Abstract
Atrial fibrillation (AF) and chronic kidney disease (CKD) are strictly related; several independent risk factors of AF are often frequent in CKD patients. AF prevalence is very common among these patients, ranging between 15% and 20% in advanced stages of CKD. Moreover, the results of several studies showed that AF patients with end stage renal disease (ESRD) have a higher mortality rate than patients with preserved renal function due to an increased incidence of stroke and an unpredicted elevated hemorrhagic risk. Direct oral anticoagulants (DOACs) are currently contraindicated in patients with ESRD and vitamin K antagonists (VKAs), remaining the only drugs allowed, although they show numerous critical issues such as a narrow therapeutic window, increased tissue calcification and an unfavorable risk/benefit ratio with low stroke prevention effect and augmented risk of major bleeding. The purpose of this review is to shed light on the applications of DOAC therapy in CKD patients, especially in ESRD patients.
Highlights
The prevalence of atrial fibrillation (AF) in the general population ranges between 0.5%and 1%, with peaks of 8% in patients over 80 years of age [1]
The aim of this review is to evaluate how treatment with Direct oral anticoagulants (DOACs) affects
Apy in Atrial fibrillation (AF) patients with diabetes mellitus (DM) and chronic kidney disease (CKD) may be more challenging because both DM and CKD have been independently associated with an increased thromboembolic and bleeding risk, which results from the prothrombotic and pro-inflammatory status [81,82,83,84,85]
Summary
The prevalence of atrial fibrillation (AF) in the general population ranges between 0.5%. Chronic kidney disease (CKD) is associated with increased cardiovascular disease risk and all-cause mortality [8,9,10] and is highly prevalent in the AF population, affecting 40–50% of patients with AF (Figure 1) [11,12,13]. < 30 mL/min) are atthese increased riskexareFurthermore, not inferior to warfarin foradvanced stroke orCKD systemic embolism; studies of cluded bleeding from uremia-induced platelet dysfunction and invasive relatedwith to patients on dialysis, those with an eGFR < 25–30. DOACs affects cluded patients on dialysis, those with an eGFR < 25–30 mL/min and those treated with strokeKand bleeding (VKA). All data concernparticular consideration is given the role of mL/min long-termcame oral anticoagulant therapy in renal ing use of DOACs in patients withtoeGFR. The aim of this review is to evaluate how treatment with DOACs affects
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