Relationship between chronic kidney disease and white matter hyperintensities on magnetic resonance imaging.

Renal dysfunction may be related to cerebral small-vessel disease. This study aimed to assess the relationship between mild renal dysfunction and various white matter hyperintensities on magnetic resonance imaging (MRI). A total of 2106 subjects (1368 men and 738 women; mean age, 56 ± 10 years) without a history of stroke were enrolled in the study. Kidney function was evaluated in terms of estimated glomerular filtration rate (eGFR), calculated using the relationship 194Cr(-1.094) × age(-0.287) × 0.739 (if female), where Cr is serum creatinine concentration. White matter hyperintensity on T2-weighted MRI was classified as deep and/or subcortical white matter hyperintensity (DSWMH), periventricular hyperintensity (PVH), or asymptomatic cerebral infarction (ACI). The prevalence of ACI, DSWMH, and PVH was significantly correlated with degree of eGFR reduction; in the subgroups with eGFR ≥ 90, 60∼89, and <60 mL/min/1.73 m(2), the following prevalences were found: ACI, 7%, 6%, and 16%; DSWMH, 18%, 21%, and 37%; PVH: 7%, 10%, and 21%. The odds ratios for ACI, DSWMH, and PVH of eGFR <60 mL/min/1.73 m(2) were significantly increased, to 2.11 (95% confidence interval [CI], 1.23-3.61; P = .006), 2.26 (1.53-3.34; P < .001), and 2.81 (1.67-4.72; P < .001), respectively. Our data indicate that mild renal dysfunction may be associated with an increase in cerebral small-vessel disease independent of hypertension.

Chronic kidney disease in patients with ischemic stroke.

To examine the significance of renal dysfunction in patients who have sustained ischemic stroke, we examined the relationship between the renal function evaluated in terms of estimated glomerular filtration rate (eGFR) and the subtype of brain infarction (BI) in patients with ischemic stroke. A total of 639 patients with BI were enrolled in this study, with 314 subjects without stroke or transient ischemic attack registered as age-matched controls. eGFR was calculated according to the equation 194 × Cr(-1.094) × Age(-0.287) (-0.739 if female), where Cr is serum creatinine concentration, and was classified into four stages: stage I, eGFR ≥ 90 mL/min/1.73 m(2); stage II, eGFR 60 ~ 89 mL/min/1.73 m(2); stage III, eGFR 30 ~ 59 mL/min/1.73 m(2); and stage IV, eGFR <29 mL/min/1.73 m(2). Stage III-IV was significantly more prevalent in the BI group (38%) than in the control group (22%; P < .001). The odds ratio for stage III-IV was significantly higher in the BI group (1.93; 95% confidence interval [CI], 1.35-2.76). Among the BI subgroups, the odds ratios of stage III-IV for the atherothrombotic type (1.81; 95% CI, 1.23-2.68) and the cardiogenic type (2.25; 95% CI, 1.32-3.83) were significantly higher than that of the control group, but that of stage III-IV for lacunar type was not (1.67; 95% CI, 0.98-2.84). Our results indicate that ischemic stroke is frequently associated with renal dysfunction. Chronic kidney disease might be independent risk factor for infarction, especially for cardiogenic and atherosclerotic types.

Is mild renal dysfunction a risk factor for carotid atherosclerosis in apparently healthy adults?

OBJECTIVE: Renal dysfunction may be related to cerebrovascular disease. The aim of this study was to assess the relationship between mild renal dysfunction and carotid artery atherosclerosis detected by ultrasonography in apparently healthy subjects. METHODS: A total of 2,106 persons (1,368 men and 738 women, mean age+/-S.D.: 56 +/- 10 years) with no history of stroke were enrolled. Kidney function was evaluated in terms of estimated glomerular filtration rate (eGFR), calculated by using the relationship 194Cr(-1.094)×Age(-0.287)×0.739 (if female), where Cr is serum creatinine concentration. Atherosclerosis on ultrasonography was defined as regional intimal thickening or nodular lesion. RESULTS: Atherosclerotic lesions were significantly more frequent in subjects with CKD stage 3 than in CKD stage 1 or 2 (p<0.001). Odds ratios for atherosclerotic lesions were significantly increased to 1.11 (95% confidence interval: 1.09-1.12, p<0.001) for increasing age, 1.66 (1.31-2.10, p<0.001) for male sex, 1.76 (1.43-2.16, p<0.001) for systolic blood pressure ≥130 mmHg and/or diastolic blood pressure ≥85 mmHg, 1.61 (1.28-2.01, p<0.001) for LDL-cholesterol ≥140 mg/dL, and 1.59 (1.23-2.05, p=0.003) for smoking habit versus no risk factor. The odds ratio of CKD stage 3 for ≥50% carotid artery stenosis was significantly increased to 3.47 (1.09-11.08, p=0.035), although CKD stage 2 and stage 3 were not significant (0.77, 95% CI: 0.59-1.01, p=0.068; 0.99, 95%CI: 0.67-1.46, p=0.981, respectively). CONCLUSION: Renal dysfunction defined in terms of eGFR might be associated with early-stage carotid atherosclerosis, but traditional vascular risk factors, including increasing age or hypertension, appear to play a major role.

Effect of edaravone on the estimated glomerular filtration rate in patients with acute ischemic stroke and chronic kidney disease.

The oxygen free radical scavenger edaravone is used in patients with acute ischemic stroke in Japan, but adverse reactions, especially decreased renal function, have raised concerns. To examine whether a patient's estimated glomerular filtration rate (eGFR) at admission can predict renal function deterioration after edaravone treatment, we retrospectively evaluated the effect of edaravone on eGFR in Japanese patients with acute ischemic stroke and chronic kidney disease (CKD). The baseline eGFR in the edaravone-treated group (73.5±20.3 mL/min/1.73 m(2); n=408) at admission was significantly (P < .05) higher than that in the non-edaravone-treated group (51.9±25.2 mL/min/1.73 m(2); n=41). The change in eGFR after treatment was categorized into 3 grades: nonexacerbation (≤10%), 10%-30% exacerbation, and >30% exacerbation. There was no significant difference in exacerbation grade between the edaravone-treated and non-edaravone-treated groups (χ(2) =3.134; P=.21). We next subdivided the edaravone-treated group according to eGFR at admission as either CKD (eGFR <60 mL/min/1.73 m(2); n=111) and non-CKD (n=297). No significant decrease in eGFR was seen even in the edaravone-treated CKD group (most of whom were in stage 3 CKD). Decreased eGFR in stroke patients was found to be associated with stroke subtype (cardiogenic stroke), but not with infection. The present study demonstrates that eGFR at admission is not a good predictor of renal deterioration in edavarone-treated acute ischemic stroke patients, including those with stage 3 CKD.