Although the renin-angiotensin system (RAS) is counter-balanced by a
salt-sensitive mechanism in the hypertensive state, both are reported to be up-regulated in
chronic kidney disease (CKD) patients. We conducted this study to evaluate the associations among the RAS, renal function,
hypertension, and
atherosclerosis, as well as to identify markers for
salt-sensitivity. A total of 213 pre-dialysis CKD patients with preserved cardiac function (EF >50 %) were enrolled. Their renal and cardiac
biochemical markers and plasma
renin activity (PRA) were measured, and echocardiography and carotid artery ultrasound were performed. Their
salt intake was estimated by the NaCl excretion from a 24-h collected urine sample. The PRA was higher in patients with
hypertension (p = 0.018), and had a significant negative correlation with the eGFR (r = -0.23, p = 0.0067). Importantly, the PRA had a strong negative correlation with the
brain natriuretic peptide (BNP) level (r = -0.28, p = 0.017) regardless of whether the patients were being treated with RAS inhibitors. The BNP level was related to the renal functions (eGFR: p = 0.001, ACR: p = 0.009). There was a significant positive correlation between the BNP level and carotid intima-media thickness (p < 0.001). A multivariate analysis revealed that older age and an excess of NaCl excretion were independent predictors of BNP elevation (p = 0.02 and 0.003, respectively). Our analysis revealed details of the counterbalance between BNP and PRA, as well as identifying that excess
salt intake is a predictor of BNP elevation. These results indicate that the BNP could be a possible valuable marker for
salt sensitivity, and that high
salt sensitivity could facilitate
atherosclerosis in CKD patients.