Comparison of the nephroprotective effects of non-steroidal anti-inflammatory drugs on cisplatin-induced nephrotoxicity in vitro and in vivo

Okamoto, Ken‐ichi; Saito, Yoshitaka; Narumi, Katsuya; Furugen, Ayako; Iseki, Ken; Kobayashi, Masaki

doi:10.1016/j.ejphar.2020.173339

Cited by 12 publications

(7 citation statements)

References 39 publications

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“…We previously reported that patients with DM develop CIN at a significantly higher rate in a short hydration method 4 . Autophagy reportedly protects against CIN 8 , 13 , 14 , and its induction at the proximal tubule, where CIN mostly appears, is significantly suppressed in type 2 DM, which all participants met in previous and present studies 4 , 15 . Thus, we consider that the main mechanism of CIN degradation in type 2 DM is the reduction in renal autophagy.…”

Section: Discussionsupporting

confidence: 79%

“…Fenske et al reported that plasma PGE 2 metabolite levels are twice as high in patients with type 2 DM than in controls 22 . In addition, we have reported that most NSAIDs do not affect renal autophagy in vitro 14 . Thus, we believe that the higher baseline PGE 2 levels in patients with DM compensate for the renal influence of NSAIDs.…”

Section: Discussionmentioning

confidence: 90%

“…Autophagy is nephroprotective against CIN 8 , 13 , 14 , and autophagic activity is induced in type 1 DM and suppressed in type 2 DM 15 . Furthermore, renal damage caused by CDDP was reportedly reduced in streptozotocin-administered mice, which are recognized as models of type 1 DM 23 , 24 .…”

Section: Discussionmentioning

confidence: 99%

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Risk factor analysis for cisplatin-induced nephrotoxicity with the short hydration method in diabetic patients

Saito,

Kobayashi,

Tamaki

et al. 2023

Sci Rep

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The occurrence of cisplatin (CDDP)-induced nephrotoxicity (CIN) has decreased with advancements in supportive care. In contrast, we reported that baseline diabetes mellitus (DM) complications significantly worsen CIN. This study aimed to determine further risk factors associated with CIN development in DM patients. Patients with thoracic cancer requiring DM pharmacotherapy, who received CDDP (≥ 60 mg/m2)-containing regimens using the short hydration method (n = 140), were enrolled in this retrospective multicenter observational study. The primary endpoint of the present study was the elucidation of risk factors (patient factors, DM medication influence, and treatment-related factors) associated with CIN development in patients with DM. Cisplatin-induced nephrotoxicity occurred in 22.1% of patients with DM. The median worst variation of serum creatinine levels and creatinine clearance (worst level − baseline level) was 0.16 mg/dL (range: − 0.12–1.41 mg/dL) and − 15.9 mL/min (− 85.5–24.3 mL/min), respectively. Multivariate logistic regression analyses identified female sex as the singular risk factor for CIN development in the DM population (adjusted odds ratio; 2.87, 95% confidence interval; 1.08–7.67, P = 0.04). Diabetes mellitus medication and treatment-related factors did not affect CIN development. In conclusion, our study revealed that female sex is significantly associated with CIN development in patients with DM and thoracic cancer.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 90%

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Risk factor analysis for cisplatin-induced nephrotoxicity with the short hydration method in diabetic patients

Saito,

Kobayashi,

Tamaki

et al. 2023

Sci Rep

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“…Furthermore, CIN worsens in autophagy-deficient mice compared to controls 29 . We showed that celecoxib, a cyclooxygenase-2 selective NSAIDs, exhibits a nephroprotective effect against CIN by activating autophagy and suppressing oxidative stress 30 . These results suggest that autophagy works nephroprotective against CIN.…”

Section: Discussionmentioning

confidence: 99%

Diabetes mellitus degenerates cisplatin-induced nephrotoxicity in short hydration method: a propensity score-matching analysis

Saito

Sakamoto²,

Takekuma³

et al. 2022

Sci Rep

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Cisplatin (CDDP)-induced nephrotoxicity (CIN) is dose-limiting. We revealed that co-administration of non-steroid anti-inflammatory drugs and baseline comorbidity of diabetes mellitus (DM) are associated with CIN development in the short hydration method; however, the results were accessorily obtained without appropriate power calculation. This study aimed to demonstrate the influence of DM complications on CIN incidence in a real-world setting. Lung cancer patients receiving CDDP (≥ 75 mg/m2)-containing regimens with a short hydration method (n = 227) were retrospectively evaluated. The patients were divided into control and baseline DM complication groups. The primary endpoint was the evaluation of CIN incidence between the groups. Propensity score-matching was performed to confirm the robustness of the primary analysis results. CIN occurred in 6.8% of control and 27.0% of DM patients, respectively, with a significant difference in all-patient populations (P = 0.001). In addition, variation of serum creatinine and creatinine clearance significantly worsened in DM patients. Similar results were obtained in a propensity-matched population. Multivariate logistic regression analysis found that DM complication is a singular risk factor for CIN development (adjusted odds ratio; 4.31, 95% confidence interval; 1.62–11.50, P = 0.003). In conclusion, our study revealed that baseline DM complications significantly worsen CIN.

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“…Moreover, cisplatin attracts different organelles and interfaces in DNA replication that proceed to alter several biological mechanisms, including necrosis and apoptosis, inflammation, and tubular derangement [ 9 , 44 ]. The mechanisms by which Cis causes nephrotoxicity are complex and intervened by different biological pathways involve oxidative stress, apoptosis, and inflammation [ 45 ]. ROS production is increased by cisplatin by mitochondria; NADPH oxidase and cellular xanthine oxidase systems are involved in the pathogenesis of Cis induced severe kidney failure [ 17 ].…”

Section: Discussionmentioning

confidence: 99%

The nephroprotective effects of Daucus carota and Eclipta prostrata against cisplatin-induced nephrotoxicity in rats

et al. 2021

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The overuse of cisplatin (>50 mg/m 2 ) is limited to nephrotoxicity, ototoxicity, gastrotoxicity, myelosuppression, and allergic reactions. The objective of this study was to investigate the nephroprotective effects of Daucus carota and Eclipta prostrata extracts on cisplatin-induced nephrotoxicity in Wistar albino rats. The study involved male Wistar albino rats of 8 weeks weighing 220–270 g. A single injection of 5 mg/kg was injected into the rats for nephrotoxicity. Rats were divided into four groups based on dose conentrations. Blood and urine samples of rats were collected on the 0, 7 th , 14 th , and 21 st days for nephrological analysis. The results showed that Cis + DC/Cis + EP (600 mg/kg) significantly (p < 0.001) increased the body weight and reduced the kidney weight of cisplatin-induced nephrotoxicity in rats (p < 0.001) as compared to Cis group. The results showed that 600 mg/kg administration of Cis + DC/Cis +EP successfully (p < 0.005) improved the urine and plasmin creatinine, Na, and K level compared to the Cis group. Histopathological results confirmed that Cis + EP/Cis + DC effectively improved the renal abnormalities. It is concluded that the co-administration of Cis + EP extract showed exceptional nephroprotective effects at a dose rate of 600 mg/kg.

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Comparison of the nephroprotective effects of non-steroidal anti-inflammatory drugs on cisplatin-induced nephrotoxicity in vitro and in vivo

Cited by 12 publications

References 39 publications

Risk factor analysis for cisplatin-induced nephrotoxicity with the short hydration method in diabetic patients

Risk factor analysis for cisplatin-induced nephrotoxicity with the short hydration method in diabetic patients

Diabetes mellitus degenerates cisplatin-induced nephrotoxicity in short hydration method: a propensity score-matching analysis

The nephroprotective effects of Daucus carota and Eclipta prostrata against cisplatin-induced nephrotoxicity in rats

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