Distribution of Cerebral Microbleeds Determines Their Association with Impaired Kidney Function

Abstract

Background and PurposeCerebral microbleeds (CMBs) are associated with various pathologies of the cerebral small vessels according to their distribution (i.e., cerebral amyloid angiopathy or hypertensive angiopathy). We investigated the association between CMB location and kidney function in acute ischemic stroke patients.MethodsWe enrolled 1669 consecutive patients with acute ischemic stroke who underwent gradient-recalled echo brain magnetic resonance imaging. Kidney function was determined using the estimated glomerular filtration rate (eGFR). CMBs were classified into strictly lobar, strictly nonlobar (i.e., only deep or infratentorial), and a combination of both lobar and nonlobar. Multinomial logistic regression analyses were used to determine the factors associated with the existence of CMBs according to their location.ResultsThe patients were aged 66±12 years (mean±standard deviation), and 61.9% (1033/1669) of them were male. CMBs were found in 27.0% (452/1669) of the patients. The stroke subtypes of small-artery occlusion and cardioembolism occurred more frequently in those with strictly nonlobar CMBs (10.8%) and strictly lobar CMBs (48.8%), respectively. The mean eGFR was lower in the strictly nonlobar CMBs group (72±28 mL/min/1.73 m2) and the both lobar and nonlobar CMBs group (72±25 mL/min/1.73 m2) than in the no-CMBs group (86±29 mL/min/1.73 m2). Multivariate multinomial logistic regression revealed that eGFR <60 mL/min/1.73 m2 was independently related to strictly nonlobar CMBs (odds ratio=2.63, p=0.001).ConclusionsImpaired kidney function is associated with strictly nonlobar CMBs. Our findings indicate that the distribution of CMBs should be considered when evaluating their relationships or prognoses.

Common Impact of Chronic Kidney Disease and Brain Microhemorrhages on Cerebral Aβ Pathology in SHRSP

“…Our experimental data suggest a temporal pathological cascade beginning with arterial hypertension [at an age of around 6 weeks, ], proceeding to CKD (and to an early cerebral endothelial dysfunction, see below), microhemorrhages and then to Aβ pathology. Initial (hypertension‐induced) tubulointerstitial damage is supported by the high CKD frequency and the young age of renal disease onset (at 14 weeks) in SHRSP ( Supporting Information Table S1 ), and is in line with published data indicating that renal dysfunction predicts cerebral microhemorrhages . Aβ deposits were depicted at 20 weeks of age, and small bleeds occurred first at later ages of 24 weeks, which may account for some independency of Aβ pathology and microhemorrhages.…”

“…Age‐dependent spontaneous systemic arteriolar and endothelial dysfunction as well as common susceptibilities of the renal and cerebral microvasculature to cardiovascular risk factors have been proposed to be the main link between CKD and cognitive decline, basically explaining the association between renal disease and the vascular dementia subtype. Recently reported relationships between impaired renal function, cerebral microbleeds and white matter hyperintensities account for a more direct link between cerebral small vessel pathology and CKD . In addition, direct associations between CKD and neurodegeneration, which are independent from microvascular pathology have been discussed , as have associations between CKD and increased serum amyloid‐β (Aβ) levels , further suggesting an impact of kidney damage on Alzheimer's disease (AD) pathology.…”

Moderate-to-severe obstructive sleep apnea is associated with cerebral small vessel disease

“…An ALI was defined as a 3-15 mm lesion showing as hyperintense on axial T2-weighted images and hypointense on axial T1-weighted images in a subject lacking a relevant history of symptoms or signs [8]. The CMBs were identified as punctate hypointense lesions <10 mm in size on GRE images [14]. The PVSs were defined as punctate or linear hyperintense lesions on T2-weighted images in the basal ganglia and <3 mm in size [12].…”

Assessment of cerebral microbleeds by susceptibility-weighted imaging at 3T in patients with end-stage organ failure

“…In the chronic kidney failure population, diminished estimated glomerular filtration rate has been found to be a risk factor for CMBs [31]. Moreover, chronic kidney failure is correlated with the number of CMBs, thus, the number of CMBs can provide an indirect estimation of chronic kidney failure severity [33][34][35][36].…”