Key result
Following intravenous saline administration, systolic blood pressure increased (P=0.016) and plasma aldosterone failed to suppress (P=0.17) in patients with CKD, unlike in non-CKD controls.
Why the study?
Does salt loading and dietary salt modification alter blood pressure and aldosterone regulation differently in patients with CKD compared to non-CKD controls?
RCT (n=27)
crossover
Does salt loading and dietary salt modification alter blood pressure and aldosterone regulation differently in patients with CKD compared to non-CKD controls?
Patients with chronic kidney disease exhibit dysregulation of aldosterone and increased systolic blood pressure in response to intravenous salt loading, but not to dietary salt modification.
Impaired aldosterone suppression after saline in CKD signals potential salt sensitivity; leaves open whether dietary modification alters BP or outcomes.
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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Taylor et al. (2018) conducted an RCT in Chronic kidney disease (n=27). Intravenous saline and dietary salt modification vs. Non-CKD controls was evaluated on Systolic blood pressure and plasma aldosterone concentration response to intravenous saline. Following intravenous saline administration, systolic blood pressure increased (P=0.016) and plasma aldosterone failed to suppress (P=0.17) in patients with CKD, unlike in non-CKD controls.
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