Diuretics & Renal Failure

Are diuretics just a way of “making urine”  or do they have inherent beneficial effects?

Diuretics actually have a number of potential beneficial effects

1. Renal cortical vasodilatation (dopaminergic agents, loop diuretics).

2. Prevention of tubular obstruction (osmotic, loop diuretics).

3. Suppression of reflex vasoconstrictive responses (dopaminergic agents, atrial natiuretic peptide [ANP]

4. Decreased tubular oxygen consumption (dopaminergic agents, loop diuretics).

5. Enhanced renal tubular oxygen balance by inhibiting the active sodium pump in the medullary thick ascending loop of Henle (mTAL) thereby conferring protection against ischemic or nephrotoxic injury.

The implication is that diuretics wash out the tubules, which may be partially blocked with necrotic debris, improve blood flow when vasoconstriction is inappropriate (such as during the stress response to surgery) and reduce the metabolic activity of the tubules (remember that the medulla is relatively hypoxic and oliguria is a defense mechanism for preventing ischemia).

What are the most commonly used diuretics in ICU?

Loop diuretics (furosemide, bumetanide, ethacrynic acid) are the agents of choice. They markedly inhibit sodium reabsorption in the thick ascending limb of the loop of Henle in the medulla (mTAL) and can induce diuresis even with marked renal impairment.

Can they prevent renal failure?

If administered prior to a renal ischemic or nephrotoxic insult, furosemide attenuates renal injury, probably through the mechanisms described; however, in clinical practice, loop diuretics usually are given post hoc; they must be given within 18 hours for any protective effect to be obtained.

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