Relationship of Intracellular Calcium and Oxygen Radicals to Cisplatin-Related Renal Cell Injury

Kawai, Yoshiko; Nakao, Takafumi; Kunimura, Naoshi; Kohda, Yuka; Gemba, Munekazu

doi:10.1254/jphs.fp0050661

Cited by 149 publications

(96 citation statements)

References 30 publications

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“…Its major adverse effect is nephrotoxicity, although ototoxicity also occurs. Both are dose-related toxicities, causing apoptosis and necrosis of cells (29)(30)(31)(32). Cisplatin injures multiple renal compartments, including blood vessels, glomeruli, and most commonly, the tubules (29).…”

Section: Tubules: Acute Tubular Injury Cisplatinmentioning

confidence: 99%

Onco-Nephrology

Perazella

2012

Clinical Journal of the American Society of Nephrology

275

197

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SummaryDespite dramatic improvements in patient survival and drug tolerability, nephrotoxicity remains an important complication of chemotherapy. Adverse renal effects occur because of innate drug toxicity and a number of patient-and drug-related factors. To provide cutting edge care for these patients, nephrologists and oncologists must be familiar with the nephrotoxicity of these drugs, particularly their associated clinical and laboratory manifestations. Rapid diagnosis, targeted treatment, and supportive care are critical to improving care for these patients. Unfortunately, some patients who develop nephrotoxicity will be left with long-term complications such as chronic tubulopathies and CKD. Onco-Nephrology is a new area that is rapidly expanding and requires a close working relationship between oncologists and nephrologists.

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Section: Tubules: Acute Tubular Injury Cisplatinmentioning

confidence: 99%

Onco-Nephrology

Perazella

2012

Clinical Journal of the American Society of Nephrology

275

197

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“…8,9 Cisplatin nephrotoxicity is mostly mediated through inflammation, 10,11 vasoconstriction 12,13 and direct cytotoxicity through reactive oxygen species. 14 Renal proximal tubules show vulnerability to cisplatin toxicity that leads to a decline in GFR. 15,16 To alleviate the nephrotoxic effects, prevention strategies such as hydration were established which allow the application of higher cisplatin doses.…”

Section: Introductionmentioning

confidence: 99%

Urinary TIMP2·IGFBP7 for the prediction of platinum-induced acute renal injury

Schanz

Hoferer²,

Shi

et al. 2017

IJNRD

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Introduction: Platinum-based chemotherapy (PBC) is a potent antineoplastic treatment, but cisplatin nephrotoxicity is often the limiting factor. Identifying the patients who are at risk for developing platinum-induced renal injury is an important issue. We tested urinary TIMP2·IGFBP7, a new US Food and Drug Administration (FDA)-cleared test to assess the risk of acute kidney injury (AKI), in a cohort of patients with malignant neoplastic disease receiving PBC. Patients and methods: A total of 58 patients with malignant neoplastic disease were enrolled in this study, of whom 32 patients had both urine samples and subsequent serum creatinine values available for detecting AKI within 72 hours. Urine samples were collected within 6 hours prior to PBC application and within 12 hours after the end of chemotherapy administration. We examined the predictive ability of TIMP2·IGFBP7 for the development of AKI as defined by KDIGO (Kidney Disease: Improving Global Outcomes) criteria within 72 hours after the administration of chemotherapy. Operating characteristics were determined for the previously validated TIMP2·IGFBP7 cutoff of 0.3 (ng/mL) 2 /1000. Results: Four (12.5%) patients developed AKI within 72 hours. Primary disease was lymphoma in 13 patients (40.6%) and solid tumors in 19 patients (59.4%). Eight patients (25.0%) received carboplatin and 24 (75.0%) cisplatin. TIMP2·IGFBP7 after PBC administration discriminated for the risk of AKI with an area under the receiver operating characteristic curve (AUC; 95% confidence interval) of 0.92 (0.80-1.00). At the cutoff of 0.3 for TIMP2·IGFBP7, sensitivity was 50%, specificity was 87%, negative predictive value was 95% and positive predictive value was 25% for the prediction of AKI within 72 hours. Conclusion: Urinary TIMP2·IGFBP7 measured in specimens gathered after PBC may be a useful tool to early identify patients who are at risk for developing platinum-induced AKI.

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“…7,8 However, it is still controversial whether oxygen therapy plays a toxic role in renal injury. Exposure to high concentrations of oxygen is known to induce injury to cells, possibly due to an increased oxygen radical formation.…”

Section: Introductionmentioning

confidence: 99%

“…10,11 Hypoxia and mitochondrial injury are also implicated in Cisplatin nephrotoxicity. 7 According to our literature review, there is no clinical human study in terms of impact of oxygen therapy before Cisplatin administration on kidney injury. This study examines whether preconditioning with normobaric hyperoxia would prevent Cisplatin-induced nephrotoxicity in patients with solid tumors.…”

Section: Introductionmentioning

confidence: 99%

Normobaric hyperoxia preconditioning ameliorates cisplatin nephrotoxicity

Saadat¹,

Maghani²,

Rahimi³

et al. 2013

Renal Failure

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Background: Cisplatin is a potent anticancer drug, but its nephrotoxicity limits the clinical use of it. To reduce the Cisplatin-induced nephrotoxicity, various interventions have been implicated. The aim of this study was to examine whether preconditioning with normobaric hyperoxia would prevent Cisplatin-induced nephrotoxicity in patient with solid tumor. Methods: In a prospective study, 80 adult patients with solid tumor who were treated with Cisplatin between February 2011 and December 2011 were included. Forty-three patients were exposed to pure oxygen via non-rebreathing reservoir mask which increased the provided oxygen rate to 60% oxygen for 2 hours at 48, 24, and 6 hours before intravenous administration of Cisplatin and 37 patients received only Cisplatin as a control group. Estimated glomerular filtration rate (eGFR) calculated in all patients on day 1 before and on days 1, 3, 6, 30 after Cisplatin exposures. Results: Patients treated with Cisplatin and 60% oxygen showed a mild improvement in eGFR and mild reduction of serum creatinine after 30 days with statistically mild significant differences (p ¼ 0.048). Conclusion: This study showed that normobaric and intermittent precondition of 60% oxygen prior to Cisplatin treatment had an acute transient adverse effect on renal function; however, the improvement of renal function will be seen after 30 days. Thus, it may help to prevent Cisplatin nephrotoxicity.

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Relationship of Intracellular Calcium and Oxygen Radicals to Cisplatin-Related Renal Cell Injury

Cited by 149 publications

References 30 publications

Onco-Nephrology

Onco-Nephrology

Urinary TIMP2·IGFBP7 for the prediction of platinum-induced acute renal injury

Normobaric hyperoxia preconditioning ameliorates cisplatin nephrotoxicity

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Relationship of Intracellular Calcium and Oxygen Radicals to Cisplatin-Related Renal Cell Injury

Cited by 149 publications

References 30 publications

Onco-Nephrology

Onco-Nephrology

Urinary TIMP2&middot;IGFBP7 for the prediction of platinum-induced acute renal injury

Normobaric hyperoxia preconditioning ameliorates cisplatin nephrotoxicity

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Urinary TIMP2·IGFBP7 for the prediction of platinum-induced acute renal injury