Increased Number and Distribution of Cerebral Microbleeds Is a Risk Factor for Cognitive Dysfunction in Hemodialysis Patients

Abstract

The aim of this study was to explore the risk factors associated with longitudinal changes in hemodialysis patients including the correlation between number and distribution of cerebral microbleeds (CMBs).Sixty-one hemodialysis patients were enrolled in this prospective study. Twenty-eight patients had follow-up examinations with a mean interval of 24.79 ± 5.17 months. The number of CMBs was manually counted on susceptibility-weighted imaging. Subjects were divided into 2 groups with and without CMBs. In the CMB group, 8 of 33 patients did not have a mini-mental state examination (MMSE) because of blurred vision. Multiple logistic regression was used to investigate the risk factors for CMBs. Partial correlation was used to explore the correlation between the increased number of CMBs and the change of MMSE scores.CMBs were seen in 33 (54%) hemodialysis patients. Both age and pre/postdialysis systolic blood pressure (SBP) positively correlated with CMBs. Serum iron (SI), and high-density lipoprotein cholesterol (HDL-c) negatively correlated with CMBs (all P < 0.05). Among 25 patients with CMBs and MMSE, 9 patients had scores <27, which was considered as subnormal and most CMBs in these patients were located in the brainstem and basal ganglia. Considering age and follow-up time as the co-confounding factors, the number of new CMBs over the 2 imaging time points negatively correlated with the change of MMSE scores (r = −0.673, P = 0.023).The presence of new CMBs was a risk factor for cognitive dysfunction and the location of CMBs may be correlated with cognitive impairment. Both SI and HDL-c were protective factors for the CMBs. The risk factors for CMBs included age, pre- and postdialysis SBP.

Hypertension impairs neurovascular coupling and promotes microvascular injury: role in exacerbation of Alzheimer’s disease

“…Cerebral microhemorrhages (CMHs; also described as microbleeds) are small chronic intracerebral hemorrhages (< 5 to 10 mm in diameter), which develop due to the rupture of small arteries, arterioles, and/or capillaries (Ungvari et al 2017b). Hypertension (Jeerakathil et al 2004;Cordonnier et al 2007;Romero et al 2014;Roob et al 1999;Sveinbjornsdottir et al 2008;Vernooij et al 2008), advanced age (Jeerakathil et al 2004;Chai et al 2016;Caunca et al 2016), and cerebral amyloid angiopathy and AD (Yates et al 2011(Yates et al , 2014Pettersen et al 2008;Benedictus et al 2013) are the major risk factors for CMHs. The prevalence of CMHs reaches 50% in patients at risk (Ungvari et al 2017b).…”

The significant effects of cerebral microbleeds on cognitive dysfunction: An updated meta-analysis

“…A subgroup analysis of MMSE with 16 studies [ 5 , 6 , 16 , 17 , 19 – 22 , 24 , 26 – 28 , 30 , 31 , 33 , 37 ] was carried out and divided into different age groups. A random-effect model was used with I 2 of 82%, and SMD: -0.3498 [-0.5624, -0.1372] ( p <0.05).…”

A Single Neonatal Exposure to BMAA in a Rat Model Produces Neuropathology Consistent with Neurodegenerative Diseases

“…Microbleeds, as observed in 86% of AD patients [ 104 ], are caused by the deposition of Aβ in cerebral vessels that leads to weakening of artery walls and thus an increased risk of vessel rupture that could subsequently cause blood-breakdown products to leak into brain tissues adjacent from the damaged fragile vessels [ 105 ]. Interestingly, Chai et al [ 106 ] reported increased cerebral microbleeds in the striatum of patients with chronic renal failure to be a significant risk factor of neurocognitive impairment. This suggests that the observed microbleeds in BMAA-exposed rats could contribute to the cognitive impairments in rats exposed to BMAA on PND3, 4 and 5 that was observed by Scott and Downing [ 55 ].…”