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[PMID]:29261470
[Au] Autor:Pursnani A; Prasad PV
[Ad] Endereço:Division of Cardiology, Department of Medicine NorthShore University HealthSystem Evanston, Ill.
[Ti] Título:Science to Practice: Can Functional MR Imaging Be Useful in the Evaluation of Cardiorenal Syndrome?
[So] Source:Radiology;286(1):1-3, 2018 Jan.
[Is] ISSN:1527-1315
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Functional magnetic resonance (MR) imaging of the kidneys has gained interest recently, especially in the detection of early changes in acute kidney injury or to predict progression of chronic kidney disease (CKD). The application of these methods to cardiorenal syndrome (CRS) is novel. CRS is widely accepted as a complex clinical problem routinely faced by clinicians. In this issue, Chang et al ( 1 ) present their preliminary experience applying blood oxygen level-dependent (BOLD) MR imaging to the kidneys in mice with experimental myocardial infarction. They showed that R2* in the kidney increases after induced myocardial infarction and that the response was higher in animals with larger infarcts and over time. The authors also for the first time correlated the BOLD MR imaging findings against hypoxia-inducible factor-1α (HIF-1α) expression, an independent marker of renal hypoxia. In addition, they showed evidence for renal injury by using a kidney injury marker, kidney injury molecule-1 (KIM-1). The results of their study support the use of renal BOLD MR imaging in subjects with heart failure, in whom the risk of subsequent renal ischemia and/or hypoxia is known to exist. These results, along with those of other recent reports ( 2 ), suggest that functional imaging methods could play a key role in evaluating changes in both the primary and secondary organs involved in complex disease processes such as CRS. Availability of such methods could facilitate translation to the clinic and improve the mechanistic understanding of the complicated and interrelated pathophysiology.
[Mh] Termos MeSH primário: Síndrome Cardiorrenal/diagnóstico por imagem
Imagem por Ressonância Magnética/métodos
[Mh] Termos MeSH secundário: Animais
Biomarcadores/análise
Insuficiência Cardíaca/diagnóstico por imagem
Receptor Celular 1 do Vírus da Hepatite A/metabolismo
Seres Humanos
Camundongos
Oxigênio/sangue
Oxigênio/metabolismo
Insuficiência Renal Crônica/diagnóstico por imagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (HAVCR1 protein, human); 0 (Hepatitis A Virus Cellular Receptor 1); S88TT14065 (Oxygen)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1148/radiol.2017171957


  2 / 605 MEDLINE  
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[PMID]:29258482
[Au] Autor:Oh SM; Park G; Lee SH; Seo CS; Shin HK; Oh DS
[Ad] Endereço:The K-herb Research Center, Korea Institute of Oriental Medicine, 1672 Yuseong-daero, Yuseong-gu, Daejeon, 34054, Republic of Korea.
[Ti] Título:Assessing the recovery from prerenal and renal acute kidney injury after treatment with single herbal medicine via activity of the biomarkers HMGB1, NGAL and KIM-1 in kidney proximal tubular cells treated by cisplatin with different doses and exposure times.
[So] Source:BMC Complement Altern Med;17(1):544, 2017 Dec 19.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Acute kidney injury (AKI) is an initial factor in many kidney disorders. Pre- and intra-renal AKI biomarkers have recently been reported. Recovery from AKI by herbal medicine has rarely been reported. Thus, this study aimed to investigate the dose- and time-dependent effects of herbal medicines to protect against AKI in cisplatin-induced human kidney 2 (HK-2) cells by assessing the activities of high-mobility group box protein 1 (HMGB1), neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1). METHODS: Proximal tubular HK-2 cell lines were treated with either 400 µM of cisplatin for 6 h or 10 µM of cisplatin for 24 h and then exposed to ten types of single herbal medicines, including Nelumbo nymphaea (NY) at a dose of 100 µg/mL. The AKI biomarkers HMGB1, NGAL and KIM-1 were repeatedly measured by an ELISA assay at 2, 4, and 6 h in the group treated with 400 µM of cisplatin to confirm necrotic cell death and at 6, 24, and 48 h in the group treated with 10 µM of cisplatin to examine apoptotic cell death. Recovery confirm was conducted through in vivo study using ICR mice for 3 day NY or Paeonia suffruticosa intake. RESULTS: Cisplatin treatment at a concentration of 10 µM decreased cell viability. Treatment with 400 µM of cisplatin reduced HMBG1 activity and resulted in lactate dehydrogenase release. In longer exposure durations (up to 48 h), NGAL and KIM-1 exhibited activity from 24 h onward. Additionally, NY treatment resulted in an approximately 50% change in all three biomarkers. The time-dependent profiles of HMGB1, NGAL and KIM-1 activities up to 48 h were notably different; HMGB1 exhibited a 7-fold change at 6 h, and NGAL and KIM-1 exhibited 1.7-fold changes at 24 h, respectively. Consistently, serum and urine NGAL and KIM-1 activities were all reduced in ICR mice. CONCLUSIONS: Several single herbal medicines, including NY, have a potential as effectors of AKI due to their ability to inhibit the activation of HMGB1, NGAL and KIM-1 in an in vitro AKI-mimicked condition and simple in vivo confirm. Furthermore, an in vivo proof-of-concept study is needed.
[Mh] Termos MeSH primário: Lesão Renal Aguda/tratamento farmacológico
Preparações de Plantas/farmacologia
Preparações de Plantas/uso terapêutico
Substâncias Protetoras/farmacologia
Substâncias Protetoras/uso terapêutico
[Mh] Termos MeSH secundário: Lesão Renal Aguda/induzido quimicamente
Lesão Renal Aguda/fisiopatologia
Animais
Morte Celular/efeitos dos fármacos
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Cisplatino/efeitos adversos
Proteína HMGB1/metabolismo
Receptor Celular 1 do Vírus da Hepatite A/metabolismo
Seres Humanos
Lipocalina-2/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos ICR
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HAVCR1 protein, human); 0 (HMGB1 Protein); 0 (Hepatitis A Virus Cellular Receptor 1); 0 (Lipocalin-2); 0 (Plant Preparations); 0 (Protective Agents); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-2055-y


  3 / 605 MEDLINE  
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[PMID]:28745689
[Au] Autor:Bulanov NM; Serova AG; Kuznetsova EI; Bulanova ML; Novikov PI; Kozlovskaya LV; Moiseev SV
[Ad] Endereço:I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia.
[Ti] Título:[Kidney injury molecules (KIM-1, MCP-1) and type IV collagen in the assessment of activity of antineutrophil cytoplasmic antibody-associated glomerulonephritis].
[Ti] Título:Molekuly povrezhdeniia pochechnoi tkani (KIM-1, MCP-1) i kollagen IV tipa v otsenke aktivnosti assotsiirovannogo s antineitrofil'nymi tsitoplazmaticheskimi antitelami glomerulonefrita..
[So] Source:Ter Arkh;89(6):48-55, 2017.
[Is] ISSN:0040-3660
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:AIM: To assess the significance of determining the serum and urinary concentrations of monocyte chemotactic protein-1 (MCP-1), kidney injury molecule-1 (KIM-1), and type IV collagen in patients with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) to estimate the activity of renal involvement in AAV. SUBJECTS AND METHODS: 78 patients (32 men and 46 women) (median age 55 (45; 61) years) with AAV were examined. The patients were divided into 3 groups according to the AAV activity estimated using the Birmingham vasculitis activity Score (BVAS): 1) 25 patients with active ANCA-associated glomerulonephritis (GN); 2) 26 patients with active AAV without renal involvement; 3) 27 patients in sustained AAV remission. The serum and urinary concentrations of the markers were measured by enzyme immunoassay. RESULTS: The urinary concentration of all 3 biomarkers was higher in patients with renal involvement (Group 1); the differences in the levels of MCP-1 and type IV collagen were statistically significant as compared to Groups 2 and 3 (p<0.01), while that in KIM-1 level was only in Group 2. There were statistically significant correlations between the urinary concentration of these biomarkers and the traditional GN activity indices (erythrocyturia, daily proteinuria (DPU), total BVAS scores that reflect renal involvement, as well as serum creatinine levels and estimated glomerular filtration rate (p<0.05). ROC curve analysis showed that the urinary MCP-1 excretion of ≥159 pg/ml had the highest (92%) sensitivity and urinary type IV collagen excretion of ≥3.09 µg/l had the highest (86%) specificity in assessing the activity of ANCA-associated GN. At the same time, their diagnostic value increased in terms of a combination of DPU and ESR (96% sensitivity, 84.9% specificity). CONCLUSION: The urinary excretion of MCP-1, KIM-1, and type IV collagen reflects the severity of local renal inflammation in AAV patients and a study of these indicators is a promising diagnostic tool for assessing the activity of ANCA-associated GN.
[Mh] Termos MeSH primário: Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos
Anticorpos Anticitoplasma de Neutrófilos/imunologia
Quimiocina CCL2
Colágeno Tipo IV
Glomerulonefrite
Receptor Celular 1 do Vírus da Hepatite A
[Mh] Termos MeSH secundário: Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/sangue
Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/imunologia
Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/urina
Biomarcadores/sangue
Biomarcadores/urina
Quimiocina CCL2/sangue
Quimiocina CCL2/imunologia
Quimiocina CCL2/urina
Colágeno Tipo IV/sangue
Colágeno Tipo IV/imunologia
Colágeno Tipo IV/urina
Feminino
Glomerulonefrite/sangue
Glomerulonefrite/imunologia
Glomerulonefrite/urina
Receptor Celular 1 do Vírus da Hepatite A/sangue
Receptor Celular 1 do Vírus da Hepatite A/imunologia
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Antineutrophil Cytoplasmic); 0 (Biomarkers); 0 (CCL2 protein, human); 0 (Chemokine CCL2); 0 (Collagen Type IV); 0 (HAVCR1 protein, human); 0 (Hepatitis A Virus Cellular Receptor 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.17116/terarkh201789648-55


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[PMID]:28792192
[Au] Autor:Benli E; Ayyildiz SN; Cirrik S; Noyan T; Ayyildiz A; Cirakoglu A
[Ad] Endereço:Department of Urology, Faculty of Medicine, Ordu University, Ordu, Turkey.
[Ti] Título:Early term effect of ureterorenoscopy (URS) on the Kidney: research measuring NGAL, KIM-1, FABP and CYS C levels in urine.
[So] Source:Int Braz J Urol;43(5):887-895, 2017 Sep-Oct.
[Is] ISSN:1677-6119
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:AIM: URS is a very commonly used procedure for treatment of ureter stones. Increased hydrostatic pressure in the collecting system linked to fluids used during the procedure may cause harmful effects on the kidney. The aim of this study is to determine whether the URS procedure has a negative effect on the kidney by investigating NGAL, KIM-1, FABP and Cys C levels in urine. MATERIAL AND METHODS: This study included 30 patients undergoing ureterorenoscopy (URS) for ureter stones. Urine samples were collected 5 times; before the URS procedure (control) and at 1, 3, 5 and 12 hours following the procedure. NGAL, KIM-1, FBAP and Cys C levels were measured in urine and compared with the control values. RESULTS: The NGAL levels in urine before the procedure and at 1, 3, 5 and 12 hours after the procedure were 34.59±35.34; 62.72±142.32; 47.15±104.48; 45.23±163.16 and 44.99±60.79ng/mL, respectively (p=0.001). Similarly, the urinary KIM-1, FABP and Cys C levels were found to increase compared to control values; however this increase did not reach statistical significance (p >0.05). CONCLUSIONS: After the URS procedure, there were important changes in NGAL, FABP, KIM-1 and Cys C levels. These changes reached statistical significance for NGAL, but did not reach significance for the other parameters. In conclusion, the URS procedure significantly affects the kidney; however, this effect disappears over time.
[Mh] Termos MeSH primário: Biomarcadores/urina
Cálculos Ureterais/cirurgia
Cálculos Ureterais/urina
Ureteroscopia/métodos
[Mh] Termos MeSH secundário: Adulto
Idoso
Cistatinas/urina
Proteínas de Ligação a Ácido Graxo/urina
Feminino
Receptor Celular 1 do Vírus da Hepatite A/análise
Seres Humanos
Lipocalina-2/urina
Masculino
Meia-Idade
Ureteroscopia/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cystatins); 0 (FABP1 protein, human); 0 (Fatty Acid-Binding Proteins); 0 (HAVCR1 protein, human); 0 (Hepatitis A Virus Cellular Receptor 1); 0 (Lipocalin-2)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171117
[Lr] Data última revisão:
171117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1590/S1677-5538.IBJU.2016.0638


  5 / 605 MEDLINE  
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[PMID]:28736945
[Au] Autor:Gu XL; He H; Lin L; Luo GX; Wen YF; Xiang DC; Qiu J
[Ad] Endereço:Department of Cardiology, Guangzhou Liuhuaqiao Hospital, Guangzhou, China.
[Ti] Título:Tim-1 B cells suppress T cell interferon-gamma production and promote Foxp3 expression, but have impaired regulatory function in coronary artery disease.
[So] Source:APMIS;125(10):872-879, 2017 Oct.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Atherosclerosis and its associated coronary artery disease (CAD) represent another chronic low-grade inflammatory disorder. Regulatory B cells (Bregs) possess essential functions in maintaining peripheral tolerance and inhibiting pathogenic inflammation through IL-10. Here, we investigated one subset of Bregs, Tim-1 B cell, and its role in atherosclerosis and CAD patients. In healthy individuals, IL-10-producing B cells were predominantly found in the Tim-1 B cells. Upon stimulation of the B cell receptor (BCR) and Toll-like receptor 9 (TLR-9) by anti-BCR antibodies and CpG, respectively, the Tim-1 B cells could further upregulate IL-10 expression. In contrast, the Tim-1 B cells were present at normal frequency in CAD patients, but showed impaired capacity to upregulate IL-10 with or without BCR + CpG stimulation. The stimulated Tim-1 B cells from healthy individuals also suppressed expression of interferon gamma (IFN-γ), an atherogenic cytokine in T cells, in an IL-10-dependent fashion, and strongly promoted the expression of Foxp3 in naive CD4 CD45RO T cells. In contrast, the Tim-1 B cells from CAD patients were unable to suppress IFN-γ secretion, and only minimally increased the expression of Foxp3 in naive CD4 CD45RO T cells. Despite this, the frequency of Tim-1 B cells in the atherosclerotic lesions from CAD patients was inversely correlated with the frequency of IFN-γ-expressing T cells. Together, these results demonstrated that CAD patients presented an inflammatory disorder in regulatory B cells, which could be used as a therapeutic target.
[Mh] Termos MeSH primário: Linfócitos B Reguladores/imunologia
Doença da Artéria Coronariana/patologia
Fatores de Transcrição Forkhead/análise
Receptor Celular 1 do Vírus da Hepatite A/análise
Interferon gama/secreção
Interleucina-10/secreção
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Idoso
Linfócitos B Reguladores/química
Feminino
Seres Humanos
Masculino
Meia-Idade
Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FOXP3 protein, human); 0 (Forkhead Transcription Factors); 0 (HAVCR1 protein, human); 0 (Hepatitis A Virus Cellular Receptor 1); 0 (IFNG protein, human); 130068-27-8 (Interleukin-10); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170725
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12729


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[PMID]:28679590
[Au] Autor:Boddu R; Fan C; Rangarajan S; Sunil B; Bolisetty S; Curtis LM
[Ad] Endereço:Division of Nephrology, Nephrology Research and Training Center, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama; and.
[Ti] Título:Unique sex- and age-dependent effects in protective pathways in acute kidney injury.
[So] Source:Am J Physiol Renal Physiol;313(3):F740-F755, 2017 Sep 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sex and age influence susceptibility to acute kidney injury (AKI), with young females exhibiting lowest incidence. In these studies, we investigated mechanisms which may underlie the sex/age-based dissimilarities. Cisplatin (Cp)-induced AKI resulted in morphological evidence of injury in all groups. A minimal rise in plasma creatinine (PCr) was seen in Young Females, whereas in Aged Females, PCr rose precipitously. Relative to Young Males, Aged Males showed significantly, but temporally, comparably elevated PCr. Notably, Aged Females showed significantly greater mortality, whereas Young Females exhibited none. Tissue KIM-1 and plasma NGAL were significantly lower in Young Females than all others. IGFBP7 levels were modestly increased in both Young groups. IGFBP7 levels in Aged Females were significantly elevated at baseline relative to Aged Males, and increased linearly through , when these levels were comparable in both Aged groups. Plasma cytokine levels similarly showed a pattern of protective effects preferentially in Young Females. Expression of the drug transporter MATE2 did not explain the sex/age distinctions. Heme oxygenase-1 (HO-1) levels (~28-kDa species) showed elevation at in all groups with highest levels seen in Young Males. Exclusively in Young Females, these levels returned to baseline on , suggestive of a more efficient recovery. In aggregate, we demonstrate, for the first time, a distinctive pattern of response to AKI in Young Females relative to males which appears to be significantly altered in aging. These distinctions may offer novel targets to exploit therapeutically in both females and males in the treatment of AKI.
[Mh] Termos MeSH primário: Lesão Renal Aguda/prevenção & controle
Envelhecimento/metabolismo
Rim/metabolismo
[Mh] Termos MeSH secundário: Lesão Renal Aguda/induzido quimicamente
Lesão Renal Aguda/metabolismo
Lesão Renal Aguda/patologia
Fatores Etários
Envelhecimento/patologia
Animais
Autofagia
Proliferação Celular
Cisplatino
Creatinina/sangue
Citocinas/sangue
Modelos Animais de Doenças
Feminino
Heme Oxigenase-1/metabolismo
Receptor Celular 1 do Vírus da Hepatite A/metabolismo
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/metabolismo
Rim/patologia
Lipocalina-2/sangue
Masculino
Proteínas de Membrana/metabolismo
Metionina Adenosiltransferase/metabolismo
Camundongos Endogâmicos C57BL
Fatores Sexuais
Transdução de Sinais
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Havcr1 protein, mouse); 0 (Hepatitis A Virus Cellular Receptor 1); 0 (Insulin-Like Growth Factor Binding Proteins); 0 (Lipocalin-2); 0 (Membrane Proteins); 0 (insulin-like growth factor binding protein-related protein 1); 126469-30-5 (Lcn2 protein, mouse); AYI8EX34EU (Creatinine); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.14.14.18 (Hmox1 protein, mouse); EC 2.5.1.6 (Methionine Adenosyltransferase); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00049.2017


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[PMID]:28614696
[Au] Autor:Miao J; Friedman E; Wu AHB; Todd JA; Estis J; Xu X; Nolan N; Bishop JJ; Lenihan DJ
[Ad] Endereço:Vanderbilt University School of Medicine, Nashville, TN, USA.
[Ti] Título:Clinical utility of single molecule counting technology for quantification of KIM-1 in patients with heart failure and chronic kidney disease.
[So] Source:Clin Biochem;50(16-17):889-895, 2017 Nov.
[Is] ISSN:1873-2933
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Acute kidney injury (AKI) is associated with high morbidity and mortality, and may lead to chronic kidney disease (CKD). Traditional serum biomarkers for acute and chronic renal dysfunction are insensitive and nonspecific. While urinary kidney injury molecule-1 (KIM-1) is a sensitive and specific measure of kidney tubular injury, it is difficult to obtain in acute settings. Thus, our objective was to develop a highly sensitive immunoassay for plasma KIM-1. METHODS: A novel plasma KIM-1 immunoassay was developed using Single Molecule Counting technology (SMC). It was clinically validated in: 120 healthy subjects to establish a preliminary reference range; 25 healthy subjects to assess biological variability; 200 patients with heart failure (CHF); and 60 patients from a CKD case control. RESULTS: SMC KIM-1 assay provided a limit of detection of 1.4pg/mL (reporting range from 2pg/mL to 1000pg/mL). Inter-assay precision was 9-15% CV. Median KIM-1 value in healthy subjects was 119pg/mL with a RR 95th percentile of 292pg/mL. KIM-1 demonstrated low weekly biological variability over 6weeks. KIM-1 was elevated in patients with CKD or CHF. Adjusted odds ratios for differentiating CHF or CKD from controls were 9.6 (95% CI 2.7-35.0) and 3.6 (95% CI 1.1-11.6), respectively. In CHF, KIM-1 values correlated inversely with eGFR (Spearman R=-0.32, p<0.0001). CONCLUSIONS: Plasma KIM-1 is quantifiable in healthy volunteers, elevated in CKD and CHF patients, and correlates with eGFR. Additional investigation is needed to determine if KIM-1 provides prognostic value for CKD and CHF patient outcomes.
[Mh] Termos MeSH primário: Insuficiência Cardíaca/sangue
Receptor Celular 1 do Vírus da Hepatite A/sangue
Imunoensaio/métodos
Insuficiência Renal Crônica/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores/sangue
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (HAVCR1 protein, human); 0 (Hepatitis A Virus Cellular Receptor 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170615
[St] Status:MEDLINE


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[PMID]:28583915
[Au] Autor:Chen H; Wang L; Wang W; Cheng C; Zhang Y; Zhou Y; Wang C; Miao X; Wang J; Wang C; Li J; Zheng L; Huang K
[Ad] Endereço:Tongji School of Pharmacy.
[Ti] Título:ELABELA and an ELABELA Fragment Protect against AKI.
[So] Source:J Am Soc Nephrol;28(9):2694-2707, 2017 Sep.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Renal ischemia-reperfusion (I/R) injury is the most common cause of AKI, which associates with high mortality and has no effective therapy. ELABELA (ELA) is a newly identified 32-residue hormone peptide highly expressed in adult kidney. To investigate whether ELA has protective effects on renal I/R injury, we administered the mature peptide (ELA32) or the 11-residue furin-cleaved fragment (ELA11) to hypoxia-reperfusion (H/R)-injured or adriamycin-treated renal tubular cells ELA32 and ELA11 significantly inhibited the elevation of the DNA damage response, apoptosis, and inflammation in H/R-injured renal tubular cells and suppressed adriamycin-induced DNA damage response. Similarly, overexpression of ELA32 or ELA11 significantly inhibited H/R-induced cell death, DNA damage response, and inflammation. Notably, treatment of mice with ELA32 or ELA11 but not an ELA11 mutant with a cysteine to alanine substitution at the N terminus (AE11C) inhibited I/R injury-induced renal fibrosis, inflammation, apoptosis, and the DNA damage response and markedly reduced the renal tubular lesions and renal dysfunction. Together, our results suggest that ELA32 and ELA11 may be therapeutic candidates for treating AKI.
[Mh] Termos MeSH primário: Lesão Renal Aguda/metabolismo
Lesão Renal Aguda/prevenção & controle
Proteínas de Transporte/farmacologia
Fragmentos de Peptídeos/farmacologia
Hormônios Peptídicos/farmacologia
RNA Mensageiro/metabolismo
Traumatismo por Reperfusão/metabolismo
Traumatismo por Reperfusão/prevenção & controle
[Mh] Termos MeSH secundário: Lesão Renal Aguda/genética
Lesão Renal Aguda/fisiopatologia
Animais
Apoptose/efeitos dos fármacos
Proteínas Mutadas de Ataxia Telangiectasia/metabolismo
Autofagia/efeitos dos fármacos
Proteínas de Transporte/genética
Proteínas de Transporte/uso terapêutico
Moléculas de Adesão Celular/genética
Hipóxia Celular
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Quinase do Ponto de Checagem 1/metabolismo
Reparo do DNA/efeitos dos fármacos
Expressão Gênica/efeitos dos fármacos
Receptor Celular 1 do Vírus da Hepatite A/genética
Histonas/metabolismo
Seres Humanos
Inflamação/genética
Inflamação/prevenção & controle
Molécula 1 de Adesão Intercelular/genética
Interleucina-6/genética
Túbulos Renais/citologia
Camundongos
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/uso terapêutico
Hormônios Peptídicos/uso terapêutico
Fosfoproteínas/metabolismo
Fosforilação
Ratos
Traumatismo por Reperfusão/genética
Traumatismo por Reperfusão/fisiopatologia
Fator de Crescimento Transformador beta1/genética
Fator de Necrose Tumoral alfa/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apela protein (22-32), human); 0 (Apela protein, mouse); 0 (Carrier Proteins); 0 (Cell Adhesion Molecules); 0 (ELA peptide, human); 0 (Havcr1 protein, mouse); 0 (Havcr1protein, rat); 0 (Hepatitis A Virus Cellular Receptor 1); 0 (Histones); 0 (ICAM1 protein, rat); 0 (Interleukin-6); 0 (Peptide Fragments); 0 (Peptide Hormones); 0 (Phosphoproteins); 0 (RNA, Messenger); 0 (Transforming Growth Factor beta1); 0 (Tumor Necrosis Factor-alpha); 0 (gamma-H2AX protein, rat); 126547-89-5 (Intercellular Adhesion Molecule-1); EC 2.7.- (ataxia telangiectasia and Rad3-related kinase, rat); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins); EC 2.7.11.1 (Checkpoint Kinase 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170607
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2016111210


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[PMID]:28579560
[Au] Autor:Wei J; Song J; Jiang S; Zhang G; Wheeler D; Zhang J; Wang S; Lai EY; Wang L; Buggs J; Liu R
[Ad] Endereço:Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa, Florida.
[Ti] Título:Role of intratubular pressure during the ischemic phase in acute kidney injury.
[So] Source:Am J Physiol Renal Physiol;312(6):F1158-F1165, 2017 Jun 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acute kidney injury (AKI) induced by clamping of renal vein or pedicle is more severe than clamping of artery, but the mechanism has not been clarified. In the present study, we tested our hypothesis that increased proximal tubular pressure (P ) during the ischemic phase exacerbates kidney injury and promotes the development of AKI. We induced AKI by bilateral clamping of renal arteries, pedicles, or veins for 18 min at 37°C, respectively. P during the ischemic phase was measured with micropuncture. We found that higher P was associated with more severe AKI. To determine the role of P during the ischemic phase on the development of AKI, we adjusted the P by altering renal artery pressure. We induced AKI by bilateral clamping of renal veins, and the P was changed by adjusting the renal artery pressure during the ischemic phase by constriction of aorta and mesenteric artery. When we decreased renal artery pressure from 85 ± 5 to 65 ± 8 mmHg, P decreased from 53.3 ± 2.7 to 44.7 ± 2.0 mmHg. Plasma creatinine decreased from 2.48 ± 0.23 to 1.91 ± 0.21 mg/dl at 24 h after renal ischemia. When we raised renal artery pressure to 103 ± 7 mmHg, P increased to 67.2 ± 5.1 mmHg. Plasma creatinine elevated to 3.17 ± 0.14 mg·dl·24 h after renal ischemia. Changes in KIM-1, NGAL, and histology were in the similar pattern as plasma creatinine. In summary, we found that higher P during the ischemic phase promoted the development of AKI, while lower P protected from kidney injury. P may be a potential target for treatment of AKI.
[Mh] Termos MeSH primário: Lesão Renal Aguda/fisiopatologia
Pressão Arterial
Isquemia/fisiopatologia
Túbulos Renais/fisiopatologia
Artéria Renal/fisiopatologia
Circulação Renal
Veias Renais/fisiopatologia
[Mh] Termos MeSH secundário: Lesão Renal Aguda/metabolismo
Lesão Renal Aguda/patologia
Lesão Renal Aguda/prevenção & controle
Animais
Constrição
Creatinina/sangue
Modelos Animais de Doenças
Receptor Celular 1 do Vírus da Hepatite A/sangue
Isquemia/metabolismo
Isquemia/patologia
Isquemia/prevenção & controle
Túbulos Renais/metabolismo
Túbulos Renais/patologia
Lipocalina-2/sangue
Masculino
Camundongos Endogâmicos C57BL
Artéria Renal/cirurgia
Veias Renais/cirurgia
Índice de Gravidade de Doença
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Havcr1 protein, mouse); 0 (Hepatitis A Virus Cellular Receptor 1); 0 (Lipocalin-2); 126469-30-5 (Lcn2 protein, mouse); AYI8EX34EU (Creatinine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00527.2016


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[PMID]:28476763
[Au] Autor:Coca SG; Nadkarni GN; Huang Y; Moledina DG; Rao V; Zhang J; Ferket B; Crowley ST; Fried LF; Parikh CR
[Ad] Endereço:Division of Nephrology, Department of Medicine, and Steven.coca@mssm.edu Chirag.parikh@yale.edu.
[Ti] Título:Plasma Biomarkers and Kidney Function Decline in Early and Established Diabetic Kidney Disease.
[So] Source:J Am Soc Nephrol;28(9):2786-2793, 2017 Sep.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Biomarkers of diverse pathophysiologic mechanisms may improve risk stratification for incident or progressive diabetic kidney disease (DKD) in persons with type 2 diabetes. To evaluate such biomarkers, we performed a nested case-control study ( =190 cases of incident DKD and 190 matched controls) and a prospective cohort study ( =1156) using banked baseline plasma samples from participants of randomized, controlled trials of early (ACCORD) and advanced (VA NEPHRON-D) DKD. We assessed the association and discrimination obtained with baseline levels of plasma TNF receptor-1 (TNFR-1), TNFR-2, and kidney injury molecule-1 (KIM-1) for the outcomes of incident DKD (ACCORD) and progressive DKD (VA-NEPHRON-D). At baseline, median concentrations of TNFR-1, TNFR-2, and KIM-1 were roughly two-fold higher in the advanced DKD population (NEPHRON-D) than in the early DKD population (ACCORD). In both cohorts, patients who reached the renal outcome had higher baseline levels than those who did not reach the outcome. Associations between doubling in TNFR-1, TNFR-2, and KIM-1 levels and risk of the renal outcomes were significant for both cohorts. Inclusion of these biomarkers in clinical models increased the area under the curve (SEM) for predicting the renal outcome from 0.68 (0.02) to 0.75 (0.02) in NEPHRON-D. Systematic review of the literature illustrated high consistency in the association between these biomarkers of inflammation and renal outcomes in DKD. In conclusion, TNFR-1, TNFR-2, and KIM-1 independently associated with higher risk of eGFR decline in persons with early or advanced DKD. Moreover, addition of these biomarkers to clinical prognostic models significantly improved discrimination for the renal outcome.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/complicações
Nefropatias Diabéticas/sangue
Receptor Celular 1 do Vírus da Hepatite A/sangue
Receptores Tipo II do Fator de Necrose Tumoral/sangue
Receptores Tipo I de Fatores de Necrose Tumoral/sangue
[Mh] Termos MeSH secundário: Idoso
Biomarcadores/sangue
Estudos de Casos e Controles
Nefropatias Diabéticas/etiologia
Nefropatias Diabéticas/fisiopatologia
Progressão da Doença
Feminino
Taxa de Filtração Glomerular
Seres Humanos
Masculino
Meia-Idade
Valor Preditivo dos Testes
Prognóstico
Estudos Prospectivos
Ensaios Clínicos Controlados Aleatórios como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (HAVCR1 protein, human); 0 (Hepatitis A Virus Cellular Receptor 1); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Receptors, Tumor Necrosis Factor, Type II)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170507
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2016101101



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