Thread by @MohitHarshMD

As promised, pt 2 in Potassium #Tweetorial series. This time, Aldosterone and Potassium Homeostasis

Another large physiology topic, so I’ll be brief and stick to highlights from reading #BurtonRose textbook, which I highly recommend for all levels of learner

Thread ⬇️

https://twitter.com/MohitHarshMD/status/1255175181854740480

Aldo is well known to provide Internal Balance of K after oral intake or fluctuation in [K]

Aldo works by augmenting K secretion in principal cells. After K load, Aldo is directly enhanced and contributes to kaliuresis via changes in Na and K channels and Na-K-ATPase activity

The initial step is ⬆️ luminal Na permeability which in turn ➡️ enhancing K secretion.

Poll: Why does increased distal Na delivery aid in Kaliuresis?

⬆️ Distal Na delivery ⬆️ Na/K ATPase activity by transporting Na out of cell and K into cell. Reabsorption of Na then makes lumen electronegative ➡️ increases electrical gradient for K secretion.

This partially explains why Distal Flow Rate plays a role in renal handling of K

Gradients matter, majority of K is reabsorbed in prox tubule + loop of henle. [K] in distal nephron is quite low but in presence of ADH can be raised 2 ⬇️ gradient

In volume depletion the high luminal [K] + low U flow leads to reduced K secretion

Poll: ⬇️ECV does what to Aldo?

In order to combat the ⬇️ gradient, hypovolemia induces secondary hyperaldosteronism. This is clinically relevant.

These two forces counteract each other, which is why in abscence of significant renal injury or severe hypovol, untreated CHF/Cirrhotic patients are normokalemic

ECV depletion ⬇️ GFR and ⬆️ prox Na + H20 reabsorption in order to expand volume

This ⬇️ distal fluid delivery which ⬇️ K secretion despite secondary hyperaldo. This is relevant in renal failure where Na conserving capability is ⬇️, making theme susceptible to volume depletion

This can happen with significant extra-renal losses, too. Case below.

Elder lady with viral gastroenteritis has diarrhea over past week, she loses 5kg and has ⬇️UOP. She has ⬇️PO intake mainly as OJ. PE w/ postural hypoTN and ⬇️skin turgor

Na 130/K 6.7/Cr 1.2/UNa 12/UK 62

Her Hx and PE show volume depletion, low Urine [Na] supports this. Although Urine [K] is elevated appropriately, her urine volume may be so low that daily excretion is not enough to Internally Balance.

Her intake of OJ (or Gatorade, etc) is high K intake which plays a role

This ends my tweetorial. Succinctly/systematically tying in basic physiology into clinical situations is challenging!

As always, please provide any feedback

All info and cases drawn from Burton Rose’s Text from the initial post. What a legacy to provide along with @UpToDate

@Charbel_Khoury @VijayanMD @kao_patricia @MDdreamchaser @always_oncall @RenalRhapsody @Maximal_Change @madmagicdoc @prathakker @GMatzumura @HumphreysLab @fernandbteich @kidney_boy @RosenelliEM @DxRxEdu @rabihmgeha @tony_breu @this_is_svenka @anuja_java @IgG4thewin @DoubleDawgMD