Cisplatin Nephrotoxicity: A Review

Yao, Xiaofeng; Panichpisal, Kessarin; Kurtzman, Neil A.; Nugent, Kenneth

doi:10.1097/maj.0b013e31812dfe1e

Cited by 1,066 publications

(914 citation statements)

References 77 publications

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“…The broad-spectrum antitumour activity and effectiveness of platinum attracted researcher dense interest and widely study. Over the half-century development platinum has become a group of widely used antitumour drugs for patients with solid tumours, and the function characteristic of platinum is in a dose-dependent manner (Yao et al, 2007). Nedaplatin is cis-glycolic diamine platinum, which molecular formula is C2H8N2O3Pt, and developed by Japanese pharmaceutical company Shionogi and launched in Japanese in 1995.…”

Section: Discussionmentioning

confidence: 99%

Intervention Effects of Nedaplatin and Cisplatin on Proliferation and Apoptosis of Human Tumour Cells in Vitro

Su¹,

Yin²,

Li³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Section: Discussionmentioning

confidence: 99%

Intervention Effects of Nedaplatin and Cisplatin on Proliferation and Apoptosis of Human Tumour Cells in Vitro

Su¹,

Yin²,

Li³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…14 For instance, inflammation, oxidative stress injury and apoptosis probably have the main roles in development of the nephrotoxicity induced by cisplatin. 15 Some human and animal studies have shown that co-administration of selenium with cisplatin could decrease the renal injury. [15][16][17] We have formerly shown that selenium deficiency exists in almost all the patients undergoing HSCT in our institution.…”

Section: Introductionmentioning

confidence: 99%

The efficacy of selenium in prevention of oral mucositis in patients undergoing hematopoietic SCT: a randomized clinical trial

Jahangard‐Rafsanjani

Gholami

Hadjibabaie

et al. 2013

Bone Marrow Transplant

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Oral mucositis (OM) is a complication of high-dose chemotherapy (HDC) followed by hematopoietic SCT (HSCT) with few effective treatments. Selenium has a cytoprotective role via the glutathione peroxidase (Glu.Px) enzyme and prevents chemotherapy-induced toxicities. We performed a double-blind, randomized, placebo-controlled study to evaluate the efficacy of selenium on the prevention of OM in 77 patients with leukemia, undergoing allogeneic HSCT. Thirty-seven patients received oral selenium tablets (200 mcg twice daily) from the starting day of HDC to 14 days after transplantation. OM was evaluated daily for 21 days after transplantation according to World Health Organization oral toxicity scale. The incidence of severe OM (grades 3-4) was significantly lower in the selenium group (10.8% vs 35.1%, Po0.05). We noted that the duration of objective OM (grades 2-4), excluding patient's selfdeclaration (grade 1), was significantly shorter in the selenium group (3.6 ± 1.84 vs 5.3 ± 2.2 days, P ¼ 0.014). Significant elevations in serum selenium level and plasma Glu.Px activity were observed 7 and 14 days after transplantation compared with baseline in the selenium group. We conclude that selenium can reduce the duration and severity of OM after HDC.

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“…Due to these cytotoxic effect, cisplatin kills not only cancer cells but also normal cells, resulting in undesirable effects in various tissues including kidney, nerves, ear and gastroenteric ones (Loehrer and Einhorn, 1984). Among these, the nephrotoxicity is most common and can be a cause for the cessation of the drug therapy (Arany and Safi rstein, 2003;Yao et al, 2007). Typically, Blood…”

mentioning

confidence: 99%

Identification of Urinary Biomarkers Related to Cisplatin-Induced Acute Renal Toxicity Using NMR-Based Metabolomics

He¹,

Yang²,

Choi³

et al. 2011

Biomolecules and Therapeutics

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Cisplatin is the founding member of the platin-group drugs that has platinum metal and ammonium group. Since its fi rst approval in 1978 by US Food and Drug Administration, it has been widely used for various types of cancer such as lung, ovarian, lymphomas, breast and bladder cancers (Smith and Talbot, 1992;von der Maase et al., 2000;Crino et al., 2001;Muggia, 2009). The mechanism of anticancer effect is cytotoxicity due to DNA cross-linking, oxidative damages and apoptosis (Gong et al., 1999;Pruefer et al., 2008). Due to these cytotoxic effect, cisplatin kills not only cancer cells but also normal cells, resulting in undesirable effects in various tissues including kidney, nerves, ear and gastroenteric ones (Loehrer and Einhorn, 1984). Among these, the nephrotoxicity is most common and can be a cause for the cessation of the drug therapy (Arany and Safi rstein, 2003;Yao et al., 2007). Typically, BloodCisplatin is widely used for various types of cancers. However, its side effects, most notably, renal toxicity often limit its clinical utility. Although previous metabolomic studies reported possible toxicity markers, they used small number of animals and statistical approaches that may not perform best in the presence of intra-group variation. Here, we identifi ed urinary biomarkers associated with renal toxicity induced by cisplatin using NMR-based metabolomics combined with Orthogonal Projections to Latent Structures-Discriminant Analysis (OPLS-DA). Male Sprague-Dawley rats (n=22) were treated with cisplatin (10 mg/kg single dose), and the urines obtained before and after treatment were analyzed by NMR. Multivariable analysis of NMR data presented clear separation between non-treated and treated groups. The OPLS-DA statistical results revealed that 1,3-dimethylurate, taurine, glucose, glycine and branched-chain amino acid (isoleucine, leucine and valine) were signifi cantly elevated in the treated group and that phenylacetylglycine and sarcosine levels were decreased in the treated group. To test the robustness of the approach, we built a prediction model for the toxicity and were able to predict all the unknown samples (n=14) correctly. We believe the proposed NMR-based metabolomics with OPLS-DA approach and the resulting urine markers can be used to augment the currently available blood markers. AbstractUrea Nitrogen (BUN), and blood creatinine are checked to monitor the expression of renal toxicity. In addition, hydration and diuretic measures are taken to minimize possible kidney damages. Still, BUN and creatinine are measured from blood and are late stage kidney functional markers (Hewitt et al.,

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Cisplatin Nephrotoxicity: A Review

Cited by 1,066 publications

References 77 publications

Intervention Effects of Nedaplatin and Cisplatin on Proliferation and Apoptosis of Human Tumour Cells in Vitro

Intervention Effects of Nedaplatin and Cisplatin on Proliferation and Apoptosis of Human Tumour Cells in Vitro

The efficacy of selenium in prevention of oral mucositis in patients undergoing hematopoietic SCT: a randomized clinical trial

Identification of Urinary Biomarkers Related to Cisplatin-Induced Acute Renal Toxicity Using NMR-Based Metabolomics

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