Cisplatin Nephrotoxicity: A Summary of Preventative Interventions

Finley, Rebecca S.; Fortner, Clarence L.; Grove, William R.

doi:10.1177/106002808501900505

Cited by 40 publications

(15 citation statements)

References 20 publications

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“…As tubular injury progresses, glomerular and interstitial cells become damaged. To decrease the concentration of cisplatin in the renal tubule, hydration [10,11] and short hydration [12][13][14] have been useful for preventing cisplatin-induced AKI. Despite these approaches, incidences of cisplatin-induced AKI remain high.…”

Section: Discussionmentioning

confidence: 99%

Lower Blood Pressure-Induced Renal Hypoperfusion Promotes Cisplatin-Induced Nephrotoxicity

et al. 2016

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Background and Aims: Cisplatin-induced nephrotoxicity primarily occurs in the proximal tubules, and tubular injuries reduce glomerular filtration rates. Lower blood pressure causes renal hypoperfusion, which promotes ischemic acute kidney injury (AKI). Our study examined the relationship between lower blood pressure-induced renal hypoperfusion and cisplatin-induced nephrotoxicity. Methods: The relationship between cisplatin use and hypoalbuminemia is not clear. This study consisted of Japanese patients who received cisplatin as the first-line chemotherapy at Fujita Health University Hospital from April 2006 to December 2012. Hypoalbuminemia was defined as serum albumin levels ≤3.5 mg/dl. Results: Patients who experienced lower blood pressure during chemotherapy were included in the lower blood pressure group (n = 229), and those who did not were included in the normal blood pressure group (n = 743). Total cisplatin dose in the normal blood pressure and lower blood pressure groups was 58.9 ± 23.8 and 55.0 ± 20.4 mg/m², respectively. The rate of severe nephrotoxicity was higher and overall survival was shorter in the lower blood pressure group than in the normal blood pressure group. In a multivariable analysis, lower blood pressure significantly correlated with hypoalbuminemia. Conclusions: To prevent ischemic AKI, nutrition and cachexia controlling are important parts of cancer treatment.

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Section: Discussionmentioning

confidence: 99%

Lower Blood Pressure-Induced Renal Hypoperfusion Promotes Cisplatin-Induced Nephrotoxicity

et al. 2016

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“…The first step in the prevention of cisplatin-induced nephrotoxicity is to ensure optimal expansion of extracellular volume with saline prior to, during, and following drug administration (Finley et al 1985). This can be accomplished by infusing 3-51 of normal saline per day beginning the day before the start of drug therapy and continuing for a day after administering the last dose.…”

Section: Antineoplastic Agentsmentioning

confidence: 99%

Drug-Induced Acute Renal Failure

Kaloyanides¹

1995

Update in Intensive Care and Emergency Medicine

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“…Various methods for reducing CDDP nephrotoxicity have been studied. Infusion and diuresis before and after CDDP administration are believed to reduce nephrotoxicity by lowering the concentration of CDDP in urine, thereby shortening the contact time between CDDP and the renal tubule [1,2]. Although renal toxicity of CDDP is reduced by infusion, it cannot be completely avoided.…”

Section: Introductionmentioning

confidence: 99%

Effect of Magnesium Supplementation to Prevent Nephrotoxicity on the Antitumor Activity of Cisplatin

Yasuda¹,

Kishimoto²,

Ebara³

et al. 2019

JCTR

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Background: Cisplatin (CDDP) is one of the most widely used anticancer drugs, but CDDP often leads to nephrotoxicity, which limits its clinical effectiveness. Magnesium (Mg) supplementation is recommended for the avoidance of CDDP-induced nephrotoxicity. However, there is a concern that exposing cancer cells to Mg may suppress the antitumor effect of CDDP. Methods: Transporter expression, intracellular platinum and Mg levels, and cytotoxicity of CDDP after Mg exposure were assessed in human hepatocellular carcinoma (HepG2) and human ovarian carcinoma (2008) cells. Results: In HepG2 cells, Mg exposure significantly increased mRNA levels of multidrug and toxin extrusion 1 (MATE1), which mediates the renal excretion of CDDP, but did not alter its protein levels, including those of organic cation transporter 1 (OCT1), which mediates CDDP uptake in renal tubular and cancer cells, and multidrug resistance-associated protein 2 (MRP2), which mediates CDDP efflux in cancer cells. In 2008 cells, MATE1 protein expression could not be detected, but a slight increase in MRP2 and OCT1 protein expression was observed after Mg exposure. Intracellular Mg levels were significantly increased due to Mg exposure in both cells. However, intracellular platinum levels and cytotoxicity of CDDP were not affected in both cells, even with 2 mM Mg co-exposure. Conclusion: This study found that Mg exposure only slightly changed transporter expression and did not affect intracellular platinum levels and CDDP cytotoxicity in HepG2 and 2008 cells. Thus, Mg supplementation can be used to avoid CDDP-induced renal toxicity without affecting the accumulation of CDDP in cancer cells and its cytotoxicity.

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Cisplatin Nephrotoxicity: A Summary of Preventative Interventions

Cited by 40 publications

References 20 publications

Lower Blood Pressure-Induced Renal Hypoperfusion Promotes Cisplatin-Induced Nephrotoxicity

Lower Blood Pressure-Induced Renal Hypoperfusion Promotes Cisplatin-Induced Nephrotoxicity

Drug-Induced Acute Renal Failure

Effect of Magnesium Supplementation to Prevent Nephrotoxicity on the Antitumor Activity of Cisplatin

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