Mycophenolic acid inhibits the phosphorylation of NF-κB and JNKs and causes a decrease in IL-8 release in H2O2-treated human renal proximal tubular cells

Andreucci, Michele; Faga, Teresa; Lucisano, Gaetano; Uccello, F.; Pisani, Antonio; Memoli, Bruno; Sabbatini, Massimo; Fuiano, Giorgio; Michael, Ashour

doi:10.1016/j.cbi.2010.03.019

Cited by 31 publications

(22 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In vitro cell culture studies have shown that all types of contrast media cause a decrease in cell viability [55–59]. The biochemical changes underlying these effects have been extended to studying changes in major intracellular signalling pathways involved in cell survival, death, and inflammation [57–60] in vitro in cultured human renal tubular cells [61]. Contrast media can cause perturbation of mitochondrial enzyme activity and mitochondrial membrane potential in proximal tubule cell line; in the more distal segments of the kidney, they can cause apoptosis [62].…”

Section: Contrast-induced Nephropathymentioning

confidence: 99%

Side Effects of Radiographic Contrast Media: Pathogenesis, Risk Factors, and Prevention

Andreucci

Solomon

Tasanarong

2014

BioMed Research International

Self Cite

218

226

View full text Add to dashboard Cite

Radiocontrast media (RCM) are medical drugs used to improve the visibility of internal organs and structures in X-ray based imaging techniques. They may have side effects ranging from itching to a life-threatening emergency, known as contrast-induced nephropathy (CIN). We define CIN as acute renal failure occurring within 24–72 hrs of exposure to RCM that cannot be attributed to other causes. It usually occurs in patients with preexisting renal impairment and diabetes. The mechanisms underlying CIN include reduction in medullary blood flow leading to hypoxia and direct tubule cell damage and the formation of reactive oxygen species. Identification of patients at high risk for CIN is important. We have reviewed the risk factors and procedures for prevention, providing a long list of references enabling readers a deep evaluation of them both. The first rule to follow in patients at risk of CIN undergoing radiographic procedure is monitoring renal function by measuring serum creatinine and calculating the eGFR before and once daily for 5 days after the procedure. It is advised to discontinue potentially nephrotoxic medications, to choose radiocontrast media at lowest dosage, and to encourage oral or intravenous hydration. In high-risk patients N-acetylcysteine may also be given.

show abstract

Section: Contrast-induced Nephropathymentioning

confidence: 99%

Side Effects of Radiographic Contrast Media: Pathogenesis, Risk Factors, and Prevention

Andreucci

Solomon

Tasanarong

2014

BioMed Research International

Self Cite

218

226

View full text Add to dashboard Cite

show abstract

“…[11][12][13][14] The direct toxic effects of CM have been studied in various cells, including renal epithelial and mesangial cells. 15 The functional and structural changes observed as a result of CM action included cell death, a decrease in cell viability, and an increase in brush border and lysosomal enzyme activity; 16 cellular DNA fragmentation; 17 downregulation of signaling molecules involved in cell survival such as Akt and upregulation of signaling molecules in cell death such as the p38 and c-Jun N-terminal kinase members of the mitogenactivated protein kinases and the transcription factor nuclear factor kB as well as caspase activation.…”

Section: Pathophysiology Of Ci-akimentioning

confidence: 99%

The potential use of biomarkers in predicting contrast-induced acute kidney injury

Andreucci¹,

Faga²,

Riccio³

et al. 2016

IJNRD

Self Cite

View full text Add to dashboard Cite

Contrast-induced acute kidney injury (CI-AKI) is a problem associated with the use of iodinated contrast media, causing kidney dysfunction in patients with preexisting renal failure. It accounts for 12% of all hospital-acquired kidney failure and increases the length of hospitalization, a situation that is worsening with increasing numbers of patients with comorbidities, including those requiring cardiovascular interventional procedures. So far, its diagnosis has relied upon the rise in creatinine levels, which is a late marker of kidney damage and is believed to be inadequate. Therefore, there is an urgent need for biomarkers that can detect CI-AKI sooner and more reliably. In recent years, many new biomarkers have been characterized for AKI, and these are discussed particularly with their use in known CI-AKI models and studies and include neutrophil gelatinase-associated lipocalin, cystatin C (Cys-C), kidney injury molecule-1, interleukin-18, N-acetyl-β-d-glucosaminidase, and L-type fatty acid-binding protein (L-FABP). The potential of miRNA and metabolomic technology is also mentioned. Early detection of CI-AKI may lead to early intervention and therefore improve patient outcome, and in future any one or a combination of several of these markers together with development in technology for their analysis may prove effective in this respect.

show abstract

“…The cell damage may be aggravated by factors such as tissue hypoperfusion and hypoxia, by properties of contrast media, such as ionic strength, high osmolarity, and/or viscosity, and by clinically unfavourable conditions, such as preexisting renal impairment particularly secondary to diabetic nephropathy, salt depletion and dehydration, congestive heart failure, and concurrent use of nephrotoxic drugs [1, 28, 42, 43]. The biochemical changes underlying the epithelial damage have been extended to study changes in major intracellular signalling pathways involved in cell survival, death, and inflammation [31, 44–51] in vitro in cultured renal tubular cells [52]. Studies in animals and in vitro studies suggest that iodinated contrast media can directly induce caspase-mediated apoptosis of renal tubular cells.…”

Section: Pathogenesismentioning

confidence: 99%

Acute Kidney Injury by Radiographic Contrast Media: Pathogenesis and Prevention

Andreucci

Faga

Pisani

et al. 2014

BioMed Research International

Self Cite

106

112

View full text Add to dashboard Cite

It is well known that iodinated radiographic contrast media may cause kidney dysfunction, particularly in patients with preexisting renal impairment associated with diabetes. This dysfunction, when severe, will cause acute renal failure (ARF). We may define contrast-induced Acute Kidney Injury (AKI) as ARF occurring within 24–72 hrs after the intravascular injection of iodinated radiographic contrast media that cannot be attributed to other causes. The mechanisms underlying contrast media nephrotoxicity have not been fully elucidated and may be due to several factors, including renal ischaemia, particularly in the renal medulla, the formation of reactive oxygen species (ROS), reduction of nitric oxide (NO) production, and tubular epithelial and vascular endothelial injury. However, contrast-induced AKI can be prevented, but in order to do so, we need to know the risk factors. We have reviewed the risk factors for contrast-induced AKI and measures for its prevention, providing a long list of references enabling readers to deeply evaluate them both.

show abstract

Mycophenolic acid inhibits the phosphorylation of NF-κB and JNKs and causes a decrease in IL-8 release in H2O2-treated human renal proximal tubular cells

Cited by 31 publications

References 45 publications

Side Effects of Radiographic Contrast Media: Pathogenesis, Risk Factors, and Prevention

Side Effects of Radiographic Contrast Media: Pathogenesis, Risk Factors, and Prevention

The potential use of biomarkers in predicting contrast-induced acute kidney injury

Acute Kidney Injury by Radiographic Contrast Media: Pathogenesis and Prevention

Contact Info

Product

Resources

About