Hemostasis, Platelet Functions, Serotonin and Serum Lipids during Omega-3 Fatty Acid Treatment in Patients with Glomerulonephritis

Małyszko, Jolanta; Pawlak, Dariusz; Buczko, Włodzimierz; Myśliwiec, Michał

doi:10.1159/000045140

Cited by 1 publication

(2 citation statements)

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“…Diminished platelet reactivity in response to other agonists such as adenosine diphosphate (ADP), arachidonic acid (AA) and collagen is also commonly found in kidney failure. 11,16,42 Impaired ADP-dependent aggregation was associated with elevated GSA levels. 34,35 Additionally, GSA stimulates the production of the vasoactive nitric oxide (NO) which prevents platelet-vessel wall and platelet-platelet interactions by producing the platelet inhibitor cyclic guanosine monophosphate (cGMP).…”

Section: Platelet Dysfunction and Thrombo-modulationmentioning

confidence: 99%

“…The GPIIb/IIIa platelet receptor was assessed in response to thrombin receptor activating peptide (TRAP) using platelet aggregometry in a study by Pluta et al 41 This test showed a significantly lower response in kidney failure patients when compared to normal controls. Diminished platelet reactivity in response to other agonists such as adenosine diphosphate (ADP), arachidonic acid (AA) and collagen is also commonly found in kidney failure 11,16,42 . Impaired ADP‐dependent aggregation was associated with elevated GSA levels 34,35 .…”

Section: Haemostatic Alterations In Kidney Failurementioning

confidence: 99%

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Navigating through the haemostatic paradox in kidney failure: A practical overview

et al. 2023

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Summary Chronic kidney disease (CKD) affects around 9.1% of humankind globally resulting in a significant health burden. Some of these individuals will also require renal replacement therapy with dialysis due to complete kidney failure. Patients with CKD are known to be at increased risk of both bleeding and thrombosis. Often it is very difficult to manage these yin and yang since both risks tend to co‐exist. Clinically, very few studies have looked at the effects of antiplatelet agents and anticoagulants in this highly vulnerable subgroup of medical patients and evidence is very limited. This review attempts to explain the current state‐of‐the‐art regarding the basic science of haemostasis in patients with end‐stage kidney disease. We also try to transfer this knowledge into the clinics by looking at some common haemostasis challenges that are encountered in this cohort of patients and what evidence and guidance there is for their optimal management.

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