Agreement Between 24-Hour Salt Ingestion and Sodium Excretion in a Controlled Environment

Lerchl, Kathrin; Rakova, Natalia; Dahlmann, Anke; Rauh, Manfred; Goller, Ulrike; Basner, Mathias; Dinges, David F.; Beck, Luis; Agureev, A. N.; Ларина, И. М.; Баранов, В. И.; Моруков, Б. В.; Eckardt, Kai‐Uwe; Vassilieva, Galina; Wabel, Peter; Vienken, Jörg; Kirsch, K.; Johannes, Bernd; Krannich, Alexander; Luft, Friedrich C.; Titze, Jens

doi:10.1161/hypertensionaha.115.05851

Cited by 180 publications

(162 citation statements)

References 31 publications

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“…A similarly interesting question is how sodium transport takes place between the subcutaneous stores and the lymphatic vessels. It is imaginable that this recruitment of salt from these stores is a regulated process (95). In that case, it may very well involve Na ϩ transporters that are similar to transporters in the kidney to facilitate movement of sodium from the intercellular space back into the lymphatic vessels.…”

Section: F966mentioning

confidence: 99%

Everything we always wanted to know about furosemide but were afraid to ask

Huang

Mees

Vos

et al. 2016

American Journal of Physiology-Renal Physiology

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Huang X, Dorhout Mees E, Vos P, Hamza S, Braam B. Everything we always wanted to know about furosemide but were afraid to ask. Am J Physiol Renal Physiol 310: F958 -F971, 2016. First published February 24, 2016 doi:10.1152/ajprenal.00476.2015.-Furosemide is a widely used, potent natriuretic drug, which inhibits the Na ϩ -K ϩ -2Cl Ϫ cotransporter (NKCC)-2 in the ascending limb of the loop of Henle applied to reduce extracellular fluid volume expansion in heart and kidney disease. Undesirable consequences of furosemide, such as worsening of kidney function and unpredictable effects on sodium balance, led to this critical evaluation of how inhibition of NKCC affects renal and cardiovascular physiology. This evaluation reveals important knowledge gaps, involving furosemide as a drug, the function of NKCC2 (and NKCC1), and renal and systemic indirect effects of NKCC inhibition. Regarding renal effects, renal blood flow and glomerular filtration rate could become compromised by activation of tubuloglomerular feedback or by renin release, particularly if renal function is already compromised. Modulation of the intrarenal renin angiotensin system, however, is ill-defined. Regarding systemic effects, vasodilation followed by nonspecific NKCC inhibition and changes in venous compliance are not well understood. Repetitive administration of furosemide induces short-term (braking phenomenon, acute diuretic resistance) and long-term (chronic diuretic resistance) adaptations, of which the mechanisms are not well known. Modulation of NKCC2 expression and activity in kidney and heart failure is ill-defined. Lastly, furosemide's effects on cutaneous sodium stores and on uric acid levels could be beneficial or detrimental. Concluding, a considerable knowledge gap is identified regarding a potent drug with a relatively specific renal target, NKCC2, and renal and systemic actions. Resolving these questions would increase the understanding of NKCCs and their actions and improve rational use of furosemide in pathophysiology of fluid volume expansion. extracellular fluid volume; natriuresis; renal function; chronic kidney disease; heart failure DIURETICS BLOCKING THE Na ϩ -K ϩ -2Cl Ϫ cotransporter (NKCC) have an important place in the treatment of fluid overload, specifically in the context of kidney disease and heart failure (64). Of the drugs that inhibit the NKCC2 in the loop of Henle (furosemide, bumetanide, torsemide, ethacrynic acid), furosemide is most commonly applied (66) and Ͼ40 million prescriptions are dispensed every year in the USA (66a). However, many uncertainties remain about intrarenal and systemic actions of furosemide, including its two main targets NKCC1 and NKCC2.Clinically, there are a number of undesirable consequences of the use of furosemide, of which the pathophysiological mechanisms have not been sufficiently investigated. Furosemide has been associated with worsening of kidney function in patients treated for volume overload admitted for acute heart failure (104) and even glomerular filtration rate (GFR) ...

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Section: F966mentioning

confidence: 99%

Everything we always wanted to know about furosemide but were afraid to ask

Huang

Mees

Vos

et al. 2016

American Journal of Physiology-Renal Physiology

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“…We recently reported ultra-long-term balance studies in 10 healthy young men simulating a flight to Mars (11,12). We found that Na + was rhythmically stored and released with about-weekly (circaseptan) and circa-monthly (circalunar) periodicity.…”

Section: Introductionmentioning

confidence: 98%

Increased salt consumption induces body water conservation and decreases fluid intake

Rakova¹,

Kitada²,

Lerchl³

et al. 2017

Journal of Clinical Investigation

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122

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BACKGROUND. The idea that increasing salt intake increases drinking and urine volume is widely accepted. We tested the hypothesis that an increase in salt intake of 6 g/d would change fluid balance in men living under ultra-long-term controlled conditions. METHODS.Over the course of 2 separate space flight simulation studies of 105 and 205 days' duration, we exposed 10 healthy men to 3 salt intake levels (12, 9, or 6 g/d). All other nutrients were maintained constant. We studied the effect of salt-driven changes in mineralocorticoid and glucocorticoid urinary excretion on day-to-day osmolyte and water balance. RESULTS.A 6-g/d increase in salt intake increased urine osmolyte excretion, but reduced free-water clearance, indicating endogenous free water accrual by urine concentration. The resulting endogenous water surplus reduced fluid intake at the 12-g/d salt intake level. Across all 3 levels of salt intake, half-weekly and weekly rhythmical mineralocorticoid release promoted free water reabsorption via the renal concentration mechanism. Mineralocorticoid-coupled increases in free water reabsorption were counterbalanced by rhythmical glucocorticoid release, with excretion of endogenous osmolyte and water surplus by relative urine dilution. A 6-g/d increase in salt intake decreased the level of rhythmical mineralocorticoid release and elevated rhythmical glucocorticoid release. The projected effect of salt-driven hormone rhythm modulation corresponded well with the measured decrease in water intake and an increase in urine volume with surplus osmolyte excretion. CONCLUSION.Humans regulate osmolyte and water balance by rhythmical mineralocorticoid and glucocorticoid release, endogenous accrual of surplus body water, and precise surplus excretion.

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“…Equally there is a significant body of evidence demonstrating that reducing salt consumption can be effective in lowering blood pressure, with projected large benefits for cardiovascular mortality and medical expenditure (3,4) . Collection of 24 h urine samples is the preferred method for determining population salt intake (5) although it does not capture the approximate 10 % of dietary salt lost through non-urinary routes (6) . In Australia, a number of small studies have measured salt consumption using 24 h urine samples but no nationally representative study has been conducted using this method (7)(8)(9)(10)(11)(12) .…”

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confidence: 99%

Dietary salt intake in the Australian population

Santos¹,

Webster²,

Land³

et al. 2017

Public Health Nutr.

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Objective: To update the estimate of mean salt intake for the Australian population made by the Australian Health Survey (AHS). Design: A secondary analysis of the data collected in a cross-sectional survey was conducted. Estimates of salt intake were made in Lithgow using the 24 h diet recall methodology employed by the AHS as well as using 24 h urine collections. The data from the Lithgow sample were age-and sex-weighted, to provide estimates of daily salt intake for the Australian population based upon (i) the diet recall data and (ii) the 24 h urine samples. Setting: Lithgow, New South Wales, Australia. Subjects: Individuals aged ≥20 years residing in Lithgow and listed on the 2009 federal electoral roll. Results: Mean (95 % CI) salt intake estimated from the 24 h diet recalls was 6·4 (6·2, 6·7) g/d for the Lithgow population compared with a corresponding figure of 6·2 g/d for the Australian population derived from the AHS. The corresponding estimate of salt intake for Lithgow adults based upon the 24 h urine collections was 9·0 (8·6, 9·4) g/d. When the age-and sex-specific estimates of salt intake obtained from the 24 h urine collections in the Lithgow sample were weighted using Australian census data, estimated salt intake for the Australian population was 9·0 (8·6, 9·5) g/d. Further adjustment for non-urinary Na excretion made the best estimate of daily salt intake for both Lithgow and Australia about 9·9 g/d. Conclusions: The dietary recall method used by the AHS likely substantially underestimated mean population salt consumption in Australia.

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Agreement Between 24-Hour Salt Ingestion and Sodium Excretion in a Controlled Environment

Cited by 180 publications

References 31 publications

Everything we always wanted to know about furosemide but were afraid to ask

Everything we always wanted to know about furosemide but were afraid to ask

Increased salt consumption induces body water conservation and decreases fluid intake

Dietary salt intake in the Australian population

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