High sodium intake, glomerular hyperfiltration, and protein catabolism in patients with essential hypertension

被引:32
|
作者
Rossitto, Giacomo [1 ,2 ]
Maiolino, Giuseppe [2 ]
Lerco, Silvia [2 ]
Ceolotto, Giulio [2 ]
Blackburn, Gavin [3 ]
Mary, Sheon [1 ]
Antonelli, Giorgia [4 ]
Berton, Chiara [2 ]
Bisogni, Valeria [2 ]
Cesari, Maurizio [2 ]
Seccia, Teresa Maria [2 ]
Lenzini, Livia [2 ]
Pinato, Alessio [4 ]
Montezano, Augusto [1 ]
Touyz, Rhian M. [1 ]
Petrie, Mark C. [1 ]
Daly, Ronan [3 ]
Welsh, Paul [1 ]
Plebani, Mario [4 ]
Rossi, Gian Paolo [2 ]
Delles, Christian [1 ]
机构
[1] Univ Glasgow, Inst Cardiovasc & Med Sci, BHF Glasgow Cardiovasc Res Ctr, 126 Univ Pl, Glasgow G12 8TA, Lanark, Scotland
[2] Univ Padua, Univ Hosp, DIMED, Clin Ipertens, Via Giustiniani 2, I-35126 Padua, Italy
[3] Univ Glasgow, Wolfson Wohl Canc Res Ctr, Glasgow Polyom, Garscube Campus, Glasgow G61 1BD, Lanark, Scotland
[4] Univ Padua, Univ Hosp, Lab Med, DIMED, Via Giustiniani 2, I-35126 Padua, Italy
基金
英国惠康基金;
关键词
Salt; Hypertension; Kidney; Glomerular hyperfiltration; Metabolism; MASS-SPECTROMETRY DATA; URINARY SODIUM; SALT INTAKE; CARDIOVASCULAR-DISEASE; POTASSIUM EXCRETION; CUSHINGS-SYNDROME; BLOOD-PRESSURE; CONSUMPTION; METABOLISM; DIAGNOSIS;
D O I
10.1093/cvr/cvaa205
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Aims A blood pressure (BP)-independent metabolic shift towards a catabolic state upon high sodium (Na+) diet, ultimately favouring body fluid preservation, has recently been described in pre-clinical controlled settings. We sought to investigate the real-life impact of high Na+ intake on measures of renal Na+/water handling and metabolic signatures, as surrogates for cardiovascular risk, in hypertensive patients. Methods and results We analysed clinical and biochemical data from 766 consecutive patients with essential hypertension, collected at the time of screening for secondary causes. The systematic screening protocol included 24h urine (24 h-u-) collec- tion on usual diet and avoidance of renin-angiotensin-aldosterone system-confounding medications. Urinary 24 hNa(+) excretion, used to define classes of Na t intake (low <= 2.3g/day; medium 2.3-5 g/day; high >5 g/day), was an independent predictor of glomerular filtration rate after correction for age, sex, BP, BMI, aldosterone, and potassium excretion [P = 0 .001; low: 94.1 (69.9-118.8) vs. high: 127.5 (108.3-147.8) mL/min/1.73 m(2)]. Renal Na+ and water handling diverged, with higher fractional excretion of Na+ and lower fractional excretion of water in those with evidence of high Na t intake [FENa+ : low 0.39% (0.30-0.47) vs. high 0.81% (0.73-0.98), P< 0.001; FEwater : low 1.13% (0.73-1.72) vs. high 0.89% (0.69-1.12), P= 0.015]. Despite higher FENa+, these patients showed higher absolute 24 h Na+ reabsorption and higher associated tubular energy expenditure, estimated by tubular Na+/ATP stoichiometry, accordingly [Delta high-low = 18 (12-24) kcal/day, P <0.001]. At non-targeted liquid chromatography/mass spectrometry plasma metabolomics in an unselected subcohort (n = 67), metabolites which were more abundant in high versus low Na+ intake (P < 0.05) mostly entailed intermediates or end products of protein catabolism/urea cycle. Conclusion When exposed to high Na+ intake, kidneys dissociate Na+ and water handling. In hypertensive patients, this comes at the cost of higher glomerular filtration rate, increased tubular energy expenditure, and protein catabolism from endogenous (muscle) or excess exogenous (dietary) sources. Glomerular hyperfiftration and the metabolic shift may have broad implications on global cardiovascular risk independent of BP. [GRAPHICS] .
引用
收藏
页码:1372 / 1381
页数:10
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