Reporter: Aviva Lev-Ari, PhD, RN
Stroke and Bleeding in Atrial Fibrillation with Chronic Kidney Disease
Original Article
Stroke and Bleeding in Atrial Fibrillation with Chronic Kidney Disease
J.B. Olesen and Others
The prevalence of both atrial fibrillation and chronic kidney disease increases with age. The prevalence of atrial fibrillation is 2.3% among persons 40 years of age or older and 5.9% among those 65 years of age or older, and the prevalence of end-stage renal disease increases from approximately 3.5% among persons 45 to 64 years of age to nearly 6% among those 75 years of age or older. Many patients have both disorders, and the number of such patients is increasing, owing in part to the aging population and the improved survival in both diseases.
Clinical Pearls
What is the effect of chronic kidney disease on the risk of stroke?
The U.S.-based Renal Data System has reported that chronic kidney disease increases the risk of stroke by a factor of 3.7, and end-stage renal disease (i.e., disease requiring renal-replacement therapy) increases the risk by a factor of 5.8. Atrial fibrillation increases the risk of stroke by a factor of 5, and chronic kidney disease increases the risk of stroke among patients without atrial fibrillation.
What is a CHA2DS2-VASc score?
This study evaluated the risk of stroke or systemic thromboembolism, with adjustment for CHA2DS2-VASc risk factors. The CHA2DS2-VASc score extends the CHADS2 algorithm to include additional nonmajor risk factors for stroke, including vascular disease (V), age between 65 to 74 years (A), and female gender (sex category or Sc).
Morning Report Questions
Q. What were the results of this study of patients with atrial fibrillation and chronic kidney disease with respect to risk of stroke or systemic embolism?
A. This study demonstrated that warfarin treatment was associated with a significantly decreased risk of stroke or systemic thromboembolism overall and among patients requiring renal-replacement therapy, and with a nonsignificantly decreased risk among patients with non–end-stage chronic kidney disease. In an analysis that compared all patients who had any renal disease with those who had no renal disease, warfarin decreased the risk of stroke or systemic thromboembolism (hazard ratio, 0.76; 95% CI, 0.64 to 0.91; P=0.003), as did warfarin plus aspirin (hazard ratio, 0.74; 95% CI, 0.56 to 0.98; P=0.04). Aspirin alone was associated with an increased risk of stroke or systemic thromboembolism overall and among patients who had any renal disease, as compared with those who had no renal disease (hazard ratio, 1.17; 95% CI, 1.01 to 1.35; P=0.04).
Table 3. Hazard Ratios for Stroke or Systemic Thromboembolism.
Q. How did the risk of bleeding differ among patients with and without kidney disease?
A. The risk of bleeding was higher among patients with non–end-stage chronic kidney disease and among patients requiring renal-replacement therapy as compared to patients without renal disease, and treatment with warfarin, aspirin, or both incrementally increased this risk. Among all patients who had any renal disease, as compared with those who had no renal disease, there was an increased risk of bleeding with warfarin (hazard ratio, 1.33; 95% CI, 1.16 to 1.53; P<0.001), aspirin (hazard ratio, 1.17; 95% CI, 1.02 to 1.34; P=0.03), and warfarin plus aspirin (hazard ratio, 1.61; 95% CI, 1.32 to 1.96; P<0.001). Among patients with non–end-stage chronic kidney disease, the risk of bleeding increased with a higher dose of loop diuretics. The risk of bleeding was highest among patients with chronic glomerulonephritis and lowest among those with chronic tubulointerstitial nephropathy.
Table 4. Hazard Ratios for Bleeding.
Stroke and Bleeding in Atrial Fibrillation with Chronic Kidney Disease
Jonas Bjerring Olesen, M.D., Gregory Y.H. Lip, M.D., Anne-Lise Kamper, M.D., D.M.Sc., Kristine Hommel, M.D., Lars Køber, M.D., D.M.Sc., Deirdre A. Lane, Ph.D., Jesper Lindhardsen, M.D., Gunnar Hilmar Gislason, M.D., Ph.D., and Christian Torp-Pedersen, M.D., D.M.Sc.
The study of stroke and CRF is interesting. The incidence of thromboembolism has to be also related to decreased cardiac output and decreased venous return, both of which would be tied to a low MAP. Of course this is managed with warfarin, which is also the most common cause of admission to a hospital in elderly people from falls with large hematomas. An inadequate warfarin doing would be in favor of thromboembolism. A TE in the presence of atrial septal defect would go from right to left without reaching the lung (uncommon), but it could be a cause of stroke. So for a stroke to develop otherwise would have to be related to thromus formation in and beyond the carotid artery.
Another allied issue has to be the development of acidemia and hyperkalemia in CRF with the dependence of H/K exchange at the tubular level. In order to lose H, it is necessary to retain K. There is a comparable molecular size, so that there can be a reciprocal loss of K. We are also looking at a patient at stage 4 or 5 CKD with eGFR of < 60, but more likely < 45 ml/min.
What about the CHF? There will be left ventricular hypertrophy, and the hs-troponin will be high as well as the amino terminal pro b-type natriuretic peptide. The understanding of the troponin part of the story is not so good. There is a huge amount of interest in the NT-proBNP. The only way to handle the NT-proBNP in the lab data requires adjustment for the eGFR.
I don't see how it is possible to get on top of this complicated situation without a much better study design and use of todays computational power.
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