Vomiting Kidney Metabolic Alkalosis Question

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coreytayloris

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So excessive vomiting causes water loss, and metabolic alkalosis (as a result of loss of H+, and presumably some K+ as well)

What response does this cause in the kidneys. I'm reading different things.

One the one hand you don't want to further exacerbate hypokalemia, so Renin release should be inhibited.

But, if blood volume is low as a result of water lost to vomiting, then renin release and thus aldosterone should be stimulated?!

Confused :confused:

Thanks

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I believe the second one is correct. With vomiting, you get an increase in aldosterone to try to maintain the blood volume. Results in Na+ and H+ absorption at the expense of K+
 
Renin releasing cells doesn't care about potassium status. if kidney is underperfused, renin will be increased, K+ be damned.

Aldosterone release increases in response to hyperkalemia but that's not part of the RAAS.
 
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So excessive vomiting causes water loss, and metabolic alkalosis (as a result of loss of H+, and presumably some K+ as well)

What response does this cause in the kidneys. I'm reading different things.

One the one hand you don't want to further exacerbate hypokalemia, so Renin release should be inhibited.

But, if blood volume is low as a result of water lost to vomiting, then renin release and thus aldosterone should be stimulated?!

Confused :confused:

Thanks

You must understand the physiology. The body isn't teleological. "Im losing K, so I should prevent the loss of K!" its physiological. Each part of the body has a specific stimulus and does one thing in response to that stimulus.

The Macula Densa, the Juxtaglomerular Aparatus, does one thing. It measures fluid status. That's it. What confuses students is that is "measures fluid status by measuring the amount of sodium in the nephron." Take that out of your knowledge vocabulary. What its really saying is "the JG apparatus measures FLOW through the nephron."

If there is too much fluid IN THE VESSELS, the kidneys are well perfused, the glomerulus filters a lot of fluid into the nephron, lots of flow through the loop of henle makes the JG apparatus turn off. On the other hand, if there is not enough fluid IN THE VESSELS, the kidneys are underperfused, the glomerulus filters less fluid into the nephron, small flow through the loop of henle turns the JG apparatus on.

Stop. Make sure you understand that. Increased flow turns it OFF decreased flow turns it ON

Ok. now what does the JG apparatus do? Its starts a chain of events, that, once initiated, goes through to completion.

JG Apparatus on --> Renin --> Angiotensinogen --> ANG II --> Aldo
- ANG II causes vasoconstriction
- Aldo causes the collecting ducts to express more Enac channels. Na is absorbed (and with it water) while K is lost.

Analyze that. When the flow to the kidney is low, JG apparatus is turned on. When the flow to the kidney is low, the kidneys feel that the body is volume depleted. It doesn't matter what the status of the body is (overloaded from CHF, or euvolemic with renal artery stenosis), if the flow through the kidney is low, the kidney thinks the body is volume down. So, the response is to tighten up the blood vessels (ANGII) and to increase the vascular volume (aldo). The cost of aldosterone activity is to lose K. The benefit is to reabsorb water.

Also note that Aldo does something else. Aldo excretes acid. You lose acid when you are volume down. Its just something aldo does. Its called a contraction alkalosis. As your fluid volume contracts (i.e. gets smaller, less flow), your aldo turns on to preserve that fluid volume. In doing so, it releases acid into the urine, retaining bicarb, making you alkalotic.

So the cost of being volume down, for any reason, burns, infection, or vomitting, is to decrease flow through the kidney. What does that do? Turns on JG apparatus, whcih turns on Renin, which turns on ANG II which turns on Aldo, which holds on to fluid, with the cost of losing K and Acid.

Now, what is the potassium sensor in the body? What is the physiologic structure that says "my K is low" or "my K is high?" you should be struggling. There isn't one. We are that sensor. We draw blood and take a look at K. If there is a derrangement in fluid status, we lose K to maintain fluid. If there is a derrangement in K, there is nothing to correct it. Instead, we, as physicians, must correct the K or the condition that has led to the bad K.

Got it?
 
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Increased flow turns it on, decreased flow turns it off.

Oops? :p

The rest looks good though, great explanation. The other big thing driving contraction alkalosis is AT2 promoting Na+/H+ exchange in the proximal tubule, which leads to more bicarb reabsorption. I only mention this because for the longest time I was confused about the mechanism for contraction alkalosis, some sources say it's Aldo at the CT and others AT2 at the PCT. Finally i figured out that it was both. :smack:
 
Oops? :p

The rest looks good though, great explanation. The other big thing driving contraction alkalosis is AT2 promoting Na+/H+ exchange in the proximal tubule, which leads to more bicarb reabsorption. I only mention this because for the longest time I was confused about the mechanism for contraction alkalosis, some sources say it's Aldo at the CT and others AT2 at the PCT. Finally i figured out that it was both. :smack:
Yes oops, and I've fixed it. Thanks!
 
Just wanted to add that the hypokalemia present in vomiting is mostly due to renal potassium wasting, NOT the (small amount of) K+ lost in the emesis.

Also, I have to disagree with the idea that people have no way to regulate their potassium levels. Were this the case, none of us would be here today, as our monkey ancestors would've arrested pretty quickly after their banana boluses.
 
Just wanted to add that the hypokalemia present in vomiting is mostly due to renal potassium wasting, NOT the (small amount of) K+ lost in the emesis.

Also, I have to disagree with the idea that people have no way to regulate their potassium levels. Were this the case, none of us would be here today, as our monkey ancestors would've arrested pretty quickly after their banana boluses.

What's the sensor?

What's the intra or extracellular signal and what's its target?

Why doesn't K get corrected if you induce hypoK with a diuretic or it gets excreted with hyperaldo?

"Its in the Kidney" just means that concentration gradients control it. The point I was making is that there is no endocrine function in relationship to regulation of potassium. Potassium is regulated as a by-product of sodium/volume. Its why potassium levels can be derranged without changes in other organ systems (i.e. no compensation) and, more pertinent to the OP, to illustrate which stimulus "wins." Volume wins because there is a hormone process designed to handle it; there is no such endocrine function exists for potassium.
 
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