How much salt is not enough?

The most common dietary rec made by physicians is sodium restriction

But to what extent?

Is an overly sodium restricted diet harmful? Especially in HF?

🔥Grab a salted pretzel and read on
#medtweetorials #nephtwitter #cardiotwitter #MedTwitter
What degree of sodium restriction to you recommend to your heart failure patients?
🔥🧂 is important

💥🧂 conservation during human evolution from sea to land was vital

In the book From Fish to Philosopher, Homer Smith wrote “The tenacious conservation of salt is one of the most primitive - if not the most primitive - of functions in the vertebrate kidney"
Throughout history🧂has triggered wars and protests

💥Roman soldiers were paid in🧂(as were American soldiers in 1812)
💥Where we got the word “salary" 💰

💥Now? There is no shortage of 🧂

👉Dietary Na intake in US adults-3660mg
👉Dietary Na intake worldwide-3660-4000mg
Major societies differ regarding Na restriction recs

CDC: <2300mg
AHA: <1500mg
WHO: <2000mg

🔥We know ⬇️Na diets = clear benefit in HTN

🔥Cochrane review (185 studies)
💥⬇️ mean Na from a whopping 11.5g➡️3.8d =
💥⬇️SBP/DBP of 1/0 if normotensive and 5.5/2.9 if hypertensive
🔥Low Na DASH diet

💥Near linear BP improvement with low Na diet (1.1g) v intermediate (2.3g) and high (3.5g) Na diets

💥The effects of dietary sodium restriction on BP appear to be heterogenous with older, hypertensive and African American patients deriving the most benefit Image
How does this translate to actual CV outcomes?
🔥Data isn't as clear

💥One observational study in JAMA assessed effects of Na restriction and CV events in 2 cohorts at high risk of CV disease
👉jamanetwork.com/journals/jama/…

💥Found a J-shaped curve with <3g Na intake = ⬆️CV events Image
The PURE study, published in the NEJM found nearly identical results

👉pubmed.ncbi.nlm.nih.gov/25119607

🔥majority of participants with no CV disease
🔥also saw ⬆️ in CV events with a <3g sodium restricted diet Image
The problem?
💥Used AM urine collections to est. 24h Na excretion via the Kawasaki formula

Apparently validated here
👉pubmed.ncbi.nlm.nih.gov/8432042/

💥Important because >90% of dietary is Na excreted in urine

💥Shown in this systematic review
👉onlinelibrary.wiley.com/doi/epdf/10.11…
🔥The TOHP study, which utilized 24h urine collections for assessment of Na intake:

💥Did not see a J shaped curve
💥Instead found a significant ⬇️ in CV events ➡️ even at the lower end of Na intake

Read it here
👉ahajournals.org/doi/epub/10.11… Image
🔥Why would Na restriction cause problems?

💥The Cochrane study above showed ⬆️ neurohumoral activation with ⬇️🧂 intake

🔥But is this really harmful?
💥The Yanomami were shown to consume <1g (!) of Na in the INTERSALT study
💥have sky high aldo/renin levels
💥but no ⬆️ in CVD ImageImage
🔥How about pts vulnerable to NH activation, i.e CHF pts?

Paterna et al randomized 232 pts w/HFrEF
💥30d post hosp. d/c
💥2.7g vs 1.8g Na diets
💥Both received diuretics +1L🥤restric + GDMT

🔥⬆️Na group had ⬇️BNP, hospital readmissions and mortality
👉pubmed.ncbi.nlm.nih.gov/19101237/ Image
🔥Another RCT by Parrinello w/173 pts
💥compensated HFrEF
💥2.7g vs 1.8g Na diets
💥30d post hosp. d/c
💥Both groups 1L 🥤 restric.+diuretics+GDMT

🔥Pts in the 1.8g Na group had ⬆️renin, aldo, inflammatory cytokines and hospital readmissions

👉pubmed.ncbi.nlm.nih.gov/19944363/ ImageImage
🔥To be clear the above studies (and societal guidelines) discuss Na restriction
💥Na can be consumed in various forms BUT

👉study …-nih-gov.offcampus.lib.washington.edu/1910064/

💥showed that table salt (NaCl) provides 90% of dietary sodium

💥So we are really talking about both Na AND Cl-
🔥The HF studies above have issues
💥Same research group
💥? duplication of data between studies
💥Rigid diuretic protocol, i.e ⬇️ Na intake with same diuretic dose = ⬆️ r/o hypovolemia

🔥BUT theoretically possible that ⬇️🧂(to a degree) = ⬆️NH activation➡️bad outcomes in CHF
🔥⬆️Na clearly has detrimental effects
💥⬆️NOX-4 + VEGF
💥⬇️NO
💥⬆️myocardial hypertrophy and glomerular fibrosis

🔥But💡⬇️ Cl- is harmful in CHF pts. 👇 and the same principal may apply here!
💥Maybe ⬇️ Cl- by⬇️🧂= ⬆️ NH activation = bad outcomes

🔥While I’m not ready to advocate for my heart failure patients to liberally use their🧂shaker

It's at least food for thought...

Thanks to @christinelimont for help with this

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More from @captainchloride

May 18, 2021
How does increasing dietary potassium improve blood pressure?

I’ve heard this, even recommended it. But how does this really work? Grab some prunes and follow along this Tuesday morning tweetorial.

#Nephtwitter #cardstwitter @MedTweetorials
Let’s establish that potassium does appear to have an inverse relationship with BP

In a meta-analysis of 22 RCTs ⬆️ K+ intake⬇️BP by an average of 5.3/3.1 mmHg

💥greatest benefit seen in hypertensive patients who ⬆️potassium intake to 90-120mEq/d

👉pubmed.ncbi.nlm.nih.gov/23558164/
This study showed a ⬇️need for antihypertensives if dietary K+ was ⬆️
💥RCT 47 pts w/ htn
💥⬆️ K+ vs usual K+ diet
💥45% ⬆️ in dietary K+ in ⬆️ K+ group
🔥Hypertensive therapy ⬇️by at least 50% in 81% of intervention group v 29% in control group at 1 yr

👉pubmed.ncbi.nlm.nih.gov/1929022/
Read 15 tweets
Aug 24, 2020
When was the last time you were paged about a serum Cl- level? Probably never.

Despite being the most abundant anion in the body, Cl- is under appreciated

🔥Here’s why it matters (esp in heart failure!)

#tweetorial #medtwitter #nephtwitter #cardiotwitter #NSMC
There is evidence supporting the use of hypertonic saline in patients with decompensated heart failure

See excellent blog post by @aldorodrig
👉 renalfellow.org/2019/04/03/the…

Mechanistically it never made sense to me, until I realized I may be focusing on the wrong ion 🤷🏾‍♂️
Chloride MAY be the 🔑 here. Something that will hopefully be more clear after the completion of ongoing trials

👉🏾 clinicaltrials.gov/ct2/show/NCT03…

In heart failure patients ⬇️ Cl- is associated with

1. Poor Prognosis
2. Neurohumoral activation
3. Diuretic Resistance
Read 10 tweets
Jun 25, 2020
Do you often check a FeNa when working up a patient with AKI?

In my experience it’s ordered reflexively

But is this a good idea? Is a FeNa actually useful?

Let’s find out #NSMCInternship #nephtwitter #tweetorial

Poll!
To differentiate between prerenal AKI and ATN you would
In normal circumstances sodium excretion = dietary intake

🔥What goes in must come out = extracellular volume is maintained within a narrow range

⬇️Volume → ⬆️RAAS →⬇️sodium excretion
⬆️Volume → ⬆️ANP → ⬆️sodium excretion

🤷‍♂️So why not just use UNa as a surrogate?
💡Remember UrNa is affected by concentration (hint: units are mEq/L)

Dilute urine = ⬇️UNa even if excretion is high
Concentrated urine = ⬆️UNa even if total excretion is low

🔥FeNa provides a measure of sodium handling that is INDEPENDENT of urinary concentration
Read 16 tweets

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