Indoxyl sulfate – the uremic toxin linking hemostatic system disturbances with the prevalence of cardiovascular disease in patients with chronic kidney disease

Background During chronic kidney disease progression, kidney-specific risk factors for cardiovascular disease come into play. The present study investigated the impact of indoxyl sulfate, dietary tryptophan-derived uremic toxin, accumulated in the blood of patients with chronic kidney disease on hemostatic parameters, markers of inflammation, oxidative stress and monocyte to macrophage transition. Methods Fifty-one CKD patients not undergoing hemodialysis were enrolled in the study. Coagulation factors, fibrinolytic parameters, adhesion molecules, endothelial dysfunction markers, oxidative stress as well as inflammation markers were examined using immune-enzymatic method. Indoxyl sulfate levels were assessed using high-performance liquid chromatography. Biochemical parameters were determined by routine laboratory techniques using an automated analyzers. All assessed parameters were compared with controls and subjected to cross-sectional statistical analysis. Results Elevated concentrations of indoxyl sulfate, the vast majority of parameters affecting hemostasis, and markers of renal insufficiency conditions were observed. Part of hemostatic factors, namely tissue factor, von Willebrand factor, thrombomodulin, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1, soluble vascular cell adhesion protein were correlated with the fraction of indoxyl sulfate. A significant quantity of assessed parameters showed strong correlations with superoxide-dismutase, renal insufficiency rate, C-reactive protein, and neopterin. Levels of indoxyl sulfate were independently associated with markers of impaired endothelial function (thrombomodulin, adhesion molecules), oxidative stress (superoxide-dismutase) and monocytes activation determinant (neopterin), which indicate unconventional links between these systems and the role of indoxyl sulfate. Furthermore, parameters that correlated with the levels of indoxyl sulfate (von Willebrand factor, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1) were positively associated with the prevalence of cardiovascular disease in a CKD patients. Conclusions The study demonstrated that in conditions of chronic exposure to uremic toxins, indoxyl sulfate seems to be one of the “missing links” between impaired renal function and prevalence of cardiovascular events, especially hemostatic disorders. The main functions of the action appear to be altered monocytes activation, intensified inflammatory process, and augmented oxidative stress by this uremic toxin. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Kamiński, Tomasz W. [verfasserIn] Pawlak, Krystyna Karbowska, Małgorzata Myśliwiec, Michał Pawlak, Dariusz

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2017

Schlagwörter:	Indoxyl sulfate Hemostatic disorder Prothrombotic state Chronic kidney disease Monocytes activation Uremic toxin Tryptophan derivatives Tissue factor von Willebrand factor Cardiovascular disease

Anmerkung:	© The Author(s). 2017

Übergeordnetes Werk:	Enthalten in: BMC nephrology - London : BioMed Central, 2000, 18(2017), 1 vom: 25. Jan.
Übergeordnetes Werk:	volume:18 ; year:2017 ; number:1 ; day:25 ; month:01

Links:	Volltext

DOI / URN:	10.1186/s12882-017-0457-1

Katalog-ID:	SPR027518620

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520			\|a Background During chronic kidney disease progression, kidney-specific risk factors for cardiovascular disease come into play. The present study investigated the impact of indoxyl sulfate, dietary tryptophan-derived uremic toxin, accumulated in the blood of patients with chronic kidney disease on hemostatic parameters, markers of inflammation, oxidative stress and monocyte to macrophage transition. Methods Fifty-one CKD patients not undergoing hemodialysis were enrolled in the study. Coagulation factors, fibrinolytic parameters, adhesion molecules, endothelial dysfunction markers, oxidative stress as well as inflammation markers were examined using immune-enzymatic method. Indoxyl sulfate levels were assessed using high-performance liquid chromatography. Biochemical parameters were determined by routine laboratory techniques using an automated analyzers. All assessed parameters were compared with controls and subjected to cross-sectional statistical analysis. Results Elevated concentrations of indoxyl sulfate, the vast majority of parameters affecting hemostasis, and markers of renal insufficiency conditions were observed. Part of hemostatic factors, namely tissue factor, von Willebrand factor, thrombomodulin, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1, soluble vascular cell adhesion protein were correlated with the fraction of indoxyl sulfate. A significant quantity of assessed parameters showed strong correlations with superoxide-dismutase, renal insufficiency rate, C-reactive protein, and neopterin. Levels of indoxyl sulfate were independently associated with markers of impaired endothelial function (thrombomodulin, adhesion molecules), oxidative stress (superoxide-dismutase) and monocytes activation determinant (neopterin), which indicate unconventional links between these systems and the role of indoxyl sulfate. Furthermore, parameters that correlated with the levels of indoxyl sulfate (von Willebrand factor, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1) were positively associated with the prevalence of cardiovascular disease in a CKD patients. Conclusions The study demonstrated that in conditions of chronic exposure to uremic toxins, indoxyl sulfate seems to be one of the “missing links” between impaired renal function and prevalence of cardiovascular events, especially hemostatic disorders. The main functions of the action appear to be altered monocytes activation, intensified inflammatory process, and augmented oxidative stress by this uremic toxin.
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allfields	10.1186/s12882-017-0457-1 doi (DE-627)SPR027518620 (SPR)s12882-017-0457-1-e DE-627 ger DE-627 rakwb eng Kamiński, Tomasz W. verfasserin aut Indoxyl sulfate – the uremic toxin linking hemostatic system disturbances with the prevalence of cardiovascular disease in patients with chronic kidney disease 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2017 Background During chronic kidney disease progression, kidney-specific risk factors for cardiovascular disease come into play. The present study investigated the impact of indoxyl sulfate, dietary tryptophan-derived uremic toxin, accumulated in the blood of patients with chronic kidney disease on hemostatic parameters, markers of inflammation, oxidative stress and monocyte to macrophage transition. Methods Fifty-one CKD patients not undergoing hemodialysis were enrolled in the study. Coagulation factors, fibrinolytic parameters, adhesion molecules, endothelial dysfunction markers, oxidative stress as well as inflammation markers were examined using immune-enzymatic method. Indoxyl sulfate levels were assessed using high-performance liquid chromatography. Biochemical parameters were determined by routine laboratory techniques using an automated analyzers. All assessed parameters were compared with controls and subjected to cross-sectional statistical analysis. Results Elevated concentrations of indoxyl sulfate, the vast majority of parameters affecting hemostasis, and markers of renal insufficiency conditions were observed. Part of hemostatic factors, namely tissue factor, von Willebrand factor, thrombomodulin, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1, soluble vascular cell adhesion protein were correlated with the fraction of indoxyl sulfate. A significant quantity of assessed parameters showed strong correlations with superoxide-dismutase, renal insufficiency rate, C-reactive protein, and neopterin. Levels of indoxyl sulfate were independently associated with markers of impaired endothelial function (thrombomodulin, adhesion molecules), oxidative stress (superoxide-dismutase) and monocytes activation determinant (neopterin), which indicate unconventional links between these systems and the role of indoxyl sulfate. Furthermore, parameters that correlated with the levels of indoxyl sulfate (von Willebrand factor, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1) were positively associated with the prevalence of cardiovascular disease in a CKD patients. Conclusions The study demonstrated that in conditions of chronic exposure to uremic toxins, indoxyl sulfate seems to be one of the “missing links” between impaired renal function and prevalence of cardiovascular events, especially hemostatic disorders. The main functions of the action appear to be altered monocytes activation, intensified inflammatory process, and augmented oxidative stress by this uremic toxin. Indoxyl sulfate (dpeaa)DE-He213 Hemostatic disorder (dpeaa)DE-He213 Prothrombotic state (dpeaa)DE-He213 Chronic kidney disease (dpeaa)DE-He213 Monocytes activation (dpeaa)DE-He213 Uremic toxin (dpeaa)DE-He213 Tryptophan derivatives (dpeaa)DE-He213 Tissue factor (dpeaa)DE-He213 von Willebrand factor (dpeaa)DE-He213 Cardiovascular disease (dpeaa)DE-He213 Pawlak, Krystyna aut Karbowska, Małgorzata aut Myśliwiec, Michał aut Pawlak, Dariusz (orcid)0000-0002-3751-0608 aut Enthalten in BMC nephrology London : BioMed Central, 2000 18(2017), 1 vom: 25. Jan. (DE-627)326643672 (DE-600)2041348-8 1471-2369 nnns volume:18 year:2017 number:1 day:25 month:01 https://dx.doi.org/10.1186/s12882-017-0457-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2017 1 25 01
spelling	10.1186/s12882-017-0457-1 doi (DE-627)SPR027518620 (SPR)s12882-017-0457-1-e DE-627 ger DE-627 rakwb eng Kamiński, Tomasz W. verfasserin aut Indoxyl sulfate – the uremic toxin linking hemostatic system disturbances with the prevalence of cardiovascular disease in patients with chronic kidney disease 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2017 Background During chronic kidney disease progression, kidney-specific risk factors for cardiovascular disease come into play. The present study investigated the impact of indoxyl sulfate, dietary tryptophan-derived uremic toxin, accumulated in the blood of patients with chronic kidney disease on hemostatic parameters, markers of inflammation, oxidative stress and monocyte to macrophage transition. Methods Fifty-one CKD patients not undergoing hemodialysis were enrolled in the study. Coagulation factors, fibrinolytic parameters, adhesion molecules, endothelial dysfunction markers, oxidative stress as well as inflammation markers were examined using immune-enzymatic method. Indoxyl sulfate levels were assessed using high-performance liquid chromatography. Biochemical parameters were determined by routine laboratory techniques using an automated analyzers. All assessed parameters were compared with controls and subjected to cross-sectional statistical analysis. Results Elevated concentrations of indoxyl sulfate, the vast majority of parameters affecting hemostasis, and markers of renal insufficiency conditions were observed. Part of hemostatic factors, namely tissue factor, von Willebrand factor, thrombomodulin, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1, soluble vascular cell adhesion protein were correlated with the fraction of indoxyl sulfate. A significant quantity of assessed parameters showed strong correlations with superoxide-dismutase, renal insufficiency rate, C-reactive protein, and neopterin. Levels of indoxyl sulfate were independently associated with markers of impaired endothelial function (thrombomodulin, adhesion molecules), oxidative stress (superoxide-dismutase) and monocytes activation determinant (neopterin), which indicate unconventional links between these systems and the role of indoxyl sulfate. Furthermore, parameters that correlated with the levels of indoxyl sulfate (von Willebrand factor, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1) were positively associated with the prevalence of cardiovascular disease in a CKD patients. Conclusions The study demonstrated that in conditions of chronic exposure to uremic toxins, indoxyl sulfate seems to be one of the “missing links” between impaired renal function and prevalence of cardiovascular events, especially hemostatic disorders. The main functions of the action appear to be altered monocytes activation, intensified inflammatory process, and augmented oxidative stress by this uremic toxin. Indoxyl sulfate (dpeaa)DE-He213 Hemostatic disorder (dpeaa)DE-He213 Prothrombotic state (dpeaa)DE-He213 Chronic kidney disease (dpeaa)DE-He213 Monocytes activation (dpeaa)DE-He213 Uremic toxin (dpeaa)DE-He213 Tryptophan derivatives (dpeaa)DE-He213 Tissue factor (dpeaa)DE-He213 von Willebrand factor (dpeaa)DE-He213 Cardiovascular disease (dpeaa)DE-He213 Pawlak, Krystyna aut Karbowska, Małgorzata aut Myśliwiec, Michał aut Pawlak, Dariusz (orcid)0000-0002-3751-0608 aut Enthalten in BMC nephrology London : BioMed Central, 2000 18(2017), 1 vom: 25. Jan. (DE-627)326643672 (DE-600)2041348-8 1471-2369 nnns volume:18 year:2017 number:1 day:25 month:01 https://dx.doi.org/10.1186/s12882-017-0457-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2017 1 25 01
allfields_unstemmed	10.1186/s12882-017-0457-1 doi (DE-627)SPR027518620 (SPR)s12882-017-0457-1-e DE-627 ger DE-627 rakwb eng Kamiński, Tomasz W. verfasserin aut Indoxyl sulfate – the uremic toxin linking hemostatic system disturbances with the prevalence of cardiovascular disease in patients with chronic kidney disease 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2017 Background During chronic kidney disease progression, kidney-specific risk factors for cardiovascular disease come into play. The present study investigated the impact of indoxyl sulfate, dietary tryptophan-derived uremic toxin, accumulated in the blood of patients with chronic kidney disease on hemostatic parameters, markers of inflammation, oxidative stress and monocyte to macrophage transition. Methods Fifty-one CKD patients not undergoing hemodialysis were enrolled in the study. Coagulation factors, fibrinolytic parameters, adhesion molecules, endothelial dysfunction markers, oxidative stress as well as inflammation markers were examined using immune-enzymatic method. Indoxyl sulfate levels were assessed using high-performance liquid chromatography. Biochemical parameters were determined by routine laboratory techniques using an automated analyzers. All assessed parameters were compared with controls and subjected to cross-sectional statistical analysis. Results Elevated concentrations of indoxyl sulfate, the vast majority of parameters affecting hemostasis, and markers of renal insufficiency conditions were observed. Part of hemostatic factors, namely tissue factor, von Willebrand factor, thrombomodulin, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1, soluble vascular cell adhesion protein were correlated with the fraction of indoxyl sulfate. A significant quantity of assessed parameters showed strong correlations with superoxide-dismutase, renal insufficiency rate, C-reactive protein, and neopterin. Levels of indoxyl sulfate were independently associated with markers of impaired endothelial function (thrombomodulin, adhesion molecules), oxidative stress (superoxide-dismutase) and monocytes activation determinant (neopterin), which indicate unconventional links between these systems and the role of indoxyl sulfate. Furthermore, parameters that correlated with the levels of indoxyl sulfate (von Willebrand factor, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1) were positively associated with the prevalence of cardiovascular disease in a CKD patients. Conclusions The study demonstrated that in conditions of chronic exposure to uremic toxins, indoxyl sulfate seems to be one of the “missing links” between impaired renal function and prevalence of cardiovascular events, especially hemostatic disorders. The main functions of the action appear to be altered monocytes activation, intensified inflammatory process, and augmented oxidative stress by this uremic toxin. Indoxyl sulfate (dpeaa)DE-He213 Hemostatic disorder (dpeaa)DE-He213 Prothrombotic state (dpeaa)DE-He213 Chronic kidney disease (dpeaa)DE-He213 Monocytes activation (dpeaa)DE-He213 Uremic toxin (dpeaa)DE-He213 Tryptophan derivatives (dpeaa)DE-He213 Tissue factor (dpeaa)DE-He213 von Willebrand factor (dpeaa)DE-He213 Cardiovascular disease (dpeaa)DE-He213 Pawlak, Krystyna aut Karbowska, Małgorzata aut Myśliwiec, Michał aut Pawlak, Dariusz (orcid)0000-0002-3751-0608 aut Enthalten in BMC nephrology London : BioMed Central, 2000 18(2017), 1 vom: 25. Jan. (DE-627)326643672 (DE-600)2041348-8 1471-2369 nnns volume:18 year:2017 number:1 day:25 month:01 https://dx.doi.org/10.1186/s12882-017-0457-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2017 1 25 01
allfieldsGer	10.1186/s12882-017-0457-1 doi (DE-627)SPR027518620 (SPR)s12882-017-0457-1-e DE-627 ger DE-627 rakwb eng Kamiński, Tomasz W. verfasserin aut Indoxyl sulfate – the uremic toxin linking hemostatic system disturbances with the prevalence of cardiovascular disease in patients with chronic kidney disease 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2017 Background During chronic kidney disease progression, kidney-specific risk factors for cardiovascular disease come into play. The present study investigated the impact of indoxyl sulfate, dietary tryptophan-derived uremic toxin, accumulated in the blood of patients with chronic kidney disease on hemostatic parameters, markers of inflammation, oxidative stress and monocyte to macrophage transition. Methods Fifty-one CKD patients not undergoing hemodialysis were enrolled in the study. Coagulation factors, fibrinolytic parameters, adhesion molecules, endothelial dysfunction markers, oxidative stress as well as inflammation markers were examined using immune-enzymatic method. Indoxyl sulfate levels were assessed using high-performance liquid chromatography. Biochemical parameters were determined by routine laboratory techniques using an automated analyzers. All assessed parameters were compared with controls and subjected to cross-sectional statistical analysis. Results Elevated concentrations of indoxyl sulfate, the vast majority of parameters affecting hemostasis, and markers of renal insufficiency conditions were observed. Part of hemostatic factors, namely tissue factor, von Willebrand factor, thrombomodulin, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1, soluble vascular cell adhesion protein were correlated with the fraction of indoxyl sulfate. A significant quantity of assessed parameters showed strong correlations with superoxide-dismutase, renal insufficiency rate, C-reactive protein, and neopterin. Levels of indoxyl sulfate were independently associated with markers of impaired endothelial function (thrombomodulin, adhesion molecules), oxidative stress (superoxide-dismutase) and monocytes activation determinant (neopterin), which indicate unconventional links between these systems and the role of indoxyl sulfate. Furthermore, parameters that correlated with the levels of indoxyl sulfate (von Willebrand factor, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1) were positively associated with the prevalence of cardiovascular disease in a CKD patients. Conclusions The study demonstrated that in conditions of chronic exposure to uremic toxins, indoxyl sulfate seems to be one of the “missing links” between impaired renal function and prevalence of cardiovascular events, especially hemostatic disorders. The main functions of the action appear to be altered monocytes activation, intensified inflammatory process, and augmented oxidative stress by this uremic toxin. Indoxyl sulfate (dpeaa)DE-He213 Hemostatic disorder (dpeaa)DE-He213 Prothrombotic state (dpeaa)DE-He213 Chronic kidney disease (dpeaa)DE-He213 Monocytes activation (dpeaa)DE-He213 Uremic toxin (dpeaa)DE-He213 Tryptophan derivatives (dpeaa)DE-He213 Tissue factor (dpeaa)DE-He213 von Willebrand factor (dpeaa)DE-He213 Cardiovascular disease (dpeaa)DE-He213 Pawlak, Krystyna aut Karbowska, Małgorzata aut Myśliwiec, Michał aut Pawlak, Dariusz (orcid)0000-0002-3751-0608 aut Enthalten in BMC nephrology London : BioMed Central, 2000 18(2017), 1 vom: 25. Jan. (DE-627)326643672 (DE-600)2041348-8 1471-2369 nnns volume:18 year:2017 number:1 day:25 month:01 https://dx.doi.org/10.1186/s12882-017-0457-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2017 1 25 01
allfieldsSound	10.1186/s12882-017-0457-1 doi (DE-627)SPR027518620 (SPR)s12882-017-0457-1-e DE-627 ger DE-627 rakwb eng Kamiński, Tomasz W. verfasserin aut Indoxyl sulfate – the uremic toxin linking hemostatic system disturbances with the prevalence of cardiovascular disease in patients with chronic kidney disease 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2017 Background During chronic kidney disease progression, kidney-specific risk factors for cardiovascular disease come into play. The present study investigated the impact of indoxyl sulfate, dietary tryptophan-derived uremic toxin, accumulated in the blood of patients with chronic kidney disease on hemostatic parameters, markers of inflammation, oxidative stress and monocyte to macrophage transition. Methods Fifty-one CKD patients not undergoing hemodialysis were enrolled in the study. Coagulation factors, fibrinolytic parameters, adhesion molecules, endothelial dysfunction markers, oxidative stress as well as inflammation markers were examined using immune-enzymatic method. Indoxyl sulfate levels were assessed using high-performance liquid chromatography. Biochemical parameters were determined by routine laboratory techniques using an automated analyzers. All assessed parameters were compared with controls and subjected to cross-sectional statistical analysis. Results Elevated concentrations of indoxyl sulfate, the vast majority of parameters affecting hemostasis, and markers of renal insufficiency conditions were observed. Part of hemostatic factors, namely tissue factor, von Willebrand factor, thrombomodulin, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1, soluble vascular cell adhesion protein were correlated with the fraction of indoxyl sulfate. A significant quantity of assessed parameters showed strong correlations with superoxide-dismutase, renal insufficiency rate, C-reactive protein, and neopterin. Levels of indoxyl sulfate were independently associated with markers of impaired endothelial function (thrombomodulin, adhesion molecules), oxidative stress (superoxide-dismutase) and monocytes activation determinant (neopterin), which indicate unconventional links between these systems and the role of indoxyl sulfate. Furthermore, parameters that correlated with the levels of indoxyl sulfate (von Willebrand factor, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1) were positively associated with the prevalence of cardiovascular disease in a CKD patients. Conclusions The study demonstrated that in conditions of chronic exposure to uremic toxins, indoxyl sulfate seems to be one of the “missing links” between impaired renal function and prevalence of cardiovascular events, especially hemostatic disorders. The main functions of the action appear to be altered monocytes activation, intensified inflammatory process, and augmented oxidative stress by this uremic toxin. Indoxyl sulfate (dpeaa)DE-He213 Hemostatic disorder (dpeaa)DE-He213 Prothrombotic state (dpeaa)DE-He213 Chronic kidney disease (dpeaa)DE-He213 Monocytes activation (dpeaa)DE-He213 Uremic toxin (dpeaa)DE-He213 Tryptophan derivatives (dpeaa)DE-He213 Tissue factor (dpeaa)DE-He213 von Willebrand factor (dpeaa)DE-He213 Cardiovascular disease (dpeaa)DE-He213 Pawlak, Krystyna aut Karbowska, Małgorzata aut Myśliwiec, Michał aut Pawlak, Dariusz (orcid)0000-0002-3751-0608 aut Enthalten in BMC nephrology London : BioMed Central, 2000 18(2017), 1 vom: 25. Jan. (DE-627)326643672 (DE-600)2041348-8 1471-2369 nnns volume:18 year:2017 number:1 day:25 month:01 https://dx.doi.org/10.1186/s12882-017-0457-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2017 1 25 01
language	English
source	Enthalten in BMC nephrology 18(2017), 1 vom: 25. Jan. volume:18 year:2017 number:1 day:25 month:01
sourceStr	Enthalten in BMC nephrology 18(2017), 1 vom: 25. Jan. volume:18 year:2017 number:1 day:25 month:01
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Indoxyl sulfate Hemostatic disorder Prothrombotic state Chronic kidney disease Monocytes activation Uremic toxin Tryptophan derivatives Tissue factor von Willebrand factor Cardiovascular disease
isfreeaccess_bool	true
container_title	BMC nephrology
authorswithroles_txt_mv	Kamiński, Tomasz W. @@aut@@ Pawlak, Krystyna @@aut@@ Karbowska, Małgorzata @@aut@@ Myśliwiec, Michał @@aut@@ Pawlak, Dariusz @@aut@@
publishDateDaySort_date	2017-01-25T00:00:00Z
hierarchy_top_id	326643672
id	SPR027518620
language_de	englisch
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author	Kamiński, Tomasz W.
spellingShingle	Kamiński, Tomasz W. misc Indoxyl sulfate misc Hemostatic disorder misc Prothrombotic state misc Chronic kidney disease misc Monocytes activation misc Uremic toxin misc Tryptophan derivatives misc Tissue factor misc von Willebrand factor misc Cardiovascular disease Indoxyl sulfate – the uremic toxin linking hemostatic system disturbances with the prevalence of cardiovascular disease in patients with chronic kidney disease
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topic_title	Indoxyl sulfate – the uremic toxin linking hemostatic system disturbances with the prevalence of cardiovascular disease in patients with chronic kidney disease Indoxyl sulfate (dpeaa)DE-He213 Hemostatic disorder (dpeaa)DE-He213 Prothrombotic state (dpeaa)DE-He213 Chronic kidney disease (dpeaa)DE-He213 Monocytes activation (dpeaa)DE-He213 Uremic toxin (dpeaa)DE-He213 Tryptophan derivatives (dpeaa)DE-He213 Tissue factor (dpeaa)DE-He213 von Willebrand factor (dpeaa)DE-He213 Cardiovascular disease (dpeaa)DE-He213
topic	misc Indoxyl sulfate misc Hemostatic disorder misc Prothrombotic state misc Chronic kidney disease misc Monocytes activation misc Uremic toxin misc Tryptophan derivatives misc Tissue factor misc von Willebrand factor misc Cardiovascular disease
topic_unstemmed	misc Indoxyl sulfate misc Hemostatic disorder misc Prothrombotic state misc Chronic kidney disease misc Monocytes activation misc Uremic toxin misc Tryptophan derivatives misc Tissue factor misc von Willebrand factor misc Cardiovascular disease
topic_browse	misc Indoxyl sulfate misc Hemostatic disorder misc Prothrombotic state misc Chronic kidney disease misc Monocytes activation misc Uremic toxin misc Tryptophan derivatives misc Tissue factor misc von Willebrand factor misc Cardiovascular disease
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title	Indoxyl sulfate – the uremic toxin linking hemostatic system disturbances with the prevalence of cardiovascular disease in patients with chronic kidney disease
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title_full	Indoxyl sulfate – the uremic toxin linking hemostatic system disturbances with the prevalence of cardiovascular disease in patients with chronic kidney disease
author_sort	Kamiński, Tomasz W.
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author_browse	Kamiński, Tomasz W. Pawlak, Krystyna Karbowska, Małgorzata Myśliwiec, Michał Pawlak, Dariusz
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title_sort	indoxyl sulfate – the uremic toxin linking hemostatic system disturbances with the prevalence of cardiovascular disease in patients with chronic kidney disease
title_auth	Indoxyl sulfate – the uremic toxin linking hemostatic system disturbances with the prevalence of cardiovascular disease in patients with chronic kidney disease
abstract	Background During chronic kidney disease progression, kidney-specific risk factors for cardiovascular disease come into play. The present study investigated the impact of indoxyl sulfate, dietary tryptophan-derived uremic toxin, accumulated in the blood of patients with chronic kidney disease on hemostatic parameters, markers of inflammation, oxidative stress and monocyte to macrophage transition. Methods Fifty-one CKD patients not undergoing hemodialysis were enrolled in the study. Coagulation factors, fibrinolytic parameters, adhesion molecules, endothelial dysfunction markers, oxidative stress as well as inflammation markers were examined using immune-enzymatic method. Indoxyl sulfate levels were assessed using high-performance liquid chromatography. Biochemical parameters were determined by routine laboratory techniques using an automated analyzers. All assessed parameters were compared with controls and subjected to cross-sectional statistical analysis. Results Elevated concentrations of indoxyl sulfate, the vast majority of parameters affecting hemostasis, and markers of renal insufficiency conditions were observed. Part of hemostatic factors, namely tissue factor, von Willebrand factor, thrombomodulin, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1, soluble vascular cell adhesion protein were correlated with the fraction of indoxyl sulfate. A significant quantity of assessed parameters showed strong correlations with superoxide-dismutase, renal insufficiency rate, C-reactive protein, and neopterin. Levels of indoxyl sulfate were independently associated with markers of impaired endothelial function (thrombomodulin, adhesion molecules), oxidative stress (superoxide-dismutase) and monocytes activation determinant (neopterin), which indicate unconventional links between these systems and the role of indoxyl sulfate. Furthermore, parameters that correlated with the levels of indoxyl sulfate (von Willebrand factor, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1) were positively associated with the prevalence of cardiovascular disease in a CKD patients. Conclusions The study demonstrated that in conditions of chronic exposure to uremic toxins, indoxyl sulfate seems to be one of the “missing links” between impaired renal function and prevalence of cardiovascular events, especially hemostatic disorders. The main functions of the action appear to be altered monocytes activation, intensified inflammatory process, and augmented oxidative stress by this uremic toxin. © The Author(s). 2017
abstractGer	Background During chronic kidney disease progression, kidney-specific risk factors for cardiovascular disease come into play. The present study investigated the impact of indoxyl sulfate, dietary tryptophan-derived uremic toxin, accumulated in the blood of patients with chronic kidney disease on hemostatic parameters, markers of inflammation, oxidative stress and monocyte to macrophage transition. Methods Fifty-one CKD patients not undergoing hemodialysis were enrolled in the study. Coagulation factors, fibrinolytic parameters, adhesion molecules, endothelial dysfunction markers, oxidative stress as well as inflammation markers were examined using immune-enzymatic method. Indoxyl sulfate levels were assessed using high-performance liquid chromatography. Biochemical parameters were determined by routine laboratory techniques using an automated analyzers. All assessed parameters were compared with controls and subjected to cross-sectional statistical analysis. Results Elevated concentrations of indoxyl sulfate, the vast majority of parameters affecting hemostasis, and markers of renal insufficiency conditions were observed. Part of hemostatic factors, namely tissue factor, von Willebrand factor, thrombomodulin, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1, soluble vascular cell adhesion protein were correlated with the fraction of indoxyl sulfate. A significant quantity of assessed parameters showed strong correlations with superoxide-dismutase, renal insufficiency rate, C-reactive protein, and neopterin. Levels of indoxyl sulfate were independently associated with markers of impaired endothelial function (thrombomodulin, adhesion molecules), oxidative stress (superoxide-dismutase) and monocytes activation determinant (neopterin), which indicate unconventional links between these systems and the role of indoxyl sulfate. Furthermore, parameters that correlated with the levels of indoxyl sulfate (von Willebrand factor, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1) were positively associated with the prevalence of cardiovascular disease in a CKD patients. Conclusions The study demonstrated that in conditions of chronic exposure to uremic toxins, indoxyl sulfate seems to be one of the “missing links” between impaired renal function and prevalence of cardiovascular events, especially hemostatic disorders. The main functions of the action appear to be altered monocytes activation, intensified inflammatory process, and augmented oxidative stress by this uremic toxin. © The Author(s). 2017
abstract_unstemmed	Background During chronic kidney disease progression, kidney-specific risk factors for cardiovascular disease come into play. The present study investigated the impact of indoxyl sulfate, dietary tryptophan-derived uremic toxin, accumulated in the blood of patients with chronic kidney disease on hemostatic parameters, markers of inflammation, oxidative stress and monocyte to macrophage transition. Methods Fifty-one CKD patients not undergoing hemodialysis were enrolled in the study. Coagulation factors, fibrinolytic parameters, adhesion molecules, endothelial dysfunction markers, oxidative stress as well as inflammation markers were examined using immune-enzymatic method. Indoxyl sulfate levels were assessed using high-performance liquid chromatography. Biochemical parameters were determined by routine laboratory techniques using an automated analyzers. All assessed parameters were compared with controls and subjected to cross-sectional statistical analysis. Results Elevated concentrations of indoxyl sulfate, the vast majority of parameters affecting hemostasis, and markers of renal insufficiency conditions were observed. Part of hemostatic factors, namely tissue factor, von Willebrand factor, thrombomodulin, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1, soluble vascular cell adhesion protein were correlated with the fraction of indoxyl sulfate. A significant quantity of assessed parameters showed strong correlations with superoxide-dismutase, renal insufficiency rate, C-reactive protein, and neopterin. Levels of indoxyl sulfate were independently associated with markers of impaired endothelial function (thrombomodulin, adhesion molecules), oxidative stress (superoxide-dismutase) and monocytes activation determinant (neopterin), which indicate unconventional links between these systems and the role of indoxyl sulfate. Furthermore, parameters that correlated with the levels of indoxyl sulfate (von Willebrand factor, soluble urokinase-type plasminogen activator receptor, soluble intercellular adhesion molecule-1) were positively associated with the prevalence of cardiovascular disease in a CKD patients. Conclusions The study demonstrated that in conditions of chronic exposure to uremic toxins, indoxyl sulfate seems to be one of the “missing links” between impaired renal function and prevalence of cardiovascular events, especially hemostatic disorders. The main functions of the action appear to be altered monocytes activation, intensified inflammatory process, and augmented oxidative stress by this uremic toxin. © The Author(s). 2017
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title_short	Indoxyl sulfate – the uremic toxin linking hemostatic system disturbances with the prevalence of cardiovascular disease in patients with chronic kidney disease
url	https://dx.doi.org/10.1186/s12882-017-0457-1
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author2	Pawlak, Krystyna Karbowska, Małgorzata Myśliwiec, Michał Pawlak, Dariusz
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