Relationship between silent brain infarction and chronic kidney disease.

BACKGROUND: The presence of silent brain infarction (SBI) increases the risk of symptomatic stroke and dementia. The association between SBI and chronic kidney disease (CKD) has not been clarified. Moreover, little is known about what factors are related to SBI in CKD patients and whether the prevalence of SBI differs in CKD stage or cause of CKD. METHODS: This is a cross-sectional study. A total of 375 subjects-335 with CKD and 40 with essential hypertension-were included. All subjects underwent magnetic resonance imaging (MRI) of the brain to detect SBI. Glomerular filtration rate (GFR) was estimated using Modification of Diet in Renal Disease equation, and cardiovascular risk factors were examined. RESULTS: The prevalence of SBI was 56.5% in all subjects. Among causes of CKD, hypertensive nephrosclerosis had a strong association with SBI. According to the estimated GFR (eGFR) stage, the more severe the stage of eGFR, the higher the prevalence of SBI (age-adjusted odds ratio [95% confidence interval] for eGFR 30-59, 15-29 and <15 versus >or=60 mL/min/1.73 m(2): 1.34 [0.68-1.99], 1.94 [1.30-2.57] and 2.51 [1.91-3.10]). In multivariate logistic analysis, eGFR was related to SBI independently, in addition to age and blood pressure (P = 0.025). However, other traditional and non-traditional risk factors were not. CONCLUSION: There was an independent association between eGFR and SBI. CKD patients should receive active detection of SBI and more intensive preventive management, especially for hypertension, should be needed in CKD patients to prevent SBI.

Loss of nocturnal decline of blood pressure in non-diabetic patients with nephrotic syndrome in the early and middle stages of chronic kidney disease.

In non-diabetic patients with nephrotic syndrome (NS) at early stages of chronic kidney disease, it remains unclear whether the degree of proteinuria affects the nocturnal blood pressure (BP) dip. We evaluated the relationship among circadian BP rhythm, proteinuria and hypoalbuminemia in these patients. We also evaluated the autonomic nervous activity. Twenty-four-hour BP was measured in NS patients (8 men and 13 women; mean age, 58.5+/-14.8 years) and age- and sex-matched normal subjects (11 men and 13 women; mean age, 54.3+/-18.2 years) as controls. Serum albumin and urinary protein concentrations were measured. Power spectral analysis of the heart rate was performed, and the high frequency (HF) and low frequency (LF) components were calculated as indices of sympathovagal balance. There were no differences in waking BP between the NS and the control groups (131+/-13/78+/-9 vs. 130+/-17/76+/-7 mm Hg; P>0.05). However, sleeping BP was significantly higher in the NS group than in the control group (127+/-18/75+/-9 vs. 115+/-14/66+/-7 mm Hg; P<0.05). Sleeping/waking BP ratios were higher in the NS group than in the control group (P<0.01). In the NS group, these ratios correlated significantly with serum albumin level (r=-0.54, P=0.011 for systolic BP; r=-0.48, P=0.030 for diastolic BP) and urinary protein excretion (r=0.47, P=0.027 for systolic BP; r=0.60, P=0.003 for diastolic BP). Both HF components and LF/HF ratios were not significantly different between the two groups. In non-diabetic NS patients, loss of nocturnal BP reduction correlates with proteinuria and hypoalbuminemia but not with circadian autonomic nervous rhythm.