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Journal of Hypertension:
doi: 10.1097/HJH.0000000000000153
Editorial Commentaries

Can we make an adequate estimation of urinary sodium excretion avoiding 24-h urine collection?

Ruilope, Luis M.

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Instituto de Investigación and Unidad de Hipertensión, Madrid, Spain

Correspondence to Luis M. Ruilope, Instituto de Investigación and Unidad de Hipertensión, Hospital 12 de Octubre, Av. Córdoba s/n, 28041 Madrid, Spain. Tel: +34914317741; fax: +34915765644; e-mail: ruilope@ad-hocbox.com

A moderate dietary sodium reduction is advocated by the European Society of Hypertension–European Society of Cardiolagy Guidelines published recently [1]. The reasons for this advice consist of a causal relationship between salt intake and blood pressure (BP) that can facilitate the development of resistant hypertension. The mechanisms underlying the increase in BP include not only an enhanced extracellular volume but also an increase vasoconstriction secondary to a stimulation of sympathetic nervous system activity [2]. A daily intake of 5–6 g of salt is recommended for the general population due to the fact that the evidence supporting the call to reduce salt intake is compelling [3]. Reducing dietary salt by 3 g per day is projected to reduce the annual number of new cases of coronary heart disease by 60 000–120 000, stroke by 32 000–66 000 and myocardial infarction by 54 000–99 000 and to reduce the annual number of deaths from any cause by 44 000–99 000 [4]. These cardiovascular benefits are parallel to the benefits of population-wide reductions in tobacco use, obesity and cholesterol levels [4]. These data indicate that in future studies with the primary objective of investigating cardiovascular or renal disease, the knowledge of the salt intake of the patients should be relevant in order to perform a more in-depth analysis of the global risk by adding that associated with an excessive amount of salt in the diet. An adequate estimation of salt intake in a representative group of individuals can be made through 24-h dietary survey as done in the National Health Nutrition Examination Survey in United States. However, the gold standard is an adequate measurement of urinary sodium excretion collected during 24 h. This methodology requires trained personnel and education of the patients that makes it impractical in big trials. This is the reason why different formulas to estimate sodium and potassium excretion from a single morning fasting urine have been considered as adequate substitutes for 24-h natriuresis. In this issue of the Journal, Mente et al.[5] validate and compare three of those formulas. The authors conclude that the Kawasaki formula is the most valid and least biased method of estimating 24-h sodium excretion from a single morning urine and could be the most suitable for population studies. The only caveat of the study is that the intraclass correlation coefficient for kaliuresis, albeit better in the Kawasaki formula than in the other two, was low. The joint measurement of sodium and potassium in urine is required for an adequate analysis of the risk [6].

Recent data [7] have described that sodium intake estimated through 24-h urinary sodium excretion is characterized by a narrow range that is remarkably reproducible over the last five decades and across 45 countries with a mean daily sodium consumption of around 160 mmol/day, clearly above the amount advised by Guidelines. One of the strengths of the article to which this editorial is devoted consist in the fact that the data analyzed were obtained from the general population in 11 countries. This fact validates the consideration for the use in multinational studies. In any case, the validation of Kawasaki or other formulas in trials is still pending.

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ACKNOWLEDGEMENTS

Conflicts of interest

There are no conflict of interests.

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REFERENCES

1. Mancia G, Fagard R, Narkiewicz K, Redon J, Zanchetti A, Bóhm M, et al. The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). 2013 ESH/ESC Guidelines for the management of arterial hypertension. J Hypertens. 2013; 31:1281–1357.

2. Guild SJ, McBryde FD, Malpas SC, Barrett CJ. High dietary salt and angiotensin II chronically increase renal sympathetic nerve activity: a direct telemetric study. Hypertension. 2012; 59:614–620.

3. Appel LJ, Anderson CAM. Compelling evidence for public health action to reduce salt intake. N Engl J Med. 2010; 362:650–651.

4. Bibbins-Domingo K, Chertow GM, Coxson PG, Moran A, Lightwood JM, Pletcher MJ, et al. Projected effect of dietary salt reduction on future cardiovascular disease. N Engl J Med. 2010; 362:590–599.

5. Mente A, O’Donnell MJ, Dagenais G, Wielgosz A, Lear SA, McQueen MJ, et al. Validation and comparison of three formulae to estimate sodium and potassium excretion from a single morning fasting urine compared to 24-h measures in 11 countries. J Hypertens. 2014; 32:1005–1015.

6. He J, Whelton PK. What is the role of dietary sodium and potassium in hypertension and target organ injury. Am J Med Sci. 1999; 317:152–159.

7. McCarron DA, Kazaks AG, Geerling JC, Stern JS, Graudal NA. Normal range of human dietary sodium intake: a perspective based on 24-h urinary sodium excretion worldwide. Am J Hypertens. 2013; 26:1218–1223.

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