Early prediction of cisplatin-induced nephrotoxicity by urinary vanin-1 in patients with urothelial carcinoma

Hosohata, Keiko; Washino, Satoshi; Kubo, Taro; Natsui, Shinsuke; Fujisaki, Akira; Kurokawa, Shinsuke; Ando, Hitoshi; Fujimura, Akio; Morita, Tatsuo

doi:10.1016/j.tox.2016.06.011

Cited by 28 publications

(29 citation statements)

References 20 publications

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“…In 33 Cis‐treated adults, urine NGAL predicted AKI with AUC over 0.85 . Another study in Cis‐treated elderly adults showed that AKI prediction using NGAL (3 days postinfusion) was modest (AUC ∼ 0.65) . An Egyptian study measured NGAL in 30 Cis‐treated children with solid tumors, pre‐Cis, 1 week after treatment start and at cancer treatment end.…”

Section: Discussionmentioning

confidence: 99%

Urine biomarkers of acute kidney injury in noncritically ill, hospitalized children treated with chemotherapy

Sterling

Al-Ismaili

McMahon

et al. 2017

Pediatric Blood & Cancer

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Section: Discussionmentioning

confidence: 99%

Urine biomarkers of acute kidney injury in noncritically ill, hospitalized children treated with chemotherapy

Sterling

Al-Ismaili

McMahon

et al. 2017

Pediatric Blood & Cancer

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“…Importantly, we showed that the urinary concentration of vanin-1 elevated before the conventional markers such as serum creatinine, urinary N -acetyl-β- d -glucosaminidase (NAG), or both increased in rats with a nephrotoxicant [70], and cisplatin [86] induced renal tubular injury in the time-course analyses. Furthermore, urinary vanin-1 was shown to be more predictive of the decline in eGFR after the dosing of cisplatin compared with KIM-1, NGAL, and NAG in patients with urothelial carcinoma [87]. …”

Section: Oxidative Stress and Vanin-1 As A Potential Biomarker Formentioning

confidence: 99%

Role of Oxidative Stress in Drug-Induced Kidney Injury

Hosohata

2016

IJMS

Self Cite

137

116

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The kidney plays a primary role in maintaining homeostasis and detoxification of numerous hydrophilic xenobiotics as well as endogenous compounds. Because the kidney is exposed to a larger proportion and higher concentration of drugs and toxins than other organs through the secretion of ionic drugs by tubular organic ion transporters across the luminal membranes of renal tubular epithelial cells, and through the reabsorption of filtered toxins into the lumen of the tubule, these cells are at greater risk for injury. In fact, drug-induced kidney injury is a serious problem in clinical practice and accounts for roughly 20% of cases of acute kidney injury (AKI) among hospitalized patients. Therefore, its early detection is becoming more important. Usually, drug-induced AKI consists of two patterns of renal injury: acute tubular necrosis (ATN) and acute interstitial nephritis (AIN). Whereas AIN develops from medications that incite an allergic reaction, ATN develops from direct toxicity on tubular epithelial cells. Among several cellular mechanisms underlying ATN, oxidative stress plays an important role in progression to ATN by activation of inflammatory response via proinflammatory cytokine release and inflammatory cell accumulation in tissues. This review provides an overview of drugs associated with AKI, the role of oxidative stress in drug-induced AKI, and a biomarker for drug-induced AKI focusing on oxidative stress.

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“…Based on these estimates, we expected a higher number of AKI episodes than resulted in this study, in which only one patient met the KDIGO criteria for stage 2 AKI . Other studies have used different AKI criteria based on arbitrary cutoffs in SCr or eGFR increase from baseline that do not conform to KDIGO criteria . The lower incidence of AKI in this study could also be due to several factors, including a limited sample size, the timing of blood collection for biomarkers, and the low to moderate cisplatin dose ranges prescribed (as low as 25 mg/m 2 ).…”

Section: Discussionmentioning

confidence: 91%

Profiling of Kidney Injury Biomarkers in Patients Receiving Cisplatin: Time‐dependent Changes in the Absence of Clinical Nephrotoxicity

George

Wen

Mercke

et al. 2017

Clin Pharma and Therapeutics

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The success of cisplatin-containing regimens to treat solid tumors is limited, in part, by nephrotoxicity. In rodents, several urinary proteins have emerged as more sensitive indicators of cisplatin-induced kidney injury. We sought to characterize time-dependent changes in the urinary concentrations of 12 proteins including KIM-1, calbindin, β2M, and TFF3 after cisplatin therapy. Urine was collected at baseline, 3 (range: 2-5), and 10 (range: 9-11) days from 57 patients with solid tumors receiving outpatient cisplatin therapy (≥ 25 mg/m2). Serum creatinine was largely unchanged after cisplatin infusion. However, compared to baseline values, several novel biomarkers were significantly increased in the urine including β2M, which was 3-fold higher by day 3 (p<0.0001). Urinary KIM-1 and TFF3 were elevated 2-fold by day 10 (p=0.002 and p=0.002, respectively) whereas calbindin levels were increased 8-fold (p<0.0001). We report novel time-dependent changes in the urinary excretion of noninvasive markers of subclinical kidney injury after cisplatin treatment.

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Early prediction of cisplatin-induced nephrotoxicity by urinary vanin-1 in patients with urothelial carcinoma

Cited by 28 publications

References 20 publications

Urine biomarkers of acute kidney injury in noncritically ill, hospitalized children treated with chemotherapy

Urine biomarkers of acute kidney injury in noncritically ill, hospitalized children treated with chemotherapy

Role of Oxidative Stress in Drug-Induced Kidney Injury

Profiling of Kidney Injury Biomarkers in Patients Receiving Cisplatin: Time‐dependent Changes in the Absence of Clinical Nephrotoxicity

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