Assessment of acute kidney injury by urinary β2-MG and NAG in pediatric cancer patients prescribed with Cisplatin, Carboplatin, and Ifosfamide as the chemotherapeutic agents

2020 ◽  
Author(s):  
Alireza Moafi ◽  
Hanieh Basirkazeruni ◽  
Nahid Reisi ◽  
Moein Dehbashi ◽  
Leila Ghanbarinia ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cancer Patients ◽  
Pediatric Cancer ◽  
Age Groups ◽  
Kidney Injury ◽  
Chemotherapeutic Agents ◽  
Pediatric Cancer Patients ◽  
The Mean ◽  
Beta 2 Microglobulin ◽  
Kidney Injury Molecule 1

Background: Acute kidney injury (AKI) is defined as a failure in renal function leading to insufficiency of fluid and electrolyte homeostasis. Thus, sensitive biomarkers of renal tubular injury are needed to detect AKI earlier. In this study, urinary beta 2-microglobulin (β2-MG) and urinary N-acetyl-β-D-glucosaminidase (NAG) were evaluated for AKI prognosis/diagnosis in pediatric patients suffering different cancers prescribed with Ifosfamide, Ifosfamide plus Carboplatin, and Ifosfamide plus Cisplatin. Materials and Methods: In this prospective study done in Isfahan, Iran, urinary β2-MG, urinary NAG, blood urea nitrogen (BUN), and serum and urinary creatinine (Cr) were measured in 40 pediatric cancer patients less than 16 years old in three age groups during 61 courses of chemotherapy on day 0, three and six after the treatment. Results: Using ANOVA and t-test, the mean levels of urinary β2-MG (p= 0.001), urinary β2-MG/Cr (p= 0.003) and urinary NAG/Cr (p= 0.001), before and on day six of the treatment were statistically significant (p< 0.05). Also, the mean levels of BUN (p= 0.01), urinary β2-MG (p= 0.001), β2-MG/Cr (p= 0.001) and NAG/Cr (p= 0.004) based on the gender groups, the mean levels of urinary NAG (p=0.001), NAG/Cr (p= 0.001) and β2-MG/Cr (p= 0.008) based on three age groups, and the mean levels of serum Cr (p= 0.047), urinary β2-MG (p= 0.005), β2-MG/Cr (p= 0.032) and NAG/Cr (p= 0.032) based on the Ifosfamide dosage were statistically significant during the time of the treatment. Conclusion: Urinary β2-MG, urinary β2-MG/Cr, and urinary NAG/Cr are more significant biomarkers than serum Cr in earlier diagnosis and treatment of AKI in cancer patients. However, urinary NAG should be further studied to prove its reliability for AKI prognosis/diagnosis. It is suggested that urinary NAG can be used along with other renal biomarkers such as urinary β2-MG, kidney injury molecule-1(KIM-1), or interleukin-18 (IL-18) for AKI prognosis/diagnosis.

The incidence, risk factors and outcomes of chemotherapy related acute kidney injury in China.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e24161-e24161
Author(s):  
Lu Li ◽  
Sheng Nie ◽  
Chen Ren ◽  
Yanqin Li ◽  
Dehua Wu
Keyword(s):  
Acute Kidney Injury ◽  
Hospital Mortality ◽  
Cancer Patients ◽  
Age Groups ◽  
Kidney Injury ◽  
Chemotherapeutic Agents ◽  
Prescription Database ◽  
Purine Analogues ◽  
Chemotherapy Drugs ◽  
Group Type

e24161 Background: Nephrotoxicity of chemotherapeutic agents remains a significant complication limiting the efficacy of the treatment. However, comprehensive data on the epidemiology and outcomes of chemotherapy related acute kidney Injury in China is lacking. Methods: We conducted a nationwide cohort study of hospitalized patients from 25 general and children’s hospitals in China during 2013-2015. Patient-level data were obtained from the electronic hospitalization information system, prescription database and laboratory databases of all cancer patients who received chemotherapy and had at least two serum creatinine tests within any 7-day window during the hospitalization. AKI was defined and staged according to Kidney Disease Improving Global Outcomes criteria. The incidence of AKI in patients with various type of cancer and chemotherapeutic agents was examined. The outcomes of AKI, including in-hospital mortality, death after discharge, kidney recovery, and length of stay, were also assessed. Results: A total of 23,232 cancer patients, including 3,120 children ( < 18 years old), 16,310 adult (19-65 years old) and 3,802 elderly patients ( > 65 years old), were analyzed. Platinum compounds and pyrimidine analogues were the most common used chemotherapy agents for cancer patients. The overall incidence of AKI was 4.9%. Patients with urinary system malignancy (12.3%), hematological malignancy (10.2%) and nerve motor system malignancy (4.1%) have the highest incidence of HA-AKI. The top three types of chemotherapy drugs with the highest incidence of AKI were Purine analogues (30.1%), folic acid analogues (15.3%) and combinations of antineoplastic agents (14.1%). The nephrotoxicity of chemotherapy drugs was different among age groups. AKI is associated with a higher risk of in-hospital mortality and death after discharge. Conclusions: The risk of AKI in cancer patients varied in different age group, type of cancer and chemotherapeutic agents.

Acute Kidney Injury in Pediatric Cancer Patients

2019 ◽  
Vol 208 ◽  
pp. 243-250.e3 ◽  
Author(s):  
Peong Gang Park ◽  
Che Ry Hong ◽  
Eunjeong Kang ◽  
Minsu Park ◽  
Hajeong Lee ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cancer Patients ◽  
Pediatric Cancer ◽  
Kidney Injury ◽  
Pediatric Cancer Patients

KIDNEY INJURY IN CANCER THERAPY

2018 ◽  
Vol 22 (5) ◽  
pp. 17-24 ◽  
Author(s):  
E. V. Burnasheva ◽  
Y. V. Shatokhin ◽  
I. V. Snezhko ◽  
A. A. Matsuga
Keyword(s):  
Risk Factors ◽  
Acute Kidney Injury ◽  
Cancer Therapy ◽  
Cancer Patients ◽  
Cytotoxic Effect ◽  
Tumor Lysis Syndrome ◽  
Kidney Injury ◽  
Chemotherapeutic Agents ◽  
Oxygen Intermediates ◽  
Circulating Blood Volume

Кidney injury is a frequent and significant complication of cancer and cancer therapy. The kidneys are susceptible to injury from malignant infiltration, damage by metabolites of malignant cells, glomerular  injury, nephrotoxic drugs including chemotherapeutic agents. Also  bone marrow transplantation complications, infections with immune  suppression (including septicemia), tumor lysis syndrome should be  taken into account. Chemotherapeutic agents are a common cause  of acute kidney injury but can potentially lead to chronic kidney  disease development in cancer patients. This article summarizes risk  factors of acute kidney injury in cancer patients. Risk factors are  divided into two groups. The systemic are decrease of total  circulating blood volume, infiltration of kidney tissue by tumor cells,  dysproteinemia, electrolyte disturbances. The local (renal) risk  factors are microcirculation disturbances, drugs biotransformation  with formation of reactive oxygen intermediates, high concentration of nephrotoxic agents in proximal tubules and its  sensitivity to ischemia. Drug-related risk factors include: drugs  combination with cytotoxic effect high doses long term use necessity, direct cytotoxic effect of not only chemotherapeutic agents but also its metabolites, mean solubility forming intratubular  precipitates. Early diagnosis, timely prevention and treatment of  these complications provide significantly improve nononcologic results of treatment.

scholarly journals Urinary protein biomarkers of kidney injury in patients receiving cisplatin chemotherapy

2017 ◽  
Vol 243 (3) ◽  
pp. 272-282 ◽  
Author(s):  
Blessy George ◽  
Melanie S Joy ◽  
Lauren M Aleksunes
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Urinary Proteins ◽  
Protein Biomarkers ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Chemotactic Protein ◽  
Trefoil Factor 3 ◽  
Beta 2 Microglobulin ◽  
Kidney Injury Molecule 1 ◽  
Neutrophil Gelatinase

Despite recent progress in the development of novel approaches to treat cancer, traditional antineoplastic drugs, such as cisplatin, remain a mainstay of regimens targeting solid tumors. Use of cisplatin is limited by acute kidney injury, which occurs in approximately 30% of patients. Current clinical measures, such as serum creatinine and estimated glomerular filtration rate, are inadequate in their ability to detect acute kidney injury, particularly when there is only a moderate degree of injury. Thus, there is an urgent need for improved diagnostic biomarkers to predict nephrotoxicity. There is also interest by the U.S. Food and Drug Administration to validate and implement new biomarkers to identify clinical and subclinical acute kidney injury in patients during the drug approval process. This minireview provides an overview of the current literature regarding the utility of urinary proteins (albumin, beta-2-microglobulin, N-acetyl-D-glucosaminidase, kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, and cystatin C) as biomarkers for cisplatin-induced AKI. Many of the well-studied urinary proteins (KIM-1, NGAL, B2M, albumin) as well as emerging biomarkers (calbindin, monocyte chemotactic protein-1, and trefoil factor 3) display distinct patterns of time-dependent excretion after cisplatin administration. Implementation of these biomarker proteins in the oncology clinic has been hampered by a lack of validation studies. To address these issues, large head-to-head studies are needed to fully characterize time-dependent responses and establish accurate cutoff values and ranges, particularly in cancer patients. Impact statement There is growing interest in using urinary protein biomarkers to detect acute kidney injury in oncology patients prescribed the nephrotoxic anticancer drug cisplatin. We aim to synthesize and organize the existing literature on biomarkers examined clinically in patients receiving cisplatin-containing chemotherapy regimens. This minireview highlights several proteins (kidney injury molecule-1, beta-2-microglobulin, neutrophil gelatinase-associated lipocalin, calbindin, monocyte chemotactic protein-1, trefoil factor 3) with the greatest promise for detecting cisplatin-induced acute kidney injury in humans. A comprehensive review of the existing literature may aid in the design of larger studies needed to implement the clinical use of these urinary proteins as biomarkers of kidney injury.

scholarly journals Role of Urinary Beta 2 Microglobulin and Kidney Injury Molecule-1 in Predicting Kidney Function at One Year Following Acute Kidney Injury

2021 ◽  
Vol Volume 14 ◽  
pp. 225-234
Author(s):  
Dhanin Puthiyottil ◽  
PS Priyamvada ◽  
Mattewada Naveen Kumar ◽  
Anand Chellappan ◽  
Bobby Zachariah ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Function ◽  
Kidney Injury ◽  
Beta 2 ◽  
One Year ◽  
Beta 2 Microglobulin ◽  
Kidney Injury Molecule 1

Different Biomarkers of Acute kidney Injury in Cancer Patients

2021 ◽  
Author(s):  
Reza Kazemi ◽  
Shirin Saberianpour ◽  
Hanieh Salehi ◽  
Mohammad Hatampour ◽  
Elnaz Sheikhpour
Keyword(s):  
Acute Kidney Injury ◽  
Cancer Patients ◽  
Early Stage ◽  
Kidney Injury ◽  
The Body ◽  
Main Task ◽  
Waste Products ◽  
Fatty Acid Binding ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Kidney Injury Molecule 1

Acute Kidney Injury (AKI) occurs if the kidneys suddenly lose their ability to remove waste products. When the kidneys lose their ability to filter, dangerous levels of waste products can accumulate, which can upset the chemical composition of the blood and urine. Chemotherapy is one of the methods used to treat or temporarily reduce cancer by using certain medications. The main task of this treatment is to kill cancer cells without seriously damaging the surrounding tissues. However, this type of treatment also has destructive effects on healthy cells and tissues in the body. Researchers studying cancer patients undergoing chemotherapy found that people undergoing this type of treatment may develop serious kidney problems and be forced to use treatments such as dialysis and kidney transplants. Research showed that people with more severe cancers and advanced tumors are more likely to have acute kidney injury than those with early-stage cancer. AKI biomarkers can be selected from the patient's serum, urine, or body imaging components. Various studies showed that urine is a source of the best markers in AKI. Biomarkers in plasma and urine, such as N-acetyl-β-glucosaminidase, Cystatin-C, β2-microglobulin , Cysteine-Rich Protein, Osteopontin, Fetuin-A, Kidney Injury Molecule-1, Liver-type fatty acid-binding protein, Netrin-1, Neutrophil gelatinase-associated lipocalin, and interleukin-18 are effective tools for early detection of AKI. In this review study, an attempt was made to collect biomarkers related to AKI disease.

Circulating myeloid-derived suppressor cells in pediatric solid tumor patients.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 9565-9565
Author(s):  
John M. Goldberg ◽  
Abdel-Aziz Zidan ◽  
Rabia Siddiqi ◽  
Myriam Zayas ◽  
Camille D. Brown ◽  
...  
Keyword(s):  
Cancer Patients ◽  
Solid Tumors ◽  
Pediatric Cancer ◽  
Suppressor Cells ◽  
Prognostic Indicators ◽  
Healthy Children ◽  
Myeloid Derived Suppressor Cells ◽  
Children With Cancer ◽  
Pediatric Cancer Patients ◽  
The Mean

9565 Background: Cure rates have reached a plateau for many pediatric solid tumors. Identifying new therapeutic targets, biomarkers of response and prognostic indicators should improve clinical outcomes. Accumulation of myeloid derived suppressor cells (MDSCs) is an important mechanism of tumor mediated immune evasion. Increased levels of MDSCs in adult cancer patients correlate with a worse prognosis, and decrease in levels with treatment is associated with benefit. Little is known about MDSCs in childhood, or in children with cancer. This pilot measured levels of MDSCs in pediatric patients with cancer and healthy children. Methods: We enrolled subjects using an Institutional Review Board approved protocol after obtaining informed consent. Blood was obtained from 14 children with newly diagnosed or recurrent solid tumors at start of therapy. In 10 of these patients, levels were also drawn after therapy. Blood was obtained once from 6 healthy children in a primary care office. Samples were obtained concurrently with complete blood counts. MDSCs were measured on fresh whole blood and were defined as Lin-1+/HLADR-/CD 33+/CD11b+/ by flow. Total MDSC numbers were then calculated. Results: The mean total number of MDSCs was 596 cells/ul at diagnosis for the 14 children with cancer and 170 cells/ul for the 6 healthy children (t(18) = 3.02, p = .0073). For the 10 children with cancer who had repeat values measured after treatment, MDSCs decreased in 4 and increased in 6. The mean initial MDSC count for these children was 494 cells/ul, and the mean post treatment count was 1716 cells/ul (t(9) = 1.81, p = .1036). Larger change scores tended to be associated with children treated with alkylator therapy followed by G-CSF. The results for percent MDSC in white cells mirrored those of total number. Conclusions: Circulating MDSCs were higher in pediatric cancer patients than healthy controls. Cancer treatment did not reliably reduce MDSC levels. After some treatments, the levels increased, potentially increasing immune tolerance. Further research is needed to determine if circulating MDSCs are a reliable predictive or prognostic marker in pediatric cancer, and whether they represent a potential target for therapeutic intervention.

scholarly journals Catalytic activity tunable ceria nanoparticles prevent chemotherapy-induced acute kidney injury without interference with chemotherapeutics

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Qinjie Weng ◽  
Heng Sun ◽  
Chunyan Fang ◽  
Fan Xia ◽  
Hongwei Liao ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Catalytic Activity ◽  
Cancer Patients ◽  
Redox Homeostasis ◽  
Kidney Injury ◽  
Chemotherapeutic Agents ◽  
Ros Generation ◽  
Ceria Nanoparticles ◽  
Clinical Prevention ◽  
The Cost

AbstractAcute kidney injury (AKI) is a prevalent and lethal adverse event that severely affects cancer patients receiving chemotherapy. It is correlated with the collateral damage to renal cells caused by reactive oxygen species (ROS). Currently, ROS management is a practical strategy that can reduce the risk of chemotherapy-related AKI, but at the cost of chemotherapeutic efficacy. Herein, we report catalytic activity tunable ceria nanoparticles (CNPs) that can prevent chemotherapy-induced AKI without interference with chemotherapeutic agents. Specifically, in the renal cortex, CNPs exhibit catalytic activity that decomposes hydrogen peroxide, and subsequently regulate the ROS-involved genes by activating the Nrf2/Keap1 signaling pathway. These restore the redox homeostasis for the protection of kidney tubules. Under an acidic tumor microenvironment, CNPs become inert due to the excessive H+ that disrupts the re-exposure of active catalytic sites, allowing a buildup of chemotherapy-mediated ROS generation to kill cancer cells. As ROS-modulating agents, CNPs incorporated with context-dependent catalytic activity, hold a great potential for clinical prevention and treatment of AKI in cancer patients.

scholarly journals Assessing Incidence of and Risk Predictors Ascertained at Diagnosis for Symptomatic Venous Thrombotic Events in Pediatric Cancer Patients: A 20-Year Population Based Study from the Maritimes, Canada

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 1117-1117
Author(s):  
Zeina Asyyed ◽  
Tamara MacDonald ◽  
Victoria E. Price ◽  
Conrad Fernandez ◽  
Mark Bernstein ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cancer Patients ◽  
Blood Group ◽  
Pediatric Cancer ◽  
Population Based ◽  
Age At Diagnosis ◽  
Axillary Vein ◽  
Large Variability ◽  
Pediatric Cancer Patients ◽  
The Mean

Abstract Background: Symptomatic venous thrombotic events (sVTE) are a well-recognized complication in pediatric cancer patients. Accurate data on true incidence of sVTE is limited due to large variability in design and methodology of previously published reports. As well, risk factors are unclear. Moreover, the limitations of several of the previously described risk factors for sVTE include (i) limited generalizability to all pediatric cancers, (ii) hemostatic protein lab values are altered by cancer itself, (iii) long turn-around times from laboratories and (iv) testing restricted to specialized labs. There is a need to identify risk factors for sVTE in pediatric cancer patients that are easily evaluated at the time of cancer diagnosis. Aims: Establish incidence of sVTE and identify risk factors associated with sVTE in pediatric cancer patients. Methods: All pediatric cancer patients in the 3 Maritime Provinces of Nova Scotia, New Brunswick and Prince Edward Island are treated at IWK Health Center (IWK) in a shared care model. This provides a population-based cohort of pediatric cancer patients from the Maritimes. After ethics approval, all pediatric cancer patients treated at the IWK from 1995 to 2014 with sVTE were identified through a conceptual framework as follows. Clinical (including sVTE) and laboratory data was extracted from the: (i) Pediatric oncology hospital database (ii) Provincial Cancer in Young People registry (iii) Electronic medical records (iv) Pharmacy database (v) IWK Central Venous Access Database and (vi) Hospital health records. After extraction, data from all sources was amalgamated and cross-verified. SPSS version 21 was used for statistical analysis. Central veins were defined as veins including and proximal to the axillary vein in the upper extremity and femoral vein in the lower extremity. sVTE was defined as radiologically documented VTE with at least one sign/symptom directly associated with VTE. Patients with VTE during relapsed disease and those with asymptomatic/incidentally diagnosed VTE were excluded from analysis. Results: Forty-seven (4.356±0.01%) of the 1079 patients had sVTE. The mean age at diagnosis for sVTE patients was 10.142 years. The mean age at diagnosis of the remaining patients (n=1032) was 7.451 years. The difference in the mean ages in the 2 categories was statistically significant (p=0.001). The gender ratio was M:F: 1.765:1 in patients with sVTE as compared to M:F: 1.123:1 in the remainder of the patients (p=0.336). Central veins were the most common location for sVTE (72.3%, n=34). Other less common locations included 1 each of sinovenous, mesenteric, cardiac, renal vein thrombosis and pulmonary embolism. On univariate analysis for risk factors, age > 10 years at diagnosis (P = 0.021), type of cancer (P = 0.028) and non-O blood group (P = 0.043) were associated with sVTE, while gender (p=0.336) and use of asparaginase (p=0.663) were not. On multivariate analysis, age > 10 years at diagnosis (odds ratio [OR]: 1.737 [1.066-2.831], p=0.027), and type of cancer (non-brain tumor; OR: 11.154 [1.527-81.451], P=0.017) were associated with sVTE. The association of non-O blood group with sVTE trended towards significance (OR: 1.886 [0.962-3.695], p=0.065) likely due to small numbers and difficulty identifying sVTE retrospectively. Conclusion: In a large population-based cohort of patients, we established incidence of sVTE in pediatric cancer patients. The study identified that sVTE occur in central veins in almost 3/4th of the patients. As well, we evaluated easily available and independent risk factors for sVTE in pediatric cancer patients. Further larger prospective and multicenter studies are needed to validate these observations and develop a risk prediction model for sVTE in pediatric cancer patients. Disclosures No relevant conflicts of interest to declare.

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