequently medullary hypoxia); direct cytotoxic effects on endothelial and tubular epithelial cells (decrease in release of NO in vasa recta); and reducing cell survival, due to decreased activation of Akt and ERK1/2, kinases involved in cell survival/proliferation. Prevention is mainly based on extracellular volume expansion, statins, and N-acetylcysteine; conflicting results have been obtained with nebivolol, furosemide, calcium-channel blockers, theophylline, and hemodialysis.

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“…Studi su animali, sia in vivo che in vitro, suggeriscono che i MC iodati possono causare direttamente un'apoptosi, mediata dalle caspasi, delle cellule tubulari renali (93). L'apoptosi indotta dai MC può essere dovuta alla attivazione di proteine shock e alla concorrente inibizione di enzimi citoprotettivi e prostaglandine (94,95). Questo tipo di ricerche sperimentali può consentire di trovare i mezzi per contrastare la citotossicità dei MC sull'epitelio tubulare (96).…”

Section: Citotossicità Dei MCunclassified

Iodinated Contrast-Induced Acute Kidney Injury. Pathophysiology and Prevention

Andreucci

2017

Giornale di Tecniche Nefrologiche e Dialitiche

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The term acute renal failure (ARF) secondary to ischemic/nephrotoxic injury should no longer be used and be replaced by acute kidney injury (AKI), indicating an abrupt (within 24–48 hours) increase in serum creatinine by 0.5 mg/dL or by 25% above baseline. Replacing “failure” with “injury” served to include the entire range of renal impairment from small changes in serum creatinine to complete loss of renal function. The term ARF should be limited to a decrease in renal function so severe as to require dialysis. When AKI is due to radiographic contrast agents, it is called contrast-induced (CI) AKI. The pathogenesis of CI-AKI is complex and not well known. Many factors are involved, including hemodynamic changes such as renal vasoconstriction, particularly in the outer medulla where tubular segments devoted to active sodium reabsorption are located; the vasoconstriction may be due to direct action of the contrast agent but may also be mediated by stimulation of angiotensin II and adenosine, or by a decrease in the local production of prostaglandins and nitric oxide, all leading to medullary hypoxia. Other factors are osmotic diuresis (with increased tubular reabsorption of sodium and tubular epithelium injury, both worsening medullary hypoxia) and production of reactive oxygen species that will cause endothelial and epithelial damage, likewise worsening medullary hypoxia. The fall in renal blood flow and tubular obstruction will decrease the glomerular filtration rate. Treatment and prevention of CI-AKI are based on opposing these factors by adequate hydration; administration of furosemide along with fluid replacement; theophylline and aminophylline; PGE1 and PGI2; N-acetylcysteine, ascorbic acid and vitamin E; nebivolol and statins.

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Effects of Gentamicin, Lipopolysaccharide, and Contrast Media on Immortalized Proximal Tubular Cells

Cited by 13 publications

References 8 publications

The possible protective effects of saccharum officinarum l. (sugar cane) juice co-supplementation on gentamicin induced acute renal toxicity in adult albino rats

The possible protective effects of saccharum officinarum l. (sugar cane) juice co-supplementation on gentamicin induced acute renal toxicity in adult albino rats

Update on the renal toxicity of iodinated contrast drugs used in clinical medicine

Iodinated Contrast-Induced Acute Kidney Injury. Pathophysiology and Prevention

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