Reduced Fibrinolytic Potential One Year After Kidney Transplantation

Patrassi, G; Sartori, Maria Teresa; Rigotti, Paolo; Landro, Domenico Di; Theodoridis, Panagiotis; Fioranelli, Massimo; Capalbo, M.; Saggiorato, Graziella; Boeri, G; Girolami, Antonio

doi:10.1097/00007890-199505270-00010

Cited by 58 publications

(31 citation statements)

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“…42 Thus, at the present state of knowledge, insulin is a modulator of PAI-1 production in humans, but this stimulatory action appears to be exerted via other tissues rather than adipose tissue. Likewise, glucocorticoids were found to induce PAI-1 biosynthesis in adipose tissue in vitro, 26,28 which is also supported by clinical data obtained in patients under treatment with glucocorticoids 43,44 and in Cushing patients. 45 The stimulatory effect of glucocorticoids was most pronounced in isolated human adipocytes and in vitro differentiated 3T3 F442A adipocytes, whereas no effect was observed in cultured human preadipocytes.…”

Section: Hormonal Regulation Of Adipose Tissue Pai-1 Expressionsupporting

confidence: 69%

Obesity and impaired fibrinolysis: role of adipose production of plasminogen activator inhibitor-1

2004

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Obesity is the central promoter of the metabolic syndrome which also includes disturbed fibrinolysis in addition to hypertension, dyslipidaemia and impaired glucose tolerance/type 2 diabetes mellitus. Plasminogen activator inhibitor-1 (PAI-1) is the most important endogenous inhibitor of tissue plasminogen activator and uro-plasminogen activator, and is a main determinant of fibrinolytic activity. There is now compelling evidence that obesity and, in particular, an abdominal type of body fat distribution are associated with elevated PAI-1 antigen and activity levels. Recent studies established that PAI-1 is expressed in adipose tissue. The greater the fat cell size and the adipose tissue mass, the greater is the contribution of adipose production to circulating PAI-1. Experimental data show that visceral adipose tissue has a higher capacity to produce PAI-1 than subcutaneous adipose tissue. Studies in human adipocytes indicate that PAI-1 synthesis is upregulated by insulin, glucocorticoids, angiotensin II, some fatty acids and, most potently, by cytokines such as tumour necrosis factor-a and transforming growth factor-b, whereas catecholamines reduce PAI-1 production. Interestingly, pharmacological agents such as thiazolidinediones, metformin and AT 1 -receptor antagonists were found to reduce adipose expression of PAI-1. In addition, weight loss by dietary restriction or comprehensive lifestyle modification is effective in lowering PAI-1 plasma levels. In conclusion, impaired fibrinolysis in obesity is probably also due to an increased expression of PAI-1 in adipose tissue. An altered function of the endocrine system and an impaired auto-/paracrine function at the fat cell levels may mediate this disturbance of the fibrinolytic system and thereby increase the risk for cardiovascular disease.

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Section: Hormonal Regulation Of Adipose Tissue Pai-1 Expressionsupporting

confidence: 69%

Obesity and impaired fibrinolysis: role of adipose production of plasminogen activator inhibitor-1

2004

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“…Our analysis also found several clinical factors and medications that may be important in predicting overall fibrinolytic and thrombotic activity. Given that some of these same factors also are known to either promote or mitigate both neointimal proliferation and atheromatous CAD, it is possible that these clinical factors could also influence the formation and/or progression of Tx CAD via mechanisms involving shifts in FA (26)(27)(28)(29)(30)(31)(32)(33)(34). This study is limited by the small, single center nature of the cohort and that some time points contain missing values, which could skew the significance of the time course.…”

Section: Discussionmentioning

confidence: 99%

Alterations in the Fibrinolytic Cascade Post-transplant: Evidence of a Bimodal Expression Pattern

Benza

Cavender

Barchue

et al. 2007

The Journal of Heart and Lung Transplantation

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Changes in the fibrinolytic system that occur after cardiac transplantation (CTx) and the factors which influence such changes are poorly described, yet may be ultimately important in determining the varying morphologic features of transplant related coronary artery disease (Tx CAD). Baselines demographic, as well as serial clinical information and plasma fibrinolytic levels were prospectively recorded preCTx and multiple times postCTx in 110 de novo cardiac transplant recipients. We noted a biphasic change in fibrinolytic activity over the first year of CTx with an early immediate decline in PAI-1 activity (p > 0.001) matched with stable PAP (plasmin) activity corresponding to an "enhanced" fibrinolytic state early post CTx followed by a significant increase at 6 months (p = 0.004) and 1 year (p < 0.001) in PAI-1 activity concomitant with a significant decline in PAP after 3 months (p = 0.005 at 3 months, p < 0.001 at 6 months, and p < 0.001 at 1 year) corresponding to an "impaired" fibrinolytic state late post CTx. This biphasic nature of the fibrinolytic system could account for the varying morphologic features of Tx CAD.

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“…Renal allografts that failed within 1 month after transplantation had a significantly greater depletion of vascular antithrombin and more extensive fibrin deposition than those that failed later. There is also biochemical evidence of impaired fibrinolysis, both systemically and regionally, on graft vessel endothelium (48,49).…”

Section: Other Thrombophilic Defects and Predisposing Factorsmentioning

confidence: 99%

Thrombophilia and Thrombotic Problems in Renal Transplant Patients

Kujovich¹

2004

Transplantation

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Reduced Fibrinolytic Potential One Year After Kidney Transplantation

Cited by 58 publications

References 0 publications

Obesity and impaired fibrinolysis: role of adipose production of plasminogen activator inhibitor-1

Obesity and impaired fibrinolysis: role of adipose production of plasminogen activator inhibitor-1

Alterations in the Fibrinolytic Cascade Post-transplant: Evidence of a Bimodal Expression Pattern

Thrombophilia and Thrombotic Problems in Renal Transplant Patients

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