OSMOTIC DIURETICS MANNITOL
Osmotically active diuretics are
filtered at the glom-erulus and undergo limited or no reabsorption in the
proximal tubule. Their presence in the proximal tubule limits the passive water
reabsorption that nor-mally follows active sodium reabsorption. Although their
major effect is to increase water excretion, in large doses, osmotically active
diuretics also increase electrolyte (sodium and potassium) excretion. The same
mechanism also impairs water and solute reab-sorption in the loop of Henle.
Mannitol is the most commonly used osmotic diuretic. It is a six-carbon
sugar that normally undergoes little or no reabsorption. In additionto its diuretic effect,
mannitol appears to increase RBF. The latter can wash out some of the medullary
hypertonicity and interfere with renal concentrat-ing ability. Mannitol appears
to activate the intrare-nal synthesis of vasodilating prostaglandins. It also
appears to be a free radical scavenger.
Many clinicians continue to administer mannitol for renal protection
and, less frequently, to convert oliguric acute kidney failure to nonoliguric
kidney failure, with the goal of lowering associated mor-bidity and mortality.
However, there is no evidence that such use of mannitol provides renal
protec-tion, lessens the severity of AKI, or lessens the morbidity or mortality
associated with AKI when compared with correction of hypovolemia and
preservation of adequate renal perfusion alone. In addition, high-dose mannitol
can be nephrotoxic, especially in patients with renal insufficiency.
Mannitol will augment urinary output in the set-ting of
hypovolemia but will have little effect in the presence of severe glomerular or
tubular injury. However, the optimal initial approach to evaluation of acute
oliguria is to correct hypovolemia and opti-mize cardiac output and renal
perfusion.
The intravenous dose for mannitol is 0.25–1 g/kg.
Mannitol solutions are hypertonic and
acutely raise plasma and extracellular osmolality. A rapid intra-cellular to
extracellular shift of water can transiently increase intravascular volume and
precipitatecardiac decompensation and pulmonary edema in
patients with limited cardiac reserve. Transient hyponatremia and reductions in
hemoglobin con-centration are also common and represent acute hemodilution
resulting from rapid movement of water out of cells; a modest, transient
increase in plasma potassium concentration may also be observed. It is also
important to note that the ini-tial hyponatremia does not represent
hypoosmo-lality but reflects the presence of mannitol . If fluid and
electrolyte losses are not replaced following diuresis, mannitol
administra-tion can result in hypovolemia, hypokalemia, and hypernatremia. The
hypernatremia occurs because water is lost in excess of sodium. As noted above,
high-dose mannitol can be nephrotoxic, especially in patients with renal
insufficiency.
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