Mannitol

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Potassium follows water around, so a hyperosmotic state tends to become hyperkalemic as well. I'm not sure about the acidosis.
 
Probable explanation:

- Mannitol draws water from cell --> increased potassium concentration in the cell --> potassium diffuses out of the cell
- Water drags potassium along with it while moving out of the cell (solvent drag) [as thehundredthone mentioned]

- Mannitol inhibits reabsorption of water and electrolytes in the renal tubules (particularly effective in the PCT as it is the site for maximum reabsorption) --> decreased bicarbonate reabsorption --> bicarbonate leaking --> metabolic acidosis

(There may be some better explanations...)
 
The Stewart model of acid-base physiology is not commonly taught in medical school, but came up often in my residency training. It is very useful for predicting and explaining changes in acid-base status in this sort of scenario which is difficult to conceptualize by other approaches. Explaining the entire model is beyond this post, but there's a lot to read online.

In this situation, mannitol-induced osmotic diuresis causes increased sodium loss. The Strong Ion Difference, a determinant of acid-base in the Stewart model, is (Na + K + Mg + Ca) - (Cl + lactate), and a decrease in SID (such as that caused by sodium loss) will lead to increased liberation of free H+ and decreased pH, ie. metabolic acidosis.

As for the hyperkalemia, I don't think there is a consensus answer. Increased serum K+ can of course be caused by all acidosis, but mannitol may also raise K+ by inducing hemolysis or by a "solvent drag" phenomenon. The latter occurs when hypertonic infusions like mannitol induce shifts of fluid from the intracellular space, taking K+ with it. Interestingly, lower doses of mannitol have been observed to decrease K+ concentration.
 
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