J Thromb Haemost. 2015 Dec 16;
Authors: Wheeler DS, Giugliano RP, Rangaswami JR
Anticoagulation-related nephropathy (ARN) is a significant but under-diagnosed complication of anticoagulation that is associated with increased renal morbidity and all-cause mortality. Originally described in patients on supratherapeutic doses of warfarin who had a distinct pattern of glomerular hemorrhage on kidney biopsy, ARN is currently defined as acute kidney injury without obvious etiology in the setting of an International Normalized Ratio greater than 3.0. The underlying molecular mechanism is thought to be due to warfarin-induced thrombin depletion, however newer studies hint at an alternate mechanism involving reduction in activate protein C and endothelial protein C receptor signaling. Prompt recognition of ARN is critical as it is associated with accelerated progression of chronic kidney disease (CKD) and a significant increase in short and long term all-cause mortality. Prior investigations into ARN have almost universally focused on anticoagulation with warfarin however recent case reports and animal studies suggest that is can also occur in patients taking novel oral anticoagulants (NOACs). Differences in the incidence and severity of ARN in patients taking warfarin as opposed to NOACs are unknown; a post-hoc analysis of routinely reported adverse renal outcomes in clinical trials comparing warfarin and NOACs finds no significant difference in the rates of acute kidney injury, a prerequisite for ARN. Given the significant impact of ARN on renal function and all-cause mortality, a thorough understanding of the pathophysiology, molecular mechanisms, clinical spectrum, and therapeutic interventions for ARN is crucial to balance the risks and benefits of anticoagulation and optimize treatment. This article is protected by copyright. All rights reserved.
PMID: 26670286 [PubMed - as supplied by publisher]