Abstract

Background: Among patients with ischemic stroke, a link between chronic kidney disease (CKD) and presence of MRI-defined cerebral microbleeds (CMB), a harbinger of future hemorrhagic stroke, has been reported. However, the association of CKD with CMB among patients with intracerebral hemorrhage (ICH) has not been systematically investigated. The objective of this analysis was to evaluate the relationship between CKD and CMB in a biracial cohort of patients with ICH. Methods: Using data from subjects with a recent ICH enrolled in a NIH-sponsored observational study between September 2007, and June 2011, we evaluated the association between CKD (defined as estimated low glomerular filtration rate (GFR) <60 ml/min per 1.73 m 2 ) and CMB. The number and location of CMBs were identified on gradient-echo T2*-weighted magnetic resonance imaging. Multivariable models were generated to determine the contribution of CKD to the presence, number, and location of CMB after adjusting for confounders (age, sex, systolic BP, history of hypertension, antihypertensive drug use, and diabetes). Results: Of 162 subjects with complete data, mean age was 59 years, 44% were female, 74% were Black, 97 (60%) had 1 or more CMBs and 47 (29%) had CKD. In univariate analyses, subjects with CKD differed from those without CKD (p<0.1): history of hypertension (100% vs. 81%), history of diabetes (34% vs. 21%), on antihypertensive drug (74% vs. 51%), on renin-angiotensin system [RAS] modulator (44% vs. 26%), higher systolic BP (186 vs. 173 mmHg), presence of CMB (75% vs. 54%), number of deep located CMB (62% vs. 44%), number of deep located CMB (median, IQR: 2 {0, 3} vs. 0 {0, 2}), and size of index ICH (median, IQR: 7.5 {2.3, 29.7} vs. 13.8 {5.2, 34.2}). Overall, CKD was independently associated with presence of CMB (adjusted OR 2.29, 95% CI: 1.00-5.22, p=0.049) and number of CMB (adjusted RR 1.91, 95% CI: 1.08-3.38, p=0.027). There was also a borderline interaction between RAS drug use and CKD for number (i.e. fewer CMB) but not presence of CMB (p=0.09). In Black subjects CKD was associated with CMB presence (adjusted OR 3.11, 95% CI: 1.47-6.59) and number (adjusted RR 3.43, 95% CI:1.22-9.67), but not CMB presence (adjusted OR 2.00, 95% CI:0.37-10.92) or number (adjusted RR 1.56, 95% CI:0.25-9.78) in Non-Hispanic White subjects (interactions by race: p=0.84 and 0.74 respectively). Conclusions: CKD is associated with presence, number and location of CMB in ICH patients. These relationships are more pronounced in Black compared to Non-Hispanic White ICH patients. Low GFR may be a CMB risk marker or potential therapeutic target for mitigating the development of CMB. Further investigation is required to see if RAS modulators may have a role to play in ameliorating CMB occurrence.

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