Impact of acute kidney injury defined by CTCAE v4.0 during first course of cisplatin-based chemotherapy on treatment outcomes in advanced urothelial cancer patients

Ishitsuka, Ryutaro; Miyazaki, Jun; Ichioka, Daishi; Inoue, Takamitsu; Kageyama, Susumu; Sugimoto, Mikio; Mitsuzuka, Koji; Matsui, Yoshiyuki; Shiraishi, Yusuke; Kinoshita, Hidefumi; Wakeda, Hironobu; Nomoto, Takuya; Kikuchi, Eiji; Kawai, Koji; Nishiyama, Hiroyuki

doi:10.1007/s10157-016-1327-z

Cited by 15 publications

(14 citation statements)

References 20 publications

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“…Adverse events related to LHRH agonists were monitored throughout the study period and the severity was recorded following the common terminology criteria for adverse events version 4.0 (CTCAE ver. 4.0) [9].…”

Section: Methodsmentioning

confidence: 99%

Effectiveness of three different luteinizing hormone-releasing hormone agonists in the chemical castration of patients with prostate cancer: Goserelin versus triptorelin versus leuprolide

Shim

Bang

et al. 2019

Investig Clin Urol

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Purpose To investigate the changes in testosterone levels and rates of chemical castration following androgen-deprivation therapy (ADT) with goserelin, triptorelin, and leuprolide. Materials and Methods We retrospectively reviewed the medical records of 125 patients with prostate cancer treated with luteinizing hormone-releasing hormone (LHRH) agonists between January 2009 and December 2015. Changes in testosterone concentration during 9 months of ADT with goserelin 11.34 mg, triptorelin 11.25 mg, and leuprolide 11.25 mg were analyzed using a mixed model. The number of patients with serum testosterone below castration levels defined as various values (<50 ng/dL, <20 ng/dL, or <10 ng/dL) at 3, 6, and 9 months were also evaluated. Results Of the 125 patients, 59 received goserelin, 44 received triptorelin, and 22 received leuprolide, respectively. The lowest mean testosterone levels during 9 months of treatment were achieved in patients treated with triptorelin, followed by those treated with leuprolide, and then by those treated with goserelin (p=0.001). Significant differences in chemical castration levels were observed only at <10 ng/dL, with 54.2% of goserelin, 93.2% of triptorelin, and 86.4% of leuprolide treated patients (p<0.001). Conclusions Three LHRH agonists showed comparable efficacy for achieving castration when the castration threshold was 50 or 20 ng/dL. However, triptorelin was the most potent LHRH agonist, achieving the lowest mean testosterone levels and the highest rate of chemical castration at <10 ng/dL testosterone.

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Section: Methodsmentioning

confidence: 99%

Effectiveness of three different luteinizing hormone-releasing hormone agonists in the chemical castration of patients with prostate cancer: Goserelin versus triptorelin versus leuprolide

Shim

Bang

et al. 2019

Investig Clin Urol

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“…In order to standardize the ICIs-AKI definition across different studies, National Cancer Institute's Common Terminology Criteria for Adverse Events (NCI-CTCAEs) ( 48 ) describes AKI, in part, by comparing changes in SCr to the “upper limit of normal” cut-off parameters. In particular, the NCI-CTCAEs recognize five different grades of renal injury based on creatinine levels (grades 1–3), dialysis requirement (grade 4), and death (grade 5).…”

Section: Clinical Features Of Icis-akimentioning

confidence: 99%

The Use of Immune Checkpoint Inhibitors in Oncology and the Occurrence of AKI: Where Do We Stand?

et al. 2020

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Immune checkpoint inhibitors (ICIs) are a novel class of immunotherapy drugs that have improved the treatment of a broad spectrum of cancers as metastatic melanoma, non-small lung cancer or renal cell carcinoma. These humanized monoclonal antibodies target inhibitory receptors (e.g. CTLA-4, PD-1, LAG-3, TIM-3) and ligands (PD-L1) expressed on T lymphocytes, antigen presenting cells and tumor cells and elicit an anti-tumor response by stimulating immune system. Nevertheless, the improved overall survival is complicated by the manifestation of Immune-related Adverse Effects (irAEs). During treatment with ICIs, the most common adverse kidney effect is represented by the development of acute kidney injury (AKI) with the acute tubulointerstitial nephritis as recurrent histological feature. The mechanisms involved in ICIs-induced AKI include the re-activation of effector T cells previously stimulated by nephrotoxic drugs (i.e. by antibiotics), the loss of tolerance versus self-renal antigens, the increased PD-L1 expression by tubular cells or the establishment of a pro-inflammatory milieu with the release of self-reactive antibodies. For renal transplant recipient treated with ICIs, the increased incidence of rejection is a serious concern. Therefore, the combination of ICIs with mTOR inhibitors represents an emerging strategy. Finally, it is relevant to anticipate which patients under ICIs would experience severe irAEs and from a kidney perspective, to predict patients with higher risk of AKI. Here, we provide a detailed overview of ICIs-related nephrotoxicity and the recently described multicenter studies. Several factors have been reported as biomarkers of ICIs-irAEs, in this review we speculate on potential biomarkers for ICIs-associated AKI.

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“…This is a multicenter, retrospective observational study performed Stage II was an increase in serum creatinine greater than 2-3-fold from baseline; or Stage III was an increase in serum creatinine greater than 3-fold from baseline or serum creatinine greater than 4 mg/dl. 9,17 The use of a predictive risk model described by Motwani et al for the development of CIN was evaluated. A risk prediction score was calculated for each patient according to Table 1.…”

Section: Me Thodsmentioning

confidence: 99%

Cisplatin‐induced nephrotoxicity in an outpatient setting

et al. 2021

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Cisplatin is a platinum-containing antineoplastic agent that has demonstrated efficacy in the treatment of various types of cancer. 1 Cisplatin exerts its antineoplastic mechanism by arresting the cell cycle and inducing apoptosis in cancer cells through alteration of DNA synthesis. 2 Cisplatin is considered a first-line agent used in the treatment of head and neck, bladder, and lung cancers, demonstrating enhanced efficacy as compared with alternative agents. The use of cisplatin is often limited by the development of nephrotoxicity with studies showing an incidence between 20 and 30%. 1,3,4 Development of nephrotoxicity may delay further cycles of cisplatin or require administration of second-line agents. It is therefore important to mitigate the risk of toxicity in order to prolong cisplatin therapy. Several pathophysiologic mechanisms have been proposed leading to the development of cisplatin-induced nephrotoxicity (CIN). Cisplatin is eliminated renally and accumulates in renal tubular cells resulting in tubular cell injury and death, inflammation, renal vasculature injury, and renal ischemia. 5,6 CIN typically presents within 7 days of initiating cisplatin therapy, manifesting primarily as a

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Impact of acute kidney injury defined by CTCAE v4.0 during first course of cisplatin-based chemotherapy on treatment outcomes in advanced urothelial cancer patients

Abstract: The present study demonstrated that AKI (CTCAE v4.0) during chemotherapy had a negative impact on both the intensity of subsequent chemotherapy and oncological outcomes.

Cited by 15 publications

References 20 publications

Effectiveness of three different luteinizing hormone-releasing hormone agonists in the chemical castration of patients with prostate cancer: Goserelin versus triptorelin versus leuprolide

Effectiveness of three different luteinizing hormone-releasing hormone agonists in the chemical castration of patients with prostate cancer: Goserelin versus triptorelin versus leuprolide

The Use of Immune Checkpoint Inhibitors in Oncology and the Occurrence of AKI: Where Do We Stand?

Cisplatin‐induced nephrotoxicity in an outpatient setting

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