Large artery stiffening as a link between cerebral lacunar infarction and renal albuminuria

Stiffening of large arteries increases pulsatile pressure and flow stresses, which extend to the microcirculation in vasodilated organs such as the brain and kidneys. Subclinical cerebral lacunar infarction and albuminuria, both of which are early manifestations of microvascular damage, have been shown to be potentially interrelated in hypertension and with aging, but the underlying pathogenesis remains unknown.

In a population of 351 general adults aged > or =50 years, urinary albumin/creatinine ratio (ACR), pulse wave velocity (PWV), and 24-h ambulatory blood pressure (BP) were measured, and cerebral lacunar lesions were assessed on magnetic resonance imaging (MRI).

Lacunar infarction was present in 86 subjects (25%). Subjects with lacunae had a higher median urinary ACR than those without (20.6 vs. 14.6 mg/g.Cr, P = 0.004). The positive association between the presence of lacunae and urinary ACR remained significant in a logistic model that adjusted for covariates including age, gender, and 24-h BP (P = 0.04); the odds ratio (OR) for lacunae was 1.32 for each 1 s.d. increase in urinary ACR. However, when PWV was added to this model, increased PWV but not urinary ACR was associated with lacunae. There was a significant interaction between urinary ACR and PWV with respect to lacunae; only subjects with a high PWV above the median showed an independent association between urinary ACR and the presence of lacunae (P = 0.03).

Microvascular damage in the brain (lacunar infarction) and kidney (albuminuria) appears to be interrelated in the general population. Large arterial stiffening may play a pivotal role in this cerebro-renal connection.