Aspects of platelet disturbances in haemodialysis patients

Abstract

Patients with mild-to-chronic kidney disease (CKD) exhibit a variety of haemostatic disorders, ranging from an increased clotting tendency and reductions in the levels of natural inhibitors of coagulation to defective fibrinolysis. In addition, platelet (PLT) abnormalities are common. In this minireview, we report on aspects of haemodialysis (HD)-induced PLT activation. It is demonstrated that PLTs from HD patients are exhausted due to repeated stimulation of HD treatment and recurrent release of PLT degranulation products. During HD, additional aberrations of the haemostatic process occur. Besides deviations of coagulation and fibrinolysis, PLT activation and a reduction in their granule content have been observed during HD treatment. As HD treatment is carried out three times per week, month after month, chronic HD patients may suffer persistently from coagulation defects and PLT disorders on top of the alterations induced by the uraemic state itself. PLT activation occurs together with thrombin and fibrin generation. However, macro fibrin depositions in clot devices are not demonstrated, microaggregates occur not only in the extracorporeal circuit (ECC) but are also present in the blood circulation. As vascular access thrombosis is a frequent complication in patients with HD treatment, it is believed that hypercoagulability could result from vascular changes combined with PLTs and activation of coagulation factors.

The Uremic Toxin Indoxyl Sulfate Accelerates Thrombotic Response after Vascular Injury in Animal Models

“…Chronic kidney disease (CKD) is a pandemic problem with a global prevalence of 11–13% [ 1 ]. Patients suffering from CKD display a broad spectrum of hemostatic disorders leading on the one hand to increased bleeding tendencies, and to thrombosis on the other [ 2 , 3 ]. Generally, CKD is connected to an increased risk for thrombotic events, including incidence of cerebrovascular disease, myocardial infarction, and pulmonary embolism, as well as postangioplasty or stent thrombosis [ 4 ].…”

Protective Effect of Apelin-13 on Kidney and Platelet Functions in Adenine-Induced Chronic Renal Failure in Rats

“…Therefore, increased platelet count may reflect a proinflammatory condition with platelet activation [63] . On contrary, Salvati and Liani [64] and Schoorl, Grooteman [19] found that platelet count was decreased in end stage renal failure. This discrepancy was explained by difference in stage of CRF as in their studies, there was an end stage CRF with platelet exhaustion from repeated stimulation by false ligands as fibrinogen fragments.…”

“…On the other hand, an increased platelet reactivity has been reported in patients with CRF [17,18] . On the contrary, Schoorl, Grooteman [19] found that there was a decrease in platelet function and an increase in the risk of hemorrhage in CRF. Moreover, Adams, Irish [20] declared that impaired renal function exposed patients to a higher risk of thrombosis.…”

Direct Oral Anticoagulants in End-Stage Renal Disease

“…17 In hemodialysis patients, repetitive activation of platelets is thought to lead to platelet "exhaustion" and consequent dysfunction. 26 Several studies have been published on bleeding risk with VKA among patients with ESRD (►Table 2). While differing in study design and methodology, most of the larger (> 100 VKA users) studies reported major bleeding rates of 10 per 100 person-years or higher.…”