Institute of Cardiovascular and Medical Sciences, University of Glasgow, U.K.
Queen Elizabeth University Hospital, Glasgow, U.K.
Clin Sci (Lond). 2018 Jan 25;132(2):285-294. doi: 10.1042/CS20171603. Print 2018 Jan 31.
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.
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.
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, =0.016 vs 125 ± 20 to 128 ± 22 mmHg, =0.38). Median PAC reduced from 184 (124,340) to 95 (80,167) pmol in controls (=0.003), but failed to suppress in CKD (230 (137,334) to 222 (147,326) pmol (=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.
We demonstrate dysregulation of aldosterone in CKD in response to salt loading with intravenous saline, but not to dietary salt modification.
高血压在慢性肾脏病(CKD)中很常见。研究表明,减少饮食盐摄入量可降低血压(BP)。我们研究了盐摄入量、BP 和肾素-血管紧张素系统调节之间的关系,以确定其在 CKD 中是否失调。
对 CKD 患者与非 CKD 对照进行机制交叉研究。参与者在随机分为低盐或高盐饮食 5 天之前接受了改良盐水抑制试验,然后交叉到另一种饮食。在两种盐状态下进行血管紧张素-II 刺激试验。测量血压、尿素和电解质以及血浆醛固酮浓度(PAC)。
共招募了 27 名受试者(12 名 CKD,15 名对照)。两组之间的年龄和基线 BP 没有差异。静脉注射生理盐水后,CKD 患者的收缩压升高,但对照组没有升高(131±16 至 139±14mmHg,=0.016 比 125±20 至 128±22mmHg,=0.38)。对照组的 PAC 中位数从 184(124,340)降至 95(80,167)pmol(=0.003),但 CKD 患者未能抑制(230(137,334)至 222(147,326)pmol(=0.17))。改变饮食盐量后,两组的 BP 均无变化。CKD 和对照组中,高盐饮食后 PAC 中位数均低于低盐饮食。两组对血管紧张素-II 的反应中,收缩压均有可比的升高。
我们证明了 CKD 患者在静脉注射盐水负荷时醛固酮失调,但在饮食盐量改变时没有失调。