Does Hypercoagulability Exist in CAPD Patients?

Bertoli, M; Gasparotto, Maria L.; Vertolli, Ugo; Ruffatti, A; Landro, Domenico Di; Romagnoli, Gian Franco

doi:10.1177/089686088400400413

Cited by 20 publications

(6 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our data indicate that increased PS exposure in uremic platelets is associated with increased procoagulant activity by those cells, as shown by their ability to support increased generation of thrombin. Thus, loss of membrane phospholipid asymmetry with PS externalization may represent a pathogenic mechanism linking platelets to the thrombotic tendency described in dialysis patients [27–29].…”

Section: Discussionmentioning

confidence: 99%

“…Though the consequences of chronic platelet activation in uremia remain to be definitely established, activated platelets may be involved in biological reactions of potential pathophysiologic significance [24–26]. Further, since alterations in the platelet reactivity state enable these activated cells to participate actively in the thrombotic process [10], activated platelets might contribute to the thrombophilic tendency of uremia [27–29], which is at present a major problem in dialysis patients [30,31].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Increased platelet phosphatidylserine exposure and caspase activation in chronic uremia

Bonomini

Dottori

Amoroso

et al. 2004

Journal of Thrombosis and Haemostasis

110

View full text Add to dashboard Cite

Summary. Platelet activation is associated with exposure of the aminophospholipid phosphatidylserine (PS) to the outer hemileaflet of the plasma membrane bilayer, which seems to be involved in the coagulation process. Because platelet activation may occur in patients suffering from chronic uremia, which is frequently associated with a thrombophilic tendency, we studied whether uremic platelets show an increased propensity to expose PS on the outer membrane leaflet and whether this process is linked with important functional and molecular changes. Flow cytometric percentage of annexin V-positive platelets, a measure of PS externalization, was significantly elevated (P < 0.001) in uremic patients when compared to normal controls under both unstimulated and agonist-stimulated conditions. Uremic platelet procoagulant activity, as measured by thrombin generation, was more than twice as high (4.13 ± 0.3 l mL ). Two independent assays showed that the enzymatic activity of caspase-3, a protease involved in the loss of membrane PS asymmetry, was significantly greater in the platelets of uremic subjects than in those of healthy controls. PS exposure in agonist-stimulated platelets was markedly reduced by inhibition of caspase-3 activity but was not affected by inhibition of calpain activity. These results support the view that the thrombophilic susceptibility of uremic patients may be partly ascribed to increased PS exposure to the outer membrane leaflet of platelets. This process seems to be causally linked to an increase in caspase-3 activity, particularly during platelet activation.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Increased platelet phosphatidylserine exposure and caspase activation in chronic uremia

Bonomini

Dottori

Amoroso

et al. 2004

Journal of Thrombosis and Haemostasis

110

View full text Add to dashboard Cite

show abstract

“…The etiology of increased thrombosis risk associated with PD is not clear. It is hypothesized that long‐term PD creates a hypercoagulable state similar to what is observed in nephrotic syndrome (14). Studies have identified an imbalance of procoagulant and fibrinolytic proteins in these patients.…”

Section: Discussionmentioning

confidence: 99%

“…Studies have identified an imbalance of procoagulant and fibrinolytic proteins in these patients. Among adult PD patients, Bertoli demonstrated evidence of accelerated fibrinolysis including increased concentrations of fibrinogen, fibrin degradation products, as well as a shorter fibrinogen half‐life (14). In addition, the loss of albumin into the dialysate leading to an increased synthesis of albumin, may contribute to increased synthesis of certain coagulation factors as seen in nephrotic syndrome (15).…”

Section: Discussionmentioning

confidence: 99%

Pretransplant peritoneal dialysis and graft thrombosis following pediatric kidney transplantation: A NAPRTCS report

McDonald

Smith

Stablein

et al. 2003

Pediatric Transplantation

View full text Add to dashboard Cite

Graft thrombosis is a common cause of graft failure in pediatric renal transplantation. Several previous studies, including a North American Pediatric Renal Transplant Cooperative Study (NAPRTCS) review of pretransplant dialysis status and graft outcomes, have described a potential correlation of peritoneal dialysis (PD) and graft thrombosis. This issue is of particular concern for pediatric transplant programs as more than 65% of children with end stage renal disease are treated with PD. We reviewed 7247 pediatric renal transplants performed between 1987 and 2001. Thrombosis was the cause of graft loss in 2.7% (199) of all the transplants performed. Among failed transplants, thrombosis was the third most common cause of graft loss in both index (11.6%) and subsequent transplants (14.5%). Thrombosis becomes the most common cause of graft failure (21%, 61/294) if one looks at transplants in the later cohort, from 1996 to 2001. This change is primarily because of a decrease in the incidence of acute rejection. In the PD group, 3.4% of all grafts were lost as a result of thrombosis. This compares with 1.9% in the hemodialysis group, 2.4% in the pre-emptive transplant group, and 4.1% among patients who received both dialysis modalities. There was a statistically significant difference in thrombosis failure risk in the different dialysis groups (p = 0.005) with those who received only peritoneal dialysis having the highest risk. Additional significant risk factors for graft thrombosis included; cadaver donor source (p < 0.001), cold ischemia time >24 h (p < 0.001), history of prior transplant (p < 0.001), donor age <6 yr (p < 0.001), and >5 pretransplant blood transfusions (p = 0.02). Using stepwise proportional hazards modeling, only pretransplant peritoneal dialysis, >24 h cold ischemia time, prior transplant, and donor age <6 yr were simultaneously associated with an increased risk of thrombosis. We conclude that pretransplant PD is associated with an increased risk of graft thrombosis. Special precautions should be undertaken in pediatric renal transplant patients who have received PD, especially infants and young children.

show abstract

“…Hypercoagulability state has been reported to occur in patients with continuous ambulatory peritoneal dialysis (PD) by a mechanism resembling that of the nephrotic syndrome due to transperitoneal protein loss (87). Kobayashi et al have found that PD patients have significantly higher levels of blood coagulation factors (e.g.…”

Section: Pre-transplant Dialysis Modalitymentioning

confidence: 99%

Acquired hypercoagulable state in renal transplant recipients

Kazory

Ducloux²

2004

Thromb Haemost

View full text Add to dashboard Cite

Stable renal transplant recipients manifest a chronic hypercoagulable state with an increased risk of thromboembolic complications, which appears to be multifactorial. While this group of patients could present the known risk factors for thromboembolism in the general population (e.g. diabetes, cancer, pregnancy), they may also suffer from other situations which are mostly related to transplantation and are consequently specific to them. Here, we review briefly the clinical aspects and controversies of the most important of these factors including immunosuppressive agents, antiphospholipid antibodies, hyper-homocysteinemia, pre-transplant dialysis modality, and post-transplant erythrocytosis. In addition, other more recent topics including hypercysteinemia, recurrent proteinuria, and acute CMV infection are discussed.

show abstract

Does Hypercoagulability Exist in CAPD Patients?

Cited by 20 publications

References 7 publications

Increased platelet phosphatidylserine exposure and caspase activation in chronic uremia

Increased platelet phosphatidylserine exposure and caspase activation in chronic uremia

Pretransplant peritoneal dialysis and graft thrombosis following pediatric kidney transplantation: A NAPRTCS report

Acquired hypercoagulable state in renal transplant recipients

Contact Info

Product

Resources

About