Trouble with solutes in kidney failure

[loveoforganic2]

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I don't think we ever really got a lecture on the pathophys (at least not yet) of electrolyte changes in renal failure. The way I've been thinking about it is that if the kidney is generally actively secretes something, serum concentration will go up in RF, and if a solute is generally actively reabsorbed, serum concentration will go down in RF. This works for potassium (hyperkalemia), organic acids (metabolic acidosis), etc., but apparently, according to qbank anyway, you get hypernatremia in RF as well. I'm hoping that we're going to cover this in more detail this coming semester, but in the meantime, does anyone have a good explanation or a link to a good explanation of the pathophysiology of serum changes in acute and chronic renal failure?

Thanks a bunch!

Edit: new smiley?

 

[Phloston]

I don't think we ever really got a lecture on the pathophys (at least not yet) of electrolyte changes in renal failure. The way I've been thinking about it is that if the kidney is generally actively secretes something, serum concentration will go up in RF, and if a solute is generally actively reabsorbed, serum concentration will go down in RF. This works for potassium (hyperkalemia), organic acids (metabolic acidosis), etc., but apparently, according to qbank anyway, you get hypernatremia in RF as well. I'm hoping that we're going to cover this in more detail this coming semester, but in the meantime, does anyone have a good explanation or a link to a good explanation of the pathophysiology of serum changes in acute and chronic renal failure?

Thanks a bunch!

Edit: new smiley?

In pre-renal failure, because there's decreased GFR, you get a compensatory SNS response to increase fluid retention at the PCT, thereby increasing Na+ reabsorption considerably. That's let alone the fact that the decreased GFR by itself will increase serum sodium.

 

[loveoforganic2]

Thanks for the reply. I attached the Qbank question to this post.

I guess my problem in this instance was thinking that at this point the patient would be in renal failure, not pre-renal failure, correct? Just intuitively thinking, if you're in intrinsic renal failure, even if the GFR is decreased, you normally reabsorb 99% of your sodium, so if your tubular epithelium is nonfunctioning, even with a low GFR, you're going to be net excreting sodium. Is this logic incorrect? If it is correct, how do you distinguish pre-renal failure from pre-renal failure that's progressed to renal failure without additional lab values (BUN/Cr ratios, FENa, etc.)?

Thanks again

 

[withrye]

Acute kidney injury (aka acute renal failure) is not limited to intrarenal failure. In the case of trauma, you can assume the blood loss is causing some serious prerenal azotemia, leading to an increased reabsorption of urea, Na, and water. I agree however that the question is vague about the specific etiology of the kidney injury.

 

[Ycut]

In this particular case I think more of crash syndrome-rhabdomyolisis-acute renal failure-obstructing pct s-increasing hydrostatic pressure in bowman's space-opposing GFR=not filtering Na

Otherwise i agree that renal failure causes Na loss

 

[loveoforganic2]

Thank you both for the input. The possibility of rhabdo didn't come to mind (I was fixating on blood loss). They very well could have been hinting at rhabdo, which would make the answer more cut and dry

 

[Suncrusher]

I agree with ycut about motor vehicle collision="crush" injury=rhabdomyolysis. And I remember doing this question! It's nice to know working these qbanks is paying off

 

[OneMoreRound]

In this particular case I think more of crash syndrome-rhabdomyolisis-acute renal failure-obstructing pct s-increasing hydrostatic pressure in bowman's space-opposing GFR=not filtering Na

Otherwise i agree that renal failure causes Na loss

👍

This seems to be the correct reasoning. Acute tubular injury / acute renal failure --> obstruction ---> decreased GFR.

Wouldn't these solutes present like this in basically any actue tubular injury? I don't think you needed to know the crush injury is nephrotoxic since they tell you that it's acute renal failure regardless.

 

[Jonari]

Lol, I made a thread about this question and so did somebody else. Isn't this question linked to a video explained by Dr. Kuthrath? As the member above mentioned, it's due to the crush injury.

 

[Ycut]

👍

This seems to be the correct reasoning. Acute tubular injury / acute renal failure --> obstruction ---> decreased GFR.

Wouldn't these solutes present like this in basically any actue tubular injury? I don't think you needed to know the crush injury is nephrotoxic since they tell you that it's acute renal failure regardless.

Yes
Any acute tubular damage whether ischemic or toxic-progressing to acute renal failure, where u have plugging tubules with tubular casts gives u the same picture

Just from case above i suspected crush syndrome

 

[Jonari]

I'm doing renal again and this topic came up in Pathoma. It still doesn't make sense, because crush injury leads to myoglobinuria...which causes obstruction and decreases the GFR, which we all know.

- the myoglobin causes injury and necrosis so you can't reabsorb sodium, so FENa is greater than 2%...so shouldnt sodium levels be decreased? also same for the B:C ratio, not reabsorbing urea because dont have intact epithelial cells...so why is this elevated?