Does the kidney injury molecule-1 predict cisplatin-induced kidney injury in early stage?

2015 ◽  
Vol 52 (1) ◽  
pp. 88-94 ◽  
Author(s):  
Buket Kin Tekce ◽  
Ummugul Uyeturk ◽  
Hikmet Tekce ◽  
Ugur Uyeturk ◽  
Gulali Aktas ◽  
...  
Keyword(s):  
Early Stage ◽  
Kidney Injury ◽  
Kidney Injury Molecule 1

scholarly journals Identification of Novel Biomarker for Early Detection of Diabetic Nephropathy

Biomedicines ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 457
Author(s):  
Kyeong-Seok Kim ◽  
Jin-Sol Lee ◽  
Jae-Hyeon Park ◽  
Eun-Young Lee ◽  
Jong-Seok Moon ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Early Stage ◽  
Kidney Injury ◽  
Diabetic Patients ◽  
High Morbidity ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Zucker Diabetic Fatty Rats ◽  
Kidney Injury Molecule 1 ◽  
Stage Renal Disease ◽  
End Stage

Diabetic nephropathy (DN) is one of the most common complications of diabetes mellitus. After development of DN, patients will progress to end-stage renal disease, which is associated with high morbidity and mortality. Here, we developed early-stage diagnostic biomarkers to detect DN as a strategy for DN intervention. For the DN model, Zucker diabetic fatty rats were used for DN phenotyping. The results revealed that DN rats showed significantly increased blood glucose, blood urea nitrogen (BUN), and serum creatinine levels, accompanied by severe kidney injury, fibrosis and microstructural changes. In addition, DN rats showed significantly increased urinary excretion of kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL). Transcriptome analysis revealed that new DN biomarkers, such as complementary component 4b (C4b), complementary factor D (CFD), C-X-C motif chemokine receptor 6 (CXCR6), and leukemia inhibitory factor (LIF) were identified. Furthermore, they were found in the urine of patients with DN. Since these biomarkers were detected in the urine and kidney of DN rats and urine of diabetic patients, the selected markers could be used as early diagnosis biomarkers for chronic diabetic nephropathy.

scholarly journals Importance of KIM-1 and MCP-1 in Determining the Leptospirosis-Associated AKI: A Sri Lankan Study

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Thilini Nisansala ◽  
Manjula Weerasekera ◽  
Nilantha Ranasinghe ◽  
Chamil Marasinghe ◽  
Chandika Gamage ◽  
...  
Keyword(s):  
Early Stage ◽  
Kidney Injury ◽  
Diagnostic Tools ◽  
Sri Lankan ◽  
Monocyte Chemoattractant Protein 1 ◽  
Median Serum ◽  
The Status ◽  
Medical Wards ◽  
Kidney Injury Molecule 1 ◽  
Prompt Diagnosis

Background. Acute kidney injury (AKI) is one of most prevalent and serious complications of leptospirosis, a prevalent zoonotic disease in tropical countries. Prompt diagnosis of the leptospirosis-associated AKI is a challenge as there are no proper diagnostic tools that can identify patients in the early stage. Kidney injury molecule-1 (KIM-1) and monocyte chemoattractant protein-1 (MCP-1) are widely used novel AKI biomarkers that are studied in various disease conditions with AKI, but not in leptospirosis. Thus, this study is aimed at seeking the importance of KIM-1 and MCP-1 in determining the leptospirosis-associated AKI. Methods. Leptospirosis-suspected patients who were admitted to medical wards of two selected hospitals in the Western province of Sri Lanka were recruited. Leptospirosis was confirmed by three diagnostic tests: PCR, MAT, and culture, and the status of AKI was determined by Kidney Disease Improving Global Outcomes (KDIGO) criteria. Results. Of 170 leptospirosis-suspected patients, 79 were leptospirosis confirmed, and among them, 24.05% of patients were diagnosed to have AKI according to KDIGO criteria. Median serum KIM-1 ( p < 0.0001 ), urine KIM-1 (0.0053), serum MCP-1 (0.0080), and urine MCP-1 (0.0019) levels in those developing AKI were significantly higher than in patients not developing AKI. The biomarker levels associated with leptospirosis AKI had AUC-ROC of 0.8565, 0.7292, 0.7024, and 0.7282 for serum KIM-1, urine KIM-1, serum MCP-1, and urine MCP-1, respectively. Conclusion. This study revealed serum KIM-1 as a promising marker for leptospirosis-associated AKI among the tested biomarkers. Thus, further validation is recommended with a larger study group.

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.

scholarly journals Kidney Injury Molecule-1 is Elevated in Nephropathy and Mediates Macrophage Activation via the Mapk Signalling Pathway

2017 ◽  
Vol 41 (2) ◽  
pp. 769-783 ◽  
Author(s):  
Lei Tian ◽  
Xinghua Shao ◽  
Yuanyuan Xie ◽  
Qin Wang ◽  
Xiajing Che ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Macrophage Activation ◽  
Mapk Pathway ◽  
Early Stage ◽  
Kidney Injury ◽  
Mitogen Activated Protein Kinase ◽  
Clinical Samples ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Kidney Injury Molecule 1

Background/Aims: Kidney injury molecule-1 (KIM-1) is highly expressed in renal tubular cells after injury and is usually regarded as an early biomarker of acute kidney injury(AKI). The aim of this study was to determine the role of KIM-1 in the development of renal tubular injury Methods: Clinical samples, three different animal models and in vitro experiments were utilized to determine the possible mechanism underlying the involvement of KIM-1 in kidney injury. Results: Both plasma and urinary KIM-1 expression levels were significantly higher in AKI and chronic kidney disease (CKD) patients than in healthy volunteers, and urinary KIM-1 expression was significantly higher in CKD patients than in AKI patients. According to the results of our research involving three different mouse models, KIM-1 expression was significantly increased during the early stage of kidney injury and was persistently elevated in renal fibrosis. Our immunofluorescence staining results indicated that KIM-1-positive tubules were surrounded by macrophage infiltrates in regions of kidney injury. Moreover, our transwell, western blotting and real-time PCR data showed that macrophage migration and phenotype transitions were mediated by KIM-1 through the mitogen-activated protein kinase (MAPK) pathway. MAPK pathway inhibition could significantly reverse the effects of KIM-1 with respect to these macrophage phenotype changes and migration. Conclusions: KIM-1 expression was markedly elevated in both acute and chronic kidney injury and may play a pivotal role in macrophage activation via the MAPK pathway in kidney disease.

Transcriptional analysis of kidneys during repair from AKI reveals possible roles for NGAL and KIM-1 as biomarkers of AKI-to-CKD transition

2010 ◽  
Vol 298 (6) ◽  
pp. F1472-F1483 ◽  
Author(s):  
Gang Jee Ko ◽  
Dmitry N. Grigoryev ◽  
Douglas Linfert ◽  
Hye Ryoun Jang ◽  
Tonya Watkins ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepatitis A Virus ◽  
Ischemia Reperfusion Injury ◽  
Early Stage ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Transcriptional Analysis ◽  
Lipocalin 2 ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Kidney Injury Molecule 1

Acute kidney injury (AKI) is being increasingly shown to be a risk factor for chronic kidney disease (CKD), but little is known about the possible mechanistic links. We hypothesized that analysis of the genomic signature in the repair stage after AKI would reveal pathways that could link AKI and CKD. Unilateral renal pedicle clamping for 45 min was performed in male C57BL/6J mice. Mice were euthanized at 3, 10, and 28 days after ischemia-reperfusion injury (IRI). Total RNA was isolated from kidney and analyzed using an Illumina mouse array. Among 24,600 tested genes, 242, 146, and 46 genes were upregulated at days 3, 10, and 28 after IRI, and 85, 35, and 0 genes were downregulated, respectively. Gene ontology analysis showed that gene expression changes were primarily related to immune and inflammatory pathways both early and late after AKI. The most highly upregulated genes late after AKI were hepatitis A virus cellular receptor 1 ( Havcr1) and lipocalin 2 ( Lcn2), which code for kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL), respectively. This was unexpected since they are both primarily potential biomarkers of the early stage of AKI. Furthermore, increases observed in gene expression in amiloride binding protein 1, vascular cell adhesion molecule-1, and endothelin 1 could explain the salt-sensitive hypertension that can follow AKI. These data suggested that 1) persistent inflammation and immune responses late after AKI could contribute to the pathogenesis of CKD, 2) late upregulation of KIM-1 and NGAL could be a useful marker for sustained renal injury after AKI, and 3) hypertension-related gene changes could underlie mechanisms for persistent renal and vascular injury after AKI.

Abstract 13920: Impact of Diabetes on Acute Kidney Injury After Myocardial Infarction: Possible Involvement of Toll-like Receptor in the Kidney

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Kohei Ohno ◽  
Atsushi Kuno ◽  
Shingo Muratsubaki ◽  
Hiromichi Murase ◽  
Hidemichi Kouzu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Early Stage ◽  
Mrna Level ◽  
Kidney Injury ◽  
Mrna Levels ◽  
Toll Like Receptor ◽  
Increased Risk ◽  
Kidney Injury Molecule 1

Background: Comorbid acute kidney injury (AKI) predicts poor prognosis in patients with acute myocardial infarction (MI). Although type 2 diabetes (T2D) is a well-known risk factor of AKI after MI, the mechanism of the increased risk remains unclear. Here we hypothesized that T2D increases AKI after MI via toll-like receptor (TLR)-mediated inflammation. Methods and Results: OLETF, a rat model of obese T2D, and LETO, non-diabetic controls, at 25-30 weeks of age were randomized into sham and permanent coronary ligation (MI) groups. At baseline, body weight (617±23 vs. 537±13 g), fasting plasma glucose (267±32 vs. 153±15 mg/dl) and urinary protein level (6.4 vs. 0.6 g/gCr), but not serum creatinine, were significantly higher in OLETF than in LETO. Histologically, glomerular size was increased by 17% without mesangial proliferation in OLETF compared to that in LETO, indicating that OLETF developed early-stage nephropathy by this age. At 12 h after MI, mRNA levels of TLR2, TLR4, IL-6 and TNF-α in the kidney were increased by 1.6-, 1.2-, 2.6-, 1.5-fold, respectively, in OLETF but not in LETO. Furthermore, immunoblot analyses showed that phosphorylation levels of p38 MAPK and JNK, downstream mediators of the TLR signal, were significantly elevated by MI in OLETF. Histological abnormalities in the kidney or increase in serum creatinine were not detected in either LETO or OLETF 12 h after MI. However, in immunohistochemical analyses, areas positive for neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) were significantly increased by 4.0- and 5.3-fold, respectively, and NGAL mRNA level was increased by 1.8-fold after MI in OLETF but not in LETO. In sham-operated LETO and OLETF, areas positive for NGAL and KIM-1 were barely detected. Infarct sizes were similar and cardiac BNP mRNA levels in the non-infarcted left ventricle were equally elevated at 12 h after MI in LETO and OLETF, suggesting that MI-induced cardiac loads were comparable in the two groups. However, mortality at 48 h after MI was significantly higher in OLETF than in LETO (68% vs. 18%, P<0.05). Conclusion: The results suggest that AKI after MI is enhanced in T2D via TLR-mediated inflammation. The cardio-renal interaction may underlie increased post-MI mortality in T2D.

scholarly journals Evaluation of Kidney Injury Molecule-1 (KIM-1) and Neutrophil Gelatinase-Associated Lipocalin (NGAL) Urinary Levels for Detecting Kidney Dysfunction in Patients With Nasopharyngeal Cancer Treated With Cisplatin-Based Treatment

2018 ◽  
Vol 12 (2) ◽  
pp. 60
Author(s):  
Marliana Sri Rejeki ◽  
Wawaimuli Arozal ◽  
Rianto Setiabudy ◽  
Djumhana Atmakusuma
Keyword(s):  
Early Stage ◽  
Nasopharyngeal Cancer ◽  
Kidney Injury ◽  
Urinary Ngal ◽  
Ngal Level ◽  
Kidney Dysfunction ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Significant Difference ◽  
Before And After ◽  
Kidney Injury Molecule 1

Background: Cisplatin has a potency of causing nephrotoxicity. Serum BUN and creatinine levels have been well-known for detecting kidney dysfunction; while KIM-1 and NGAL urine levels are relatively new measurements. The study was aimed to evaluate urinary KIM-1 and NGAL level to detect kidney dysfunction in patients with advanced stage NPC who received cisplatin-based chemotherapy.Methods: The study was a cohort-prospective study with 3 subject groups, i.e. patients who had never received and who had received 75-100 mg/m2 cisplatin-based chemotherapy as well as those who had never received 40 mg/m2 cisplatin-based chemotherapy. The levels of urinary KIM-1, NGAL and serum level of BUN and creatinine were measured before and after receiving cisplatin. Statistical analyses were ANOVA, Pearson, Spearman, Kolmogorov-Smirnov test and SPSS version 22.0.Result: There was a significant difference of delta BUN level (p=0.0001) and delta urinary NGAL level (p = 0.025) before and after treatment in all three groups; while delta KIM-1 level showed no significant difference in all three groups (p=0.275). Cisplatin may cause accumulated nephrotoxicity, which has dose-dependent manner.Conclusion: Measuring urinary NGAL level can detect an early stage of kidney dysfunction; however, it still cannot replace the role of BUN. Measurement of urinary KIM-1 level cannot detect kidney dysfunction.

scholarly journals Kidney injury molecule-1: potential biomarker of acute kidney injury and disease severity in patients with COVID-19

2021 ◽  
Author(s):  
Manuel J. Vogel ◽  
Julian Mustroph ◽  
Stephan T. Staudner ◽  
Simon B. Leininger ◽  
Ute Hubauer ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Respiratory Infections ◽  
Early Stage ◽  
Severe Disease ◽  
Kidney Injury ◽  
Clinical Endpoints ◽  
Potential Biomarker ◽  
Tubular Markers ◽  
Kidney Injury Molecule 1 ◽  
Additional Value

Abstract Aims The aim of the current study was to evaluate whether tubular markers kidney injury molecule-1 (KIM-1) and N-acetyl-ß-glucosaminidase (NAG) are related to acute kidney injury (AKI) and severe disease in patients with COVID-19. Methods and results In this prospective observational clinical trial we examined a cohort of 80 patients with proof of acute respiratory infection and divided them into a COVID-19 cohort (n = 54) and a control cohort (n = 26). KIM-1 and NAG were measured from urine samples collected in the emergency department. We assessed the development of AKI, admission to the intensive care unit (ICU) and intrahospital death as clinical endpoints. Urinary KIM-1 and NAG were not significantly different between patients with SARS-CoV-2 and those with other respiratory infections (each p = n.s.). Eight patients from the COVID-19 cohort and five of the non-COVID-19-patients suffered from acute kidney injury during their stay. Nine COVID-19 patients and two non-COVID-19 patients were admitted to the ICU. KIM-1 was significantly elevated in COVID-19 patients with, compared to those without AKI (p = 0.005), as opposed to NAG and creatinine (each p = n.s.). Furthermore, KIM-1 was significantly elevated in the patients with COVID-19 that had to be transferred to the ICU (p = 0.015), in contrast to NAG and creatinine (each p = n.s.). Conclusion Assessing KIM-1 in patients with COVID-19 might provide additional value in recognizing AKI at an early stage of disease. Further, KIM-1 might indicate higher risk for clinical deterioration as displayed by admission to the ICU. Graphical abstract

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