Plasma thrombomodulin levels are dependent on renal function

Hergesell, Olaf; Andrássy, K.; Geberth, Steffen K.; Nawroth, Peter P.; Gabath, Stefanie

doi:10.1016/0049-3848(93)90246-k

Cited by 37 publications

(27 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We failed to observe a significant elevation in TM and AT before IVIG in this study; this agrees with previous findings that urinary TM levels are significantly elevated in the acute phase and decline to within the normal range in the recovery phase [30]. Hypoalbuminemia is often associated with KD and is thought to result from extravasation due to enhanced vascular permeability [31] and/or to increased renal excretion [32,33]. As both soluble TM and AT have a mass close to that of albumin, their levels will likely decrease in KD patients with hypoalbuminemia.…”

Section: Discussionsupporting

confidence: 81%

Persistent Endothelial Damage after Intravenous Immunoglobulin Therapy in Kawasaki Disease

Sakurai¹,

Takatsuka²,

Onaka³

et al. 2014

Int Arch Allergy Immunol

View full text Add to dashboard Cite

Background: Kawasaki disease (KD) is an acute systemic vasculitis of unknown etiology. Although endothelial cell damage associated with vasculitis might lead to the hypercoagulability that is involved in coronary artery disease, the changes in coagulation after intravenous immunoglobulin therapy (IVIG) have not been well investigated in KD. The aims of this study were to address the changes in coagulation before and after IVIG in KD, and to further elucidate the coagulation-inflammation axis, with special attention to endothelial damage. Methods: We retrospectively collected the laboratory data before and after IVIG in 26 pediatric KD patients treated at the Nara Prefecture Western Medical Center between May 2010 and April 2012. Prothrombin time (PT), activated partial thromboplastin time (APTT) and levels of fibrin/fibrinogen degradation products (FDP) and D-dimer were assessed as coagulation markers. Fibrinogen, ferritin, serum amyloid A, procalcitonin and urine F2 microglobulin were assessed as inflammation markers. Thrombomodulin, antithrombin, factor VIII activity (FVIII:C), and von Willebrand factor antigen (VWF:Ag) were used to assess endothelial damage. Results: Prolonged PT and APTT before IVIG were significantly shortened after IVIG, and elevated levels of FDP and D-dimer were significantly decreased. Elevated levels of inflammation markers had decreased significantly after IVIG, but levels of FVIII:C and VWF:Ag remained high, even after IVIG. Conclusions: Ameliorated inflammation by IVIG might improve the hypercoagulable state. Nevertheless, our results suggest that endothelial damage might be prolonged in IVIG-treated patients. Control of endothelial damage in KD is critical. i 2014 S. Karger AG, Basel

show abstract

Section: Discussionsupporting

confidence: 81%

Persistent Endothelial Damage after Intravenous Immunoglobulin Therapy in Kawasaki Disease

Sakurai¹,

Takatsuka²,

Onaka³

et al. 2014

Int Arch Allergy Immunol

View full text Add to dashboard Cite

show abstract

“…Therefore, its level rises in renal failure and this increase is significantly associated with creatininemia and inversely correlated to creatinine clearance values (42). When creatininemia is increased, pTM should be expressed as a ratio, pTM/ serum creatinine, in order to distinguish pTM increase due to renal failure from that resulting from endothelial injury.…”

Section: Tm Metabolism and Regulationmentioning

confidence: 99%

Considering cellular thrombomodulin distribution and its modulating factors can facilitate the use of plasma thrombomodulin as a reliable endothelial marker?

Boffa

1996

Pathophysiol Haemos Thromb

View full text Add to dashboard Cite

“…Although elevated TM levels have been associated with atheroembolic risk [23,24], TM levels were normal in different stages of atherosclerosis and did not correlate with the degree of the disease as measured by angiograms of large portions of the arterial system [27]. Also, it was recorded to be of little clinical interest in reflecting atherogenesis, as smoking and serum creatinine levels markedly affected it [16,23,28]. Platelet activation has been shown to precede signs of endothelial damage [13].…”

Section: Discussionmentioning

confidence: 99%

“…The plasma TM level was quantified using a two-site ELISA from Diagnostica Stago (Asserachrom, Asnières, France) [16]. vWF was measured by electroimmunoassay (Laurell) with reagents from Behring (Marburg, Germany).…”

Section: Plasma Assaysmentioning

confidence: 99%

Relation between Carotid Intima-Media Thickness, Platelet Surface Activation and Endothelial Cell Markers

Ramsis

Elhawary²,

Ismail³

1998

Pathophysiol Haemos Thromb

View full text Add to dashboard Cite

Background: The role of platelet activation and endothelial cell damage in the pathogenesis of atherosclerosis was investigated. Methods: Flow-cytometric detection of platelet activity was accomplished by measuring the surface expression of activated platelet glycoprotein IIb/IIIa (activated CD41) and the lysosomal integral membrane protein (CD63). Levels of thrombomodulin (TM) and von Willebrand factor (vWF) were estimated by the ELISA technique as markers of endothelial cell damage. These procedures were performed in healthy male subjects without obvious signs of atherosclerosis. Also, the intima-media thickness of the carotid artery was measured with high-resolution B- mode ultrasound to quantitate the presence and/or the extent of carotid atherosclerosis. Results: According to ultrasound findings patients were divided into those with apparent evidence of atherosclerosis (AS+) with intima-media thickness >1.1 mm (n = 19) and those without such evidence (AS–) with intima-media thickness <1.1 mm (n = 17). The percentages of activated CD41 and CD63 surface antigen expression were significantly increased in the AS+ compared to AS– subjects. TM levels were elevated in the former group compared to the latter, while vWF levels were not different in the two groups. Multivariate analysis indicated the independent association of carotid atherosclerosis with each of the expression of activated CD41, CD63 as well as TM levels after adjustment of other risk factors. Conclusion: This study demonstrates that platelets circulate in an enhanced activation state in asymptomatic atherosclerosis, which is closely related to the degree of endothelial cell damage as expressed by increased plasma levels of TM. The detection of platelet activation can be used as a potential marker for oncoming atherosclerosis.

show abstract

Plasma thrombomodulin levels are dependent on renal function

Cited by 37 publications

References 9 publications

Persistent Endothelial Damage after Intravenous Immunoglobulin Therapy in Kawasaki Disease

Persistent Endothelial Damage after Intravenous Immunoglobulin Therapy in Kawasaki Disease

Considering cellular thrombomodulin distribution and its modulating factors can facilitate the use of plasma thrombomodulin as a reliable endothelial marker?

Relation between Carotid Intima-Media Thickness, Platelet Surface Activation and Endothelial Cell Markers

Contact Info

Product

Resources

About