PROGRESSION OF ANTICOAGULANT-RELATED NEPHROPATHY AFTER ANTICOAGULANT THERAPY

7 Feb 2025 12 a.m. 12 a.m.
WCN25-AB-3811, Poster Board= FRI-143

Introduction:

Anticoagulant-related nephropathy (ARN) is a recently discovered cause of AKI and possibly, progressive CKD as well. It occurs in patients receiving oral anticoagulant therapy, namely warfarin or a novel oral anticoagulant (NOAC). Many multi-center studies indicate that ARN occurs in up to 30 % of patients exposed to supratherapeutic INR when treated with vitamin K antagonists but little is known about ARN in direct oral anticoagulants. Our aim was to determine the incidence of ARN in patients with atrial fibrillation initiating (AF) oral anticoagulant treatment.

Methods:

We included consecutive anticoagulant-naive patients with AF referred to our anticoagulation clinic. Before initiation of therapy and after 6 months of treatment, urine and blood samples were collected. We defined ARN as a rise in serum creatinine by at least 27 mmol/l (SCr >0.3 mg/dl) or by at least 50 % after initiation of anticoagulant therapy. We also followed concentration of cystatin C and presence of proteinuria and erythrocyturia as markers of renal damage.

Results:

We included 137 consecutive patients. All patients required anticoagulant treatment for AF. Patients received apixaban 55 (40.1%), rivaroxaban 39 (28.5%), dabigatran 27 (19.7%) or warfarin 16 (11.7%) (Table 1). None of the patients received direct oral anticoagulants developed ARN. The only significant difference was a slight rise in concentration of cystatin C but the absolute difference was not significant. Despite the similar basal renal function between the warfarin and DOAC groups, the sCr level was higher and the eGFR was lower in patients with warfarin than DOAC group after follow-up period. The independent risk factors for the development of warfarin related nephropathy (WRN) in this study were coexisting congestive heart failure (CHF) and low serum basal albumin level.

Conclusions:

ARN appears to be rare during the follow-up period after initiating anticoagulant treatment. It is important that irrespective of renal dysfunction, a lower basal serum albumin level, a higher serum AST level at post INR elevation, and comorbidity such as CHF were independent predictors of WRN.

I have no potential conflict of interest to disclose.

I did not use generative AI and AI-assisted technologies in the writing process.