A randomized trial of sodium-restriction on kidney function, fluid volume and adipokines in CKD patients

被引:44
作者
Campbell, Katrina L. [1 ,2 ,3 ]
Johnson, David W. [1 ,2 ,3 ]
Bauer, Judith D. [2 ]
Hawley, Carmel M. [1 ,2 ,3 ]
Isbel, Nicole M. [1 ,2 ,3 ]
Stowasser, Michael [1 ,2 ,3 ]
Whitehead, Jonathan P. [2 ,3 ,4 ]
Dimeski, Goce [2 ,5 ]
McMahon, Emma [1 ,2 ]
机构
[1] Princess Alexandra Hosp, Woolloongabba, Qld, Australia
[2] Univ Queensland, Brisbane, Qld, Australia
[3] Translat Res Inst, Brisbane, Qld, Australia
[4] Univ Queensland, Mater Res Inst, Brisbane, Qld, Australia
[5] Princess Alexandra Hosp, Brisbane, Qld 4102, Australia
关键词
Dietary sodium; Nutrition; Chronic kidney disease; Cardiovascular disease; Blood pressure; Kidney function; Inflammation; SALT INTAKE; DIETARY-SODIUM; BLOOD-PRESSURE; PLASMA ADIPONECTIN; RENAL-FAILURE; HYPERTENSION; DISEASE; HYPERFILTRATION; MORTALITY; INFLAMMATION;
D O I
10.1186/1471-2369-15-57
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Background: Dietary sodium restriction is a key management strategy in chronic kidney disease (CKD). Recent evidence has demonstrated short-term reduction in blood pressure (BP) and proteinuria with sodium restriction, however the effect on other cardiovascular-related risk factors requires investigation in CKD. Methods: The LowSALT CKD study involved 20 hypertensive Stage III-IV CKD patients counselled by a dietitian to consume a low-sodium diet (< 100 mmol/day). The study was a randomised crossover trial comparing 2 weeks of high-sodium (additional 120 mmol sodium tablets) and low-sodium intake (placebo). Measurements were taken after each crossover arm including BP (peripheral and central), adipokines (inflammation markers and adiponectin), volume markers (extracellular-to-intracellular [E/I] fluid ratio; N-terminal pro-brain natriuretic peptide [NT-proBNP]), kidney function (estimated Glomerular Filtration Rate [eGFR]) and proteinuria (urine protein-creatinine ratio [ PCR] and albumin-creatinine ratio [ACR]). Outcomes were compared using paired t-test for each cross-over arm. Results: BP-lowering benefits of a low-sodium intake (peripheral BP (mean +/- SD) 148/82 +/- 21/12 mmHg) from high-sodium (159/87 +/- 15/10 mmHg) intake were reflected in central BP and a reduction in eGFR, PCR, ACR, NTproBNP and E/I ratio. There was no change in inflammatory markers, total or high molecular weight adiponectin. Conclusions: Short-term benefits of sodium restriction on BP were reflected in significant change in kidney function and fluid volume parameters. Larger, long-term adequately powered trials in CKD are necessary to confirm these results.
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页数:6
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