Prevention of cisplatin nephrotoxicity: state of the art and recommendations from the European Society of Clinical Pharmacy Special Interest Group on Cancer Care

Launay-Vacher, Vincent; Rey, Jean‐Baptiste; Bagnis, Corinne Isnard; Deray, Gilbert; Daouphars, Mikaël

doi:10.1007/s00280-008-0711-0

Cited by 235 publications

(178 citation statements)

References 41 publications

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“…However, cisplatin also induces undesired side effects in normal tissues or organs, especially in the kidney (3)(4)(5)(6)(7)(8). Nephrotoxicity or acute kidney injury (AKI) 4 occurs in over one quarter of the patients receiving cisplatin treatment and AKI has been reported to be related to the increased mortality in the long-term survivors of these patients (3)(4)(5)(6)(7). Years of research has led to the identification of the main signaling pathways that are activated by cisplatin in kidneys and contribute to AKI, such as mitogen-activated protein kinase (MAPK), P53 and related DNA damage response, NF-B, and other signaling pathways.…”

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confidence: 99%

MicroRNA-375 Is Induced in Cisplatin Nephrotoxicity to Repress Hepatocyte Nuclear Factor 1-β

Hao

Lou

Wei

et al. 2017

Journal of Biological Chemistry

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Edited by Joel GottesfeldNephrotoxicity is a major adverse effect of cisplatin-mediated chemotherapy in cancer patients. The pathogenesis of cisplatininduced nephrotoxicity remains largely unclear, making it difficult to design effective renoprotective approaches. Here, we have examined the role of microRNAs (miRNAs) in cisplatininduced nephrotoxicity. We show that cisplatin nephrotoxicity was not affected by overall depletion of both beneficial and detrimental miRNAs from kidney proximal tubular cells in mice in which the miRNA-generating enzyme Dicer had been conditionally knocked out. To identify miRNAs involved in cisplatin nephrotoxicity, we used microarray analysis to profile miRNA expression and identified 47 up-regulated microRNAs and 20 down-regulated microRNAs in kidney cortical tissues. One upregulated miRNA was miR-375, whose expression was also induced in cisplatin-treated renal tubular cells. Interestingly, inhibition of miR-375 decreased cisplatin-induced apoptosis, suggesting that miR-375 is a cell-damaging or pro-apoptotic agent. Blockade of P53 or NF-B attenuated cisplatin-induced miR-375 expression, supporting a role of P53 and NF-B in miR-375 induction. We also identified hepatocyte nuclear factor 1 homeobox B (HNF-1␤) as a key downstream target of miR-375. Of note, we further demonstrated that HNF-1␤ protected renal cells against cisplatin-induced apoptosis. Together, these results suggest that upon cisplatin exposure, P53 and NF-B collaboratively induce miR-375 expression, which, in turn, represses HNF-1␤ activity, resulting in renal tubular cell apoptosis and nephrotoxicity.

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confidence: 99%

MicroRNA-375 Is Induced in Cisplatin Nephrotoxicity to Repress Hepatocyte Nuclear Factor 1-β

Hao

Lou

Wei

et al. 2017

Journal of Biological Chemistry

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“…In addition, several investigators have reported that persistent hypomagnesemia might be associated with renal damage after chemotherapy. 30,31 Therefore, management of longterm hypomagnesemia is one candidate, although it is not clear at present whether correction of hypomagnesemia improves renal function.…”

Section: Discussionmentioning

confidence: 99%

Risk factors for chronic kidney disease after chemotherapy for testicular cancer

et al. 2012

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Abbreviations & Acronyms BMI = body mass index CDDP = cisplatin CI = confidence interval CKD = chronic kidney disease eGFR = estimated glomerular filtration rate GFR = glomerular filtration rate IGCC = International Germ Cell Consensus IGCCCG = International Germ Cell Consensus Collaborative Group RPLN = retroperitoneal lymph node RPLND = retroperitoneal lymph node dissection sCR = serum creatinine Objective: To elucidate the patterns of and risk factors for deterioration of renal function after chemotherapy in metastatic testicular cancer survivors using the estimated glomerular filtration rate. Methods: A total of 96 patients who were treated with cisplatin-based chemotherapy for metastatic testicular cancer between January 1981 and December 2010 were enrolled in this study. The estimated glomerular filtration rate was based on the serum creatinine concentration using the formula of the Japanese Society of Nephrology. Risk factors for chronic kidney disease were examined by multivariate logistic-regression analysis. Results:The median follow-up period was 70 months (range 15-342). The median pretreatment estimated glomerular filtration rate was 98 mL/min/1.73 m 2 (range 44-216), and it gradually decreased for 1 year after the end of chemotherapy, although there was no significant change in estimated glomerular filtration rate beyond 1 year. One year after chemotherapy, 22 of 96 patients (23%) showed chronic kidney disease (less than 60 mL/min/1.73 m 2 estimated glomerular filtration rate). The multivariate analysis showed that the patients with mild renal damage (estimated glomerular filtration rate 60-89 mL/min/1.73 m 2 ) and elevated blood pressure (higher than 130/ 80 mmHg) before treatment had a significant risk with odds ratios of 2.63 (95% confidence interval 1.09-6.73) and 4.22 (95% confidence interval 1.45-12.6), respectively. Conclusions: Close monitoring of renal function is important for at least 1 year after chemotherapy for testicular cancer, especially in patients having elevated blood pressure and/or mild renal damage before chemotherapy.

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“…Oxaliplatin, unlike cisplatin, has been reported to have minimal effect on kidneys in humans and rats. 18,19 In their study of the pharmacokinetic and toxicodynamic relationships of platinum compounds, Hanada et al reported that the reason for the differential in vivo susceptibility of oxaliplatin and cisplatin to nephrotoxicity (at the doses used in their work) is pharmacokinetic in origin and the oxaliplatin total clearance was the highest among other platinum compounds. 20 In this work we have shown that both cisplatin and oxaliplatin are equi-effective in inducing a state of oxidative stress in HEK cells.…”

Section: Discussionmentioning

confidence: 99%

Effect of Curcumin on Cisplatin- and Oxaliplatin-Induced Oxidative Stress in Human Embryonic Kidney (HEK) 293 Cells

2011

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Generation of reactive oxygen species (ROS) is involved in the nephrotoxicity of platinum anticancer drugs. This study involved incubation of human embryonic kidney (HEK) 293 cells in cell culture media supplemented with cisplatin or oxaliplatin in the presence or absence of curcumin, a well-studied antioxidant. Thereafter several indices of oxidative stress have been measured, which included glutathione (GSH), total antioxidant capacity (TAC), and antioxidant enzymes [(superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidases (GPX)]. The impact of platinum drugs on cells viability, lipid peroxidation, and lactate dehydrogenase leakage was also examined. The results show that at both acute (60 min) and chronic (24 h) durations of incubation, cisplatin and oxaliplatin induced oxidative stress as evidenced by significant inhibition of the activities of SOD, CAT, and GPX enzymes as well as significant reduction of the concentrations of GSH and TAC. Curcumin ameliorated the oxidative stress induced by these insults by significantly restoring the measured oxidative indices. Our findings provide evidence that curcumin significantly ameliorates oxidative stress induced by both cisplatin and oxaliplatin in HEK cells.

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Prevention of cisplatin nephrotoxicity: state of the art and recommendations from the European Society of Clinical Pharmacy Special Interest Group on Cancer Care

Cited by 235 publications

References 41 publications

MicroRNA-375 Is Induced in Cisplatin Nephrotoxicity to Repress Hepatocyte Nuclear Factor 1-β

MicroRNA-375 Is Induced in Cisplatin Nephrotoxicity to Repress Hepatocyte Nuclear Factor 1-β

Risk factors for chronic kidney disease after chemotherapy for testicular cancer

Effect of Curcumin on Cisplatin- and Oxaliplatin-Induced Oxidative Stress in Human Embryonic Kidney (HEK) 293 Cells

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