if you drink large amounts of salt water what will happen to your urinary output
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J Clin Invest. 2017 May 1;127(v):1932-1943. doi: ten.1172/JCI88530. Epub 2017 April 17.
Increased table salt consumption induces torso water conservation and decreases fluid intake.
Rakova Due north, Kitada K, Lerchl K, Dahlmann A, Birukov A, Daub S, Kopp C, Pedchenko T, Zhang Y, Beck 50, Johannes B, Marton A, Müller DN, Rauh M, Luft FC, Titze J.
PMID: 28414302 Bachelor for Free at JCI: Full Text
Accompanying Editorial (gated)
Introduction
The sodium physiology that yous were taught, the physiology Edelman, is nether assault. In fact everything we know about sodium physiology is crumbling nether the weight of imaginative inquiry and novel techniques. The kickoff I learned about the assault was in Ingelfinger's 2015 sodium review in the NEJM:
When it became known that much of the sodium in the body is bound to bone, cartilage, and connective tissue, information technology was hypothesized that these tissues could serve as sodium reservoirs, taking upwards or releasing sodium in response to the needs of the body. Despite early testify supporting the concept of a sodium reservoir, this theory lost favor and was not pursued for half a century. However, the by decade has seen renewed interest in stored sodium.11 In patients who eat high-salt diets, sodium can accumulate in the body, seemingly disappearing without a change in the plasma sodium concentration, body weight, or extracellular fluid book. Sodium, potassium, and water balance practice not always account for changes in the plasma sodium concentration during recovery from hyponatremia. Proteoglycans in skin serve every bit a sodium reservoir, and the number of negative charges available to bind sodium varies in response to the sodium concentration of interstitial tissue. In experiments in rats, chronic hyponatremia has been shown to be a more potent cause of osteopenia than vitamin D deficiency, and loss of sodium from bone exceeded the loss of calcium from bone. The action of osteoclasts is increased in chronic hyponatremia attributable to a direct upshot of sodium and possibly vasopressin on these cells.
In case you TL;DR'd it, here is the essential renal heresy
"Sodium, potassium, and h2o residue practice not e'er business relationship for changes in the plasma sodium concentration"
As if millions of voices suddenly cried out in terror and were suddenly silenced. I fear something terrible has happened.
This week'due south NephJC continues the assail and you know the walls of knowledge have been breached when the New York Times runs with this headline:
It is a proficient commodity with quotes by #NephMadness Blueish Ribbon Panel Member, Melanie Hoenig
The primary study question investigates the relationship of sodium intake to urine book. The dogma is that increased sodium intake leads to increased thirst which and so stimulates fluid intake. This is a central tenet for one of the theories explaining the obesity epidemic: increased dietary sodium stimulates thirst leading to increased consumption of carbohydrate-sweetened beverages and thus increased obesity.
However previous piece of work had non been able to find a relationship between sodium intake and urine volume.
Methods: We are going to Mars
The study used two fake Mars missions for the study. Mars105 and Mars520 had 12 men in fake space flight for 105 days and 520 days respectively. The participants were kept in a hermetically sealed environment while they lived and worked like cosmonauts. Environmental factors were kept abiding.
During the Mars105 study common salt intake was sequentially adapted from 12 grams a twenty-four hour period to 9 g/d to 6 g/d. During the Mars520 the salt intake was was adjusted from 12 g/d to 9 one thousand/d to 6 thou/d then back to 12 g/d. The article plays a little loose with the terms salt and sodium and in fact at times confuses them. Conversion tabular array:
Each salt level was maintained for 29 days. Calories and other minerals were stock-still. Patients had unrestricted access to water and beverages. Fluid and sodium intake along with urine output were all rigorously tracked. (They measured urine output volumetrically, just similar your hospital does, and gravimetrically, which is JCI-speak for "past weight")
The subjects went to 24-hour urine school. They had four ane-hour classroom sessions to teach the cosmonauts how to collect the 24-hour urine samples. For comparison I get 5 hours divided into 2 sessions (one lecture and 1 flipped classroom) to teach 2nd year medical students everything they need to know about sodium water balance. The investigators monitored compliance and kicked out the losers:
We excluded subjects from analysis when their weekly urinary sodium recovery was repeatedly less than 80% of sodium intake or when the subjects did non attach to our daily menu plans. Only this strict focus on experimental accurateness immune us to implement a long- term balance approach. Because 2 subjects did non comply with these criteria, nosotros had to exclude them from further analysis.
When they say 24-hour urine, they mean 24-hour urine.
In addition to sodium intake and excretion, fluid intake and excretion, the investigators also recorded serial cortisone, and aldosterone excretion; urine Na+, K+, and urea concentration; and urine osmolality.
Results
And so the principal assessments were on urine sodium and urine volume on the three different common salt diets.
Commencement with panels F and K. They prove a straight forwards increment in urine sodium over 24 hours as the diet goes from 6 to 9 to 12 grams of salt a day. Easy. Panels B and C bear witness decreasing water intake as dietary salt intake rises. That makes no sense. Panels D and Eastward wait at urine book beyond dietary salt intake. No clear pattern emerged, with the lowest urine volume with the centre table salt diet. The dark-green lines look at the measured variable not by dietary intake but by 24-hour urine sodium. The authors presented data that dietary sodium in does non equal urinary sodium out in a nifty 24-hour cycle. That people agree on to sodium and that the diuresis can be delayed for days. To account this temporal discrepancy they presented the information using tertiles of urine sodium and then the urine volume makes more than sense with increasing urine output with increased urine sodium.
In trying to explain why water intake went down with increasing h2o excretion the investigators looked to urine concentration and the concept of free water clearance. Urine that is hyperosmotic compared to plasma results in a negative complimentary water clearance (FWC). Meaning that when the patient generates urine they are creating h2o that is added back to the apportionment.
The investigators showed that with higher dietary salt intake urine concentration rose and so did gratuitous h2o generation. To the indicate that at 12 grams of salt a 24-hour interval patients were generating a liter of free water everyday. This endogenuos water creation suppressed thirst.
The investigators then looked at what was driving the increase in urine osmolality. They institute that the rise in urine osmolality was about entirely from increased sodium and an associated anion, while urine urea actually fell. The authors speculate that the urea was accumulated in the renal medullary interstitium to let ADH-driven concentration of the urine.
Note the fall in urine urea every bit the salt intake rises
There was a stepwise increase in serum and 24-hour urinary aldosterone equally patients went from 6 g to 12 one thousand salt diets. Additionally, while salt was fixed the investigators noted a cyclical rise and fall of urine aldosterone and urine cortisol.
However, as reported earlier (11), UAldoV and UCortisoneV showed additional rhythmical one-half-weekly and weekly patterns of modify that were contained of salt intake.
And so the authors stratified their findings beyond loftier, medium and depression aldosterone and cortisol levels for each dietary salt intake. They noted the following findings:
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Increased aldosterone was associated with less urine book and more water intake. So total trunk water (and body weight) went upward
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Increased cortisol was associated with increased urine book without increased water intake. In that location was also no loss of body weight, suggesting that this increased urine book was endogenously created water.
Rhythmical glucocorticoid release was therefore linked to increased diuresis in the context of the urine dilution mechanism by increasing FWC
The author then projected the combined glucocorticoid and mineralocorticoid furnishings in response to changes in dietary salt claiming and estimated that a six gram increase in dietary table salt would increment urine book by 358 ml/day and decrease oral intake of water by 60 ml.
At that place is also an accompanying paper, from the same group, which was done in mice, and which supports these conclusions.
Give-and-take
At that place are a few key lines in the word that I desire to call out. Showtime is this gem to try to wrap your brain around:
the excretion of a Na+ and Cl– osmolyte surplus of 201 ± 8 mmol/d at the 12-grand/d salt intake level eventually reduced fluid intake, fifty-fifty though urine volume was increased.
Try to square that with your classical nephrology education, increased sodium intake increases urine volume and reduces h2o intake.
And so this line blew me away:
"The resulting rhythmical Na+ storage and release reduced the predictive value of an accurately collected 24-60 minutes urine sample to correctly estimate a 3-g/d divergence in salt intake to only fifty%"
Think of how many studies on sodium, hypertension and kidney stones have relied on the intuitive, uncomplicated principle of sodium in = sodium out . Burn it all downward.
The authors then propose three interconnected hypotheses to explain long-term control of body fluids in humans.
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Hypothesis 1: Increasing salt intake promotes accrual of endogenous water
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Hypothesis 2: Dietary salt modulates endogenous infradian- rhythmical control of osmolyte and water accrual and release.
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Hypothesis iii: High salt intake induces glucocorticoid-driven metabolic h2o production.
This is an important written report that reveals truths of the human body that evidence sodium and water treatment is more complex than the models we accept used for over half a century. We have built entire kingdoms on the assumption that sodium excretion is equal to dietary sodium intake in neat 24-hour intervals. Like any research, this needs to be replicate. Only getting people to sign upwards for 100-day metabolic studies is not going to be forthcoming. Information technology is amazing that it took ten cosmonauts sealed into a simulated space station for 500 days to topple those ideas.
If these data are accurate
We need to end relying on the 24-hour urine as unquestioned truth
and
We need to start thinking of glucocorticoid as a major influencer in sodium and water metabolism
Information technology'due south a dauntless new globe.
Source: http://www.nephjc.com/news/2017/5/31/spookysodium
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