Salt sensitivity of blood pressure in non-dialysis patients with chronic kidney disease

Abstract

Background: Chronic kidney disease (CKD) is a world-wide public health problem. Hypertension is both a cause and a complication of CKD, and a risk factor for progression of kidney disease. The effect of salt intake on blood pressure (BP) and the salt sensitivity in non-dialysis patients with CKD were studied. Methods: One hundred and thirty non-dialysis patients with CKD were enrolled in the present study. Daily urinary excretion of sodium (representative of daily sodium intake) and BP was monitored in conditions of original eating habits. Estimated glomerular filtration rate (eGFR) was measured by the creatinine clearance (Ccr). Results: There was a linear positive relationship between the salt intake and systolic blood pressure (SBP) (b ¼ 0.250, p ¼ 0.004). It had been found that the log of BP/24-h urinary sodium (salt sensitivity index) had linear relationship with the log of eGFR (b syst ¼ À0.364, p ¼ 0.000, b diast ¼ À0.345, p ¼ 0.000, respectively). Multi-stepwise regression analysis showed SBP was mainly influenced by salt intake and eGFR. There was a negative correlation between diastolic blood pressure (DBP) and age. Conclusion: These results demonstrated a linear relationship between the salt intake and SBP in non-dialysis patients with CKD. The salt sensitivity of BP rose with the decline of renal function.

Pooled analysis of Phase III trials indicate contrasting influences of renal function on blood pressure, body weight, and HbA1c reductions with empagliflozin

“…As a consequence of the functional changes in counterregulatory pathways, patients with CKD may have enhanced sodium sensitivity due in part to changes in tubular sodium handling. 33,34 Hence, patients with eGFR impairment may show greater downstream effects on circulating fluid volume and/or BP in response to changes in tubular sodium loss. Effects of SGLT2 inhibition on sodium or volume have not been characterized in relation to renal function.…”

Cardiovascular Autonomic Dysfunction in Chronic Kidney Disease: a Comprehensive Review

“…The exact mechanism by which high salt intake aggravates sympathetic stimulation and hypertension in CKD is an active area of research, with salt restriction now being considered more frequently as a means of controlling BP in CKD/ESRD patients [148]. In nondialysis CKD patients, a linear relationship between salt intake and systolic BP has been identified, with salt sensitivity of BP increasing as renal function declines [149]. An inhibitory action for salt on neuronal NOS expression in the posterior hypothalamic nuclei, the locus coeruleus, and the PVN was suggested by Campese et al [150] as a possible mechanism related to the high-salt-mediated action of the SNS.…”

Urinary Sodium-to-Potassium Ratio and Blood Pressure in CKD

“…17 Short-term randomized trials in patients with moderate to severe CKD have shown that clinically relevant BP reductions follow dietary sodium restriction. 18,19 In observational studies, high sodium intake based on 24-hour urinary sodium excretion has been associated with increased systolic BP at CKD stages 3-4, 20,21 but not at stages 1-2, 22 whereas findings from studies that reported association of potassium intake with BP led to contradictory conclusions. [23][24][25] As far as the effects of sodium and potassium intake on renal outcomes are concerned, most reports indicate that high sodium intake is associated with more rapid CKD progression, 24,26 whereas potassium intake remains a matter of debate.…”