Risk of overanticoagulation during acute kidney injury in patients treated with vitamin K antagonists.
acute kidney injury
anticoagulant therapy
bleeding
chronic kidney disease
drug interactions
Journal
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
ISSN: 1460-2385
Titre abrégé: Nephrol Dial Transplant
Pays: England
ID NLM: 8706402
Informations de publication
Date de publication:
25 03 2022
25 03 2022
Historique:
received:
14
09
2020
pubmed:
19
1
2021
medline:
28
4
2022
entrez:
18
1
2021
Statut:
ppublish
Résumé
Vitamin K antagonists (VKAs) are still in use for oral anticoagulation, but not all indications allow their replacement by direct oral anticoagulants. Although formal dose reduction is not required in patients with impaired kidney function, case reports indicate that acute kidney injury (AKI) might be associated with derailment of VKA therapy. The study retrospectively collected patients from a tertiary nephrology care centre who experienced AKI while being treated with VKA. In these individuals, the international normalized ratio (INR) as a measure of anticoagulant effect during renal failure was compared with a reference time point with stable kidney function. A total of 100 patients with AKI and ongoing VKA therapy met the inclusion criteria. The majority (76%) of patients had AKI with CKD. Volume depletion (n = 43), septic renal failure (n = 22), decompensated heart failure (n = 18) and toxic renal damage (n = 11) were the most important causes of AKI. The average INR values at the time of AKI were higher than at the reference time point [median 3.17 (range 1.10-13.0) versus 2.24 (1.07-5.17); P < 0.0001]. Fifty-four patients had INR values above the recommended therapeutic range for their indication at the time point of AKI. Bleeding complications occurred in 24 patients during AKI and the VKA dose had to be reduced in 55. Women, patients with low body mass index and patients with diabetes were predisposed to overanticoagulation during AKI. The effect of AKI on anticoagulation by VKA has not been systematically described. This risk should be considered in patients at high risk for AKI.
Sections du résumé
BACKGROUND
Vitamin K antagonists (VKAs) are still in use for oral anticoagulation, but not all indications allow their replacement by direct oral anticoagulants. Although formal dose reduction is not required in patients with impaired kidney function, case reports indicate that acute kidney injury (AKI) might be associated with derailment of VKA therapy.
METHODS
The study retrospectively collected patients from a tertiary nephrology care centre who experienced AKI while being treated with VKA. In these individuals, the international normalized ratio (INR) as a measure of anticoagulant effect during renal failure was compared with a reference time point with stable kidney function.
RESULTS
A total of 100 patients with AKI and ongoing VKA therapy met the inclusion criteria. The majority (76%) of patients had AKI with CKD. Volume depletion (n = 43), septic renal failure (n = 22), decompensated heart failure (n = 18) and toxic renal damage (n = 11) were the most important causes of AKI. The average INR values at the time of AKI were higher than at the reference time point [median 3.17 (range 1.10-13.0) versus 2.24 (1.07-5.17); P < 0.0001]. Fifty-four patients had INR values above the recommended therapeutic range for their indication at the time point of AKI. Bleeding complications occurred in 24 patients during AKI and the VKA dose had to be reduced in 55. Women, patients with low body mass index and patients with diabetes were predisposed to overanticoagulation during AKI.
CONCLUSIONS
The effect of AKI on anticoagulation by VKA has not been systematically described. This risk should be considered in patients at high risk for AKI.
Identifiants
pubmed: 33459792
pii: 6103794
doi: 10.1093/ndt/gfab008
pmc: PMC8951229
doi:
Substances chimiques
Anticoagulants
0
Fibrinolytic Agents
0
Vitamin K
12001-79-5
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
681-686Informations de copyright
© The Author(s) 2021. Published by Oxford University Press on behalf of the ERA.
Références
J Clin Pharmacol. 1976 Oct;16(10 Pt 1):468-72
pubmed: 977790
J Am Soc Nephrol. 2009 Oct;20(10):2223-33
pubmed: 19713308
Arch Intern Med. 2005 May 23;165(10):1095-106
pubmed: 15911722
Clin Pharmacol Ther. 2003 May;73(5):427-34
pubmed: 12732843
Eur Heart J. 2017 Sep 21;38(36):2739-2791
pubmed: 28886619
Eur Heart J. 2016 Oct 7;37(38):2893-2962
pubmed: 27567408
Ugeskr Laeger. 2009 Mar 16;171(12):1012
pubmed: 19284926
Clin Pharmacokinet. 2005;44(12):1227-46
pubmed: 16372822
J Am Soc Nephrol. 2018 Dec;29(12):2787-2793
pubmed: 30420420
Expert Opin Drug Metab Toxicol. 2008 Aug;4(8):1065-74
pubmed: 18680441
Ann Intern Med. 2009 May 5;150(9):604-12
pubmed: 19414839
Chest. 2016 Apr;149(4):951-9
pubmed: 26378611
Arch Intern Med. 2000 Jun 12;160(11):1612-7
pubmed: 10847254
Clin Pharmacol Ther. 2003 May;73(5):475-7
pubmed: 12732848
J Gen Intern Med. 2007 Jun;22(6):727-35
pubmed: 17401605
Br J Pharmacol. 1979 Jun;66(2):275-81
pubmed: 465881
Clin J Am Soc Nephrol. 2019 Aug 7;14(8):1183-1192
pubmed: 31311818
JAMA Intern Med. 2014 Mar;174(3):409-16
pubmed: 24445404
Am J Kidney Dis. 2015 May;65(5):701-9
pubmed: 25468385
Br J Anaesth. 1993 Aug;71(2):282-90
pubmed: 8123408
Eur J Clin Pharmacol. 1977;11(1):27-32
pubmed: 832654
Br J Haematol. 2003 Feb;120(3):526-8
pubmed: 12580973