Hemostatic and Fibrinolytic Response to Nasal Desmopressin in Hemodialysis Patients

Ulusoy, Şükrü; Ovalı, Ercüment; Aydin, Faruk; Erem, Cihangir; Özdemir, Feyyaz; Kaynar, Kubra

doi:10.1159/000080471

Cited by 14 publications

(4 citation statements)

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“…the current study showed that there were statistically significant differences between the mean of APTT in HD patients and those of the control group. This finding agreed with the results obtained by Ulusoy et al, (2004).…”

Section: Discussionsupporting

confidence: 93%

Impact of Hemodialysis on Bleeding Tendency in End Stage Renal Disease Patients

2023

JPTCP

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Background: Heparin is a potent anticoagulant with diverse pleiotropic effects through cytokine release. In hemodialysis, anticoagulation using systemic heparinization is crucial to prevent blood clots within the extracorporeal circuit. However, the risk of bleeding complications and substantial hemostatic defects are increased in maintenance HD patients. Aim of work: the aim of the presented study was to investigate the effect of systemic heparinization during hemodialysis on the coagulation profile of maintenance HD patients and whether heparin free dialysis would be beneficial for specific patients. Patients and Methods: Sixty ESRD patients on regular HD three times per week and 25 healthy controls were recruited to this study. Complete blood count, prothrombin time, activated partial prothrombin time, fibrinogen and D-dimer levels pre and post hemodialysis were evaluated. Results:The presented study demonstrated prolongation of PTand APTT associated with increased levels of fibrinogen and D-dimer post HD (p-value: <0.0001). Conclusion:The prolonged PT and APTT in addition to the rise in fibrinogen and D-dimer levels post HD indicates that the prophylactic anticoagulantion using unfractionated heparin could increase the risk of bleeding in HD patients.

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Section: Discussionsupporting

confidence: 93%

Impact of Hemodialysis on Bleeding Tendency in End Stage Renal Disease Patients

2023

JPTCP

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“…But the finding in this study is not consistent with Yeniçerioglu et al 16 who reported a significant decrease in circulating platelets post-HD when compared to the pre-HD counts. The decrease in platelets counts post-HD may be due to either the HD procedure itself, through the interaction of blood with membranes that may activate complement (Galbusera et al 14 ) or to the heparin used during dialysis was one of the factors accounting for the increased platelet aggregation after dialysis as previously reported by Charvát et al 17 . In a previous study by Docci et al 18 stated that the dialysis membrane composition is a major factor influencing haemodialysis-associated platelet loss.…”

Section: Resultsmentioning

confidence: 76%

A Comparative Study on Haematological Changes before and One hour after Haemodialysis in Patients with End Stage Renal Disease

Rahman¹,

Giti²,

Khan³

et al. 2022

J. Armed Forces Med. Coll.

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Introduction: Normal kidney function is very important for maintaining homeostasis. Any deviation of normal renal function leads to deviation of normal homeostasis. End-stage renal disease (ESRD) is the last stage of chronic kidney disease (CKD) resulting from different aetiologies. Different haematological abnormalities in patients with ESRD result from multiple pathogenesis. Treatment of this condition requires multidisciplinary approach. Among all the treatment options haemodialysis (HD) is the most common, widely accepted and available treatment option. Objective: To find out the effectiveness of haemodialysis in the improvement of different haematological deviations developed during the course of ESRD. Materials and Methods: A total of 72 patients with ESRD of both sexes with the age ranging from 25 years to 70 years were included in this comparative cross sectional study and carried out in Combined Military Hospital and Armed Forces Institute of Pathology, Dhaka Cantonment from November 2014 to October 2015. Results: The pre dialysis haematological parameters found in this study were TRBC: 3.4 ± 0.5 X 1012/L, haemoglobin (Hb) level : 9.5 ± 1.4 gm/dL, Haematocrit (HCT): 29.1 ± 4.4%, Mean corpuscular volume (MCV): 83.5 ± 7 fl, Mean corpuscular Hb (MCH): 28 ± 1.8 pg, Mean corpuscular Hb concentration (MCHC): 31.0 ± 2.9 gm/dl, Total leucocyte count (TLC): 6.6 ± 1.9 X109/L, Neutrophil: 66.3 ± 7.8 %, Lymphocyte: 24.5 ± 6.9 %, Monocyte: 5.0 ± 1.8%, Eosinophil: 4.1 ± 2.4 %, Platelet: 184.3 ± 66.5 X 109/L. One hour post HD values are: TRBC: 3.6 ± 0.6 X1012/L, Hb level:10.1 ± 1.6 gm/dl, Hct: 30.9 ± 5 %, MCV:82.6 ± 6.9 fl, MCH: 29.1 ± 2.3 pg, MCHC: 32.2 ± 3.4 gm/dl,TLC: 7.3 ± 2.3 X 109/L, Neutrophil: 69.2 ± 7 %, Lymphocyte: 21.6 ± 5.5 %, Monocyte: 5.3 ± 2 %, Eosinophil: 3.9 ± 2.3%. Platelet: 206.1 ± 63.6 X109/L. Among these values TRBC, Hb level, Hct, MCH, MCHC, TLC, Neutrophil, Lymphocyte and Platelet count significantly improved after HD (p value < .05). Conclusion: Haemodialysis in the management of patients with CKD/ESRD played a pivotal role in improving haematological parameters deranged by these conditions. JAFMC Bangladesh. Vol 18, No 1 (June) 2022: 39-42

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“…DDAVP's reducing effect on bleeding time starts within 1 h and continues for 4-8 h. Bleeding time returns to normal in 24 h (Mannucci et al, 1983;Galbusera et al, 2009). DDAVP has been shown to effectively reduce bleeding time when administered intravenously (0.3 microg⁄kg) by the subcutaneous and intranasal routes (Mannucci et al, 1983;Shapiro & Kelleher, 1984;Ulusoy et al,2004;Viganò et al, 1989). One of the things that must not be forgotten in desmopressin therapy is that efficacy may decline with increasing use, probably in association with a decline in endothelial vWF stores (Canavese et al, 1985).…”

Section: Desmopressinmentioning

confidence: 99%

Bleeding Diathesis in Hemodialysis Patients

Özkan¹,

Ulusoy²

2013

Hemodialysis

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A knowledge of normal hemostasis is needed in order to understand hemostatic disorders in uremic patients. The normal hemostatic process establishes blood viscosity inside the vessel and rapid plaque formation as a result of vascular injury. Hemostasis consists of three phases primary hemostasis, coagulation and fibrinolysis Galbusera et al.,. Platelets assume the main role in primary hemostasis. Under normal conditions, it prevents vascular endothelium platelet aggregation and adhesion. In the event of vascular injury, plateletmediated hemostatic plaque formation begins Stassen et al.,. Two main platelet receptors, glycoprotein Ib GPIb and activation-dependent glycoprotein IIb-IIIa GPIIb-IIIa complex, and the adhesion molecule von Willebrand factor VWF and fibrinogen are involved in the adhesion process in hemostatic plaque formation. Various modifications take place in the platelets after the adhesion phase, and molecules assisting platelet activation and adhesion, such as ADP, serotonin, epinephrine, fibrinogen, thromboxane and VWF, are released from the platelet granules Ruggeri et al.,. The coagulation phase consists of intrinsic and extrinsic coagulation pathways. A number of coagulation proteins are involved in these coagulation pathways, including Tissue Factor TF , and factors VII, IX, X, V, VIII, XI and XIII. Natural inhibitors of the coagulation cascade are protein C, Tissue factor TF pathway inhibitor and antithrombin III Stassen et al.,. The fibrinolytic system leads to plasmin-mediated dissolution of fibrin. Molecules serving in this system are the plasminogen activator inhibitors PAI-and PAI-, the plasmin inhibitor alpha--antiplasmin, alpha--macroglobulin and thrombin activatable fibrinolysis inhibitor TAFI Fay et al., . . Bleeding diathesis in uremic patientsThe relation between uremia and bleeding diathesis has been known for many years. Uremic patients used to be lost from bleeding from vital organs. Despite today's improvement in anemia with modern HD techniques and erythropoietin therapy, bleeding diathesis continues to represent a significant problem. There may be serious, life-threatening bleeding, and surgical procedures may be delayed or not performed at all out of concern over bleeding diathesis. This causes a rise in patient morbidity. The most common cause of uremic bleeding diathesis is impaired primary hemostasis. The most frequent complications seen as a reflection of primary hemostasis disorders are petechiae, purpura, and bleeding in the arteriovenous fistula puncture site and regions where the HD catheter is inserted Galbusera et al., Remuzzi et al., . In addition, bleeding in vital organs may also be seen in uremia, leading to less frequently observed but fatal complications. In HD patients in particular, various HD therapy-related factors mean that bleeding complications to be seen more frequently. Although various rates have been citied in HD patients in different publications, the bleeding diathesis rate is around %-%, and bleeding-associated morbidity around % Davenport et a...

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Hemostatic and Fibrinolytic Response to Nasal Desmopressin in Hemodialysis Patients

Cited by 14 publications

References 14 publications

Impact of Hemodialysis on Bleeding Tendency in End Stage Renal Disease Patients

Impact of Hemodialysis on Bleeding Tendency in End Stage Renal Disease Patients

A Comparative Study on Haematological Changes before and One hour after Haemodialysis in Patients with End Stage Renal Disease

Bleeding Diathesis in Hemodialysis Patients

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