Epidemiologic data suggest that individuals at all stages of CKD have a higher risk of developing cognitive disorders and dementia. This risk is generally explained by the high prevalence of both symptomatic and subclinical ischemic cerebrovascular lesions. However, other potential mechanisms, including direct neuronal injury by uremic toxins, could also be involved, especially in the absence of obvious cerebrovascular disease. We discuss the prevalence and characteristics of cognitive disorders and dementia in patients with CKD, brain imaging findings, and traditional and nontraditional risk factors. Understanding the pathophysiologic interactions between renal impairment and brain function is important in order to minimize the risk for future cognitive impairment.

Chronic kidney disease (CKD) is associated with vascular calcifications and atherosclerosis. There is a need for novel predictors to allow earlier diagnosis of these disorders, predict disease progression, and improve assessment of treatment response. We focused on microRNAs since they are implicated in a variety of cellular functions in cardiovascular pathology. We examined changes of microRNA expression in aortas of CKD and non-CKD wild type mice and apolipoprotein E knock-out mice, respectively. Both vascular smooth muscle-specific miR-143 and miR-145 expressions were decreased in states of atherosclerosis and/or CKD or both, and the expression level of protein target Myocardin was increased. The inflammatory miR-223 was increased in more advanced stages of CKD, and specific protein targets NFI-A and GLUT-4 were dramatically decreased. Expression of miR-126 was markedly increased and expression of protein targets VCAM-1 and SDF-1 was altered during the course of CKD. The drug sevelamer, commonly used in CKD, corrected partially these changes in microRNA expression, suggesting a direct link between the observed microRNA alterations and uremic vascular toxicity. Finally, miR-126, -143 and -223 expression levels were deregulated in murine serum during the course of experimental CKD. In conclusion, these miRNAs could have role(s) in CKD vascular remodeling and may therefore represent useful targets to prevent or treat complications of CKD.

Background and objectives: Intracranial artery calcification (IAC) is frequently observed on brain computed tomography (CT) scans in stroke patients. This retrospective study was designed to determine the prevalence, risk factors, and clinical relevance of IAC in a cohort of patients with ischemic stroke.Design, setting, participants, & measurements: We included all eligible patients admitted to Amiens University Hospital for acute ischemic stroke between January and December 2006 and assessed using 64-slice multidetector-row CT (n ‫؍‬ 340). Patients were classified according to the presence or absence of IAC in the internal carotid arteries, middle cerebral arteries, vertebral arteries, and basilar artery. GFR was estimated using the MDRD equation. Chronic kidney disease (CKD) was defined as a GFR < 60 ml/min/1.73 m 2 . We also studied a control group of patients admitted for neurologic diseases other than stroke.Results: Two hundred fifty-nine stroke patients (76.2%) displayed IAC, which was independently associated with carotid atherosclerosis > 50%, age, and GFR. One hundred three nonstroke patients (60.2%) had IAC, with age, arterial hypertension, and GFR as independently associated factors. For all patients taken together, age, arterial hypertension, stroke, and GFR were independently associated with IAC.Conclusion: These results confirm the high prevalence of IAC in patients with and without ischemic stroke and show for the first time that IAC is associated with the presence of CKD in these patients. The frequency of IAC was significantly higher in stroke patients than in nonstroke patients. The association between IAC and stroke outcome requires further investigation.

In cryptogenic ischaemic stroke, the NDAF score can be used to target patients at high risk of developing AF after hospital discharge, as a score of 0-1 was highly predictive of the absence of NDAF during follow-up. These results need to be confirmed in prospective studies.