Step I Mannitol

[iA-MD2013]

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Does mannitol cause hypernatremia or hyponatremia?

I believe UWorld contradicts itself:
- "Common SEs of mannitol are N/V, headache, and hyponatremia"
- "Mannitol is not used as maintenace therapy for any indication because it causes a brisk free water diuresis that leads to hypernatremia with chronic use"

 

[Encephalectomy]

Does mannitol cause hypernatremia or hyponatremia?

I believe UWorld contradicts itself:
- "Common SEs of mannitol are N/V, headache, and hyponatremia"
- "Mannitol is not used as maintenace therapy for any indication because it causes a brisk free water diuresis that leads to hypernatremia with chronic use"

I think that it can cause both. Mannitol-->transfer of water from interstitial space/cells into plasma-->hyponatremia

mannitol--> diuresis of free water-->hypernatremia

so I guess maybe it can acutely case hyponatremia and then hypernatremia?

 

[iA-MD2013]

I think that it can cause both. Mannitol-->transfer of water from interstitial space/cells into plasma-->hyponatremia

mannitol--> diuresis of free water-->hypernatremia

so I guess maybe it can acutely case hyponatremia and then hypernatremia?

Ahh that makes sense. Thanks!

 

[raynor123456]

Also, with chronic use I'd imagine that RAA system would go into full effect due to hypovolemia.

 

[iA-MD2013]

Also, with chronic use I'd imagine that RAA system would go into full effect due to hypovolemia.

Ahh also explains it...thanks!

I have another UWorld renal question and don't want to make a new thread:
During the recovery phase of acute tubular necrosis, the high volume hypotonic urine causes sodium retention and decreased concentrations of K, Mg, Pi, and Ca.
Can someone explain that?

 

[raynor123456]

Ahh also explains it...thanks!

I have another UWorld renal question and don't want to make a new thread:
During the recovery phase of acute tubular necrosis, the high volume hypotonic urine causes sodium retention and decreased concentrations of K, Mg, Pi, and Ca.
Can someone explain that?

Just a guess in case nobody comes in here with anything definitive:

The only way I can think of that sodium would be retained is via the RAA system. If Na+ is being retained via RAA, then K+ is being lost. If K+ is being lost, then Mg and Ca won't have the K+-derived intratubular positive potential driving them through the paracellular spaces and are also lost. No good ideas about phosphate though.

 

[ArcGurren]

Ahh also explains it...thanks!

I have another UWorld renal question and don't want to make a new thread:
During the recovery phase of acute tubular necrosis, the high volume hypotonic urine causes sodium retention and decreased concentrations of K, Mg, Pi, and Ca.
Can someone explain that?

When you recover from ATN you have vigorous diuresis - that is your body reflexively needs to get rid of the extra volume retention during the time your kidneys were effed up and as a result the diuresis can actually cause hypo-everything. The most dangerous of these is hypokalemia, so you constantly need to monitor this.

I don't know the exact mechanism of the massive diuresis but I hope that makes sense.

 

[iA-MD2013]

When you recover from ATN you have vigorous diuresis - that is your body reflexively needs to get rid of the extra volume retention during the time your kidneys were effed up and as a result the diuresis can actually cause hypo-everything. The most dangerous of these is hypokalemia, so you constantly need to monitor this.

I don't know the exact mechanism of the massive diuresis but I hope that makes sense.

Kind of...
If you're loosing a hypotonic solution, shouldn't this cause hyper everything? What's the stimulus to pee out all the ions in the blood but Na?

And the RAAS resulting in sodium retention doesn't make sense to me because ATN was in an oliguric state before, so the body already had a tone of fluid...no need to add more. Also the kidneys tubules aren't very happy, so I doubt the DCT macula densa cells have any energy to stimulate the RAAS.

 

[raynor123456]

I don't know the exact mechanism of the massive diuresis but I hope that makes sense.

Another guess (lack time to look it up 😛)

A person with ATN is oliguric and hypervolemic. I'm sure that the diuresis would come directly from the hypervolemic state and is probably ANP mediated.