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Updated: Feb 15, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Non-uniform relationship between salt status and aldosterone activity in patients with chronic kidney disease
Alison H M Taylor1, Alastair J Rankin2,3, Emily P McQuarrie3
1Institute of Cardiovascular and Medical Sciences, University of Glasgow, U.K.
Insights
In chronic kidney disease (CKD), aldosterone regulation is disordered with intravenous salt loading, but not dietary salt changes. This impacts blood pressure management in CKD patients.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Endocrinology
Background:
- Hypertension is common in chronic kidney disease (CKD).
- Dietary salt intake reduction may lower blood pressure (BP).
- Renin-angiotensin system (RAS) regulation in CKD requires further study.
Purpose of the Study:
- To investigate the relationship between salt intake, BP, and RAS regulation in CKD.
- To determine if salt intake and BP regulation are disordered in CKD patients.
Main Methods:
- A crossover study compared CKD patients and non-CKD controls.
- Participants underwent saline suppression and angiotensin-II stimulation tests.
- Diets were modified to low and high salt intake; BP and plasma aldosterone concentration (PAC) were measured.
Main Results:
- Systolic BP increased in CKD patients after intravenous saline, unlike controls.
- Plasma aldosterone concentration (PAC) failed to suppress in CKD patients following saline administration.
- Dietary salt modification did not alter BP in either group, though PAC levels varied with salt intake.
Conclusions:
- Aldosterone regulation is dysregulated in CKD patients in response to intravenous salt loading.
- Dietary salt modification did not reveal significant changes in BP or aldosterone suppression in CKD.
- Findings suggest a specific impairment in CKD's response to acute salt challenges.
Background:
Hypertension is prevalent in chronic kidney disease (CKD). Studies suggest that reduction in dietary salt intake reduces blood pressure (BP). We studied relationships between salt intake, BP and renin-angiotensin system regulation in order to establish if it is disordered in CKD.
Methods:
Mechanistic crossover study of CKD patients versus non-CKD controls. Participants underwent modified saline suppression test prior to randomization to either low or high salt diet for 5 days and then crossed over to the alternate diet. Angiotensin-II stimulation testing was performed in both salt states. BP, urea and electrolytes, and plasma aldosterone concentration (PAC) were measured.
Results:
Twenty-seven subjects were recruited (12 CKD, 15 control). There was no difference in age and baseline BP between the groups. Following administration of intravenous saline, systolic BP increased in CKD but not controls (131 ± 16 to 139 ± 14 mmHg, P=0.016 vs 125 ± 20 to 128 ± 22 mmHg, P=0.38). Median PAC reduced from 184 (124,340) to 95 (80,167) pmol in controls (P=0.003), but failed to suppress in CKD (230 (137,334) to 222 (147,326) pmol (P=0.17)). Following dietary salt modification, there was no change in BP in either group. Median PAC was lower following high salt compared with low salt diet in CKD and controls. There was a comparable increase in systolic BP in response to angiotensin-II in both groups.
Discussion:
We demonstrate dysregulation of aldosterone in CKD in response to salt loading with intravenous saline, but not to dietary salt modification.
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