🤔🔬Why are kidney stones so interesting?
Because the 🔑tubules > glomeruli

Disagree if you like, but it’s true.

A short thread on some mechanisms associated with calcium stones...

#nephtwitter #FOAMed #MedEd #uronephrology #kidneystone #nephrolith Image
Which is a risk factor for calcium oxalate stones?
Correct!

Risk factors for calcium oxalate stones classically include 📌hypercalciuria and 📌hyperoxaluria along with 💧low urine volume.

#Hypercalciuria can stem from a LOT of different causes and clinical settings. The most common in adults is idiopathic. Image
There is debate about whether hyperuricosuria can serve as a nidus for CaOx stones.

pubmed.ncbi.nlm.nih.gov/18059457/

Hypocitraturia and high urine pH (>7.0) tend to be stronger risk factors for CaP stones (we’ll discuss that later!)

Photo courtesy of @porische ImageImage
What is the link between hypercalciuria and salt (🧂NaCl) intake?
Right! ⬆️More NaCl --> ⬆️ Urine Calcium

❓How does this happen?!
💡The kidney has the answer.

In the proximal tubule, 🦴Ca reabsorption is linked with 🧂Na reabsorption.

With more 🧂Na reabsorption, 💧H2O follows paracellularly and “drags” 🦴Ca along with it. #solventdrag Image
In the DCT, ⬆️increased 🧂Na delivery reduces the stimulus for Na/Ca exchange on the basolateral membrane

This results in ⬇️less Ca influx via TRVP5 channel.

🌟If you understand this, you understand why normal saline is effective in hypercalcemia.

pubmed.ncbi.nlm.nih.gov/27009338/ Image
Now, what is the link between hypercalciuria and 🍋acidosis?
Essentially besides leaching Ca from 🦴bones, acidosis 🖇️uncouples Na reabs from Ca reabs in the DCT.

In acidosis,
📌PT: Na and Ca reabs linked
📌DCT: ⬇️LESS Ca influx due to inhibition of TRPV5 and reduced TRPV5 mRNA due to H+

🌟Net effect: ⬆️more UrCa

pubmed.ncbi.nlm.nih.gov/27468975/ Image
In the work up of hypercalciuria in calcium stone formers, it is important to consider 🧬monogenetic causes (esp in pediatrics)

pubmed.ncbi.nlm.nih.gov/15689405/
pubmed.ncbi.nlm.nih.gov/18446382/
pubmed.ncbi.nlm.nih.gov/18836558/ Image
When the initial screen and/or work up are negative, we’re stuck with 🤷‍♀️idiopathic hypercalciuria.
❓You may ask, should you counsel patients to reduce Ca intake to reduce risk of Ca stones and hypercalciuria?!
Correct, you should not.

Calcium intake has been found to reduce risk of stone formation likely by binding intestinal oxalate and reducing oxalate absorption.

pubmed.ncbi.nlm.nih.gov/8441427/ Image
But, (a) #PUSHing fluid💧 increases urine volume (ie lower the concentration of urinary calcium and reduce the relative supersaturation)

Coffee, tea, wine, beer, high citrate juices seem ok.👌


pubmed.ncbi.nlm.nih.gov/23676355/
Encourage low salt diet (UrNa goal < 80-100 mEq per day) and consider thiazide diuretics.

pubmed.ncbi.nlm.nih.gov/20042524/ Image
Hope that helps the next time you have a calcium stone former with hypercalciuria.

Suggestions/comments are always welcome! #uronephrology #kidneystone #nephrolith

Next up?
Lol I just realized answers A and B are the same. Why didn't anyone say anything?!!! #babybrain

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More from @amyaimei

13 Sep
⁉️What is the difference between mineral and organic acidosis?
⁉️Why does one cause more hyperkalemia than the other?

Join me on this 🐇🕳️rabbit hole #tweetorial on metabolic acidosis and it's effect on potassium.

📊To start, which type of acidosis causes more hyperkalemia?
Metabolic acidosis is defined as a ⬇️low pH due to a ⬇️decrease in bicarbonate extracellularly

💎Mineral acids (aka inorganic acids) are “synthesized from earth minerals.”

🥬Organic acids are metabolized by the cell and occur naturally.
Both can have a 🩸high anion-gap...just depends on anion accumulated.

💎Mineral acids are often (not always) a hyperchloremic normal anion gap metabolic acidosis

Think of 🥬organic acidosis as high anion gap metabolic acidosis (though not always true)
Read 19 tweets

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