Elevated pulse pressure preceded incident chronic kidney disease in the general older population in Sweden.

Arterial stiffness (AS) and chronic kidney disease (CKD) are common in the older population. AS results in increased pulsatile pressure, elevated pulse pressure (PP), and is linked to hypertension. PP is a surrogate for AS. The kidney has low vascular resistance mechanisms, presumably making it vulnerable to the increased pulsatile pressure and hypertension associated with AS. The aims of this study were to investigate the impact of PP elevation on incident CKD (glomerular filtration rate < 60 ml/min/1.73 m2) and all-cause mortality. The data was collected from the general population cohort study "Good Aging in Skåne". Cox proportional hazard regression models adjusted for age, sex, diabetes, and smoking habits were used to investigate the impact of three levels of PP elevation on incident CKD (n = 2693) and all-cause mortality (n = 5253). For PP < 60 mmHg, the median survival time was 18.7 years (event incident CKD) and first quartile survival time (event all-cause mortality) 15.4 years. Elevated PP ≥ 80 mmHg was associated with incident CKD (hazard ratio 1.59, CI 1.28-1.97), but not all-cause mortality. Our results suggest that a finding of PP ≥ 80 mmHg in older age should raise concern of kidney function.

Chronic kidney disease and its association with cerebral small vessel disease in the general older hypertensive population.

BACKGROUND: Cerebral small vessel disease can be identified using magnetic resonance imaging, and includes white matter hyperintensities, lacunar infarcts, cerebral microbleeds, and brain atrophy. Cerebral small vessel disease and chronic kidney disease share many risk factors, including hypertension. This study aims to explore an association between chronic kidney disease and cerebral small vessel disease, and also to explore the role of hypertension in this relationship. METHODS: With a cross sectional study design, data from 390 older adults was retrieved from the general population study Good Aging in Skåne. Chronic kidney disease was defined as glomerular filtration rate < 60 ml/min/1,73m2. Associations between chronic kidney disease and magnetic resonance imaging markers of cerebral small vessel disease were explored using logistic regression models adjusted for age and sex. In a secondary analysis, the same calculations were performed with the study sample stratified based on hypertension status. RESULTS: In the whole group, adjusted for age and sex, chronic kidney disease was not associated with any markers of cerebral small vessel disease. After stratification by hypertension status and adjusted for age and sex, we observed that chronic kidney disease was associated with cerebral microbleeds (OR 1.93, CI 1.04-3.59, p-value 0.037), as well as with cortical atrophy (OR 2.45, CI 1.34-4.48, p-value 0.004) only in the hypertensive group. In the non-hypertensive group, no associations were observed. CONCLUSIONS: In this exploratory cross-sectional study, we observed that chronic kidney disease was associated with markers of cerebral small vessel disease only in the hypertensive subgroup of a general population of older adults. This might indicate that hypertension is an important link between chronic kidney disease and cerebral small vessel disease. Further studies investigating the relationship between CKD, CSVD, and hypertension are warranted.

Associations of carotid artery flow parameters with MRI markers of cerebral small vessel disease and patterns of brain atrophy.

OBJECTIVES: A growing body of evidence links age related brain pathologies to systemic vascular processes. We aimed to study the prevalence and interrelations between magnetic resonance imaging (MRI) markers of cerebral small vessel disease and patterns of brain atrophy, and their association to carotid duplex ultrasound flow parameters. MATERIALS AND METHODS: We investigated a population based randomised cohort of older adults (n=391) aged 70-87, part of the Swedish Good Aging in Skåne Study. Peak systolic and end diastolic velocities of the carotid arteries were measured by ultrasound, and resistivity- and pulsatility indexes were calculated. Subjects with increased peak systolic velocity indicating carotid stenosis were excluded from analysis. Nine MRI findings were rated by visual scales: white matter changes, pontine white matter changes, microbleeds, lacunar infarctions, medial temporal lobe atrophy, global cortical atrophy, parietal atrophy, precuneus atrophy and central atrophy. RESULTS: MRI pathologies were found in 80% of subjects. Mean end diastolic velocity in common carotid arteries was inversely associated with white matter hyperintensities (OR=0.92; p=0.004), parietal lobe atrophy (OR=0.94; p=0.039), global cortical atrophy (OR=0.90; p=0.013), precuneus atrophy (OR=0.94; p=0.022), "number of CSV pathologies" (ß=-0.07; p<0.001) and "MRI-burden score" (ß=-0.11; p<0.001), after adjustment for age and sex. The latter three were also associated with pulsatility and resistivity indexes. CONCLUSIONS: Low carotid end diastolic velocity, as well as increased carotid resistivity and pulsatility, were associated with signs of cerebral small vessel disease and patterns of brain atrophy, indicating a vascular component in the process of brain aging.

Association between cerebral microbleeds and hypertension in the Swedish general population "Good Aging in Skåne" study.

Cerebral microbleeds (CMB) on MRI are frequent in healthy aging individuals but precede ischemic and hemorrhagic stroke and dementia. Different etiologies have been suggested for nonlobar CMB, which have a stronger connection to hypertension (HT) than do lobar CMB. This study aimed to investigate the prevalence of CMB and the association between nonlobar/lobar CMB and different blood pressure (BP) and HT treatment conditions in a longitudinal, population-based cohort of the Good Aging in Skåne (GÅS) study. White matter hyperintensities (WMH), CMB, atrophies, and infarctions were identified with brain 3T MRI, and BP parameters were examined in 344 randomly selected subjects between 70 and 87 years old. CMB were observed in 26% of the whole cohort, increasing from 19% of subjects in their 70s to 30% of those over 80 years of age. Of these subjects, 38% had multiple CMB, and 59% had a lobar localization. CMB were associated with severe confluent WMH (odds ratio = 7.02; 2.16-18.84). Increasing age, being male, and having HT, impaired cognition, or a history of angina pectoris were associated with CMB. Both lobar and nonlobar CMB were associated with HT. Nonlobar CMB were particularly associated with increased BP, pulse pressure, controlled HT, and uncontrolled HT. After controlling for sex and HT, age was no longer a risk factor for CMB In conclusion, sex and HT are the major risk factors for CMB, especially nonlobar CMB, which suggests stricter implementation of recommended guidelines for HT treatment in the elderly.

Influence of early-life parental severe life events on the risk of type 1 diabetes in children: the DiPiS study.

AIMS: Stress and severe life events (SLEs) modify autoimmune disease susceptibility. Here, we aimed to establish if SLEs reported by parents during the first 2 years of life influence the risk of developing type 1 diabetes (T1D) using data from the prospective Diabetes Prediction in Skåne (DiPiS) study. METHODS: Prospective questionnaire data recorded at 2 months (n = 23,187) and 2 years of age (n = 3784) from the DiPiS cohort of children were included in the analysis. SLEs were analyzed both by groups and as a combined variable. A Cox proportional hazards model was used to calculate hazard ratios (HRs) for T1D diagnosis for the total cohort and for the HLA-DQ2/8 high-risk population. Affected first-degree relatives, HLA-DQ risk group, paternal education level, and parents' country of birth were included as covariates. RESULTS: There was a significantly increased risk of T1D in children with SLEs occurring during the child's first 2 years of life for both the total cohort (HR 1.67; 95% CI 1.1, 2.7; p = 0.03) and the DQ2/8 cohort (HR 2.2; 95% CI 1.1, 4.2; p = 0.018). Subgroup analysis of events related to unemployment, divorce, or family conflict showed a significant hazard for these events occurring both during and after pregnancy in the DQ2/8 cohort (HR 2.17; 95% CI 1.1, 4.3; p = 0.03 and HR 4.98; 95% CI 2.3, 11; p < 0.001, respectively) and after pregnancy in the total cohort (multiple regression HR 2.07; 95% CI 1.01, 4.2; p = 0.047). CONCLUSIONS: Children of parents experiencing an SLE during the child's first 2 years of life were at increased risk of T1D. Further studies including those measuring immune and stress-related biomarkers are necessary to validate the findings.