Regarding loop diuretics, all of the following statements are correct EXCEPT:

Explanation

## Loop Diuretics: Mechanism and Clinical Effects ### Mechanism of Action **Key Point:** Loop diuretics (furosemide, torsemide, bumetanide, ethacrynic acid) inhibit the Na-K-2Cl cotransporter (NKCC2) in the thick ascending limb of the loop of Henle, blocking reabsorption of ~25% of filtered sodium. ### Why Each Statement Is Evaluated | Statement | Correctness | Rationale | |-----------|-------------|----------| | Na-K-2Cl cotransporter action | ✓ Correct | Hallmark mechanism of loop diuretics | | Hyperuricemia via urate secretion competition | ✓ Correct | Loop diuretics compete with uric acid at URAT1 in proximal tubule, reducing uric acid excretion | | Torsemide pharmacokinetics | ✓ Correct | Torsemide has longer half-life (~3–4 h vs 1–2 h for furosemide) and more consistent oral bioavailability (>90% vs 10–60% for furosemide) | | Increased renal perfusion in acute decompensation | ✗ **INCORRECT** | Loop diuretics *decrease* renal perfusion and GFR in acute decompensated heart failure by reducing intravascular volume and renal perfusion pressure | ### Clinical Pearl **Warning:** In acute decompensated heart failure (ADHF), loop diuretics reduce preload and improve pulmonary congestion, but they do NOT improve renal perfusion — in fact, they may worsen renal function if the patient is volume-depleted or hypotensive. This is a common exam trap. Renal perfusion improves only when systemic perfusion is restored (e.g., after inotropic support or mechanical support). ### High-Yield Adverse Effects of Loop Diuretics **Mnemonic: HALE** — Hyperuricemia, Ototoxicity, Alkalosis, Electrolyte depletion (hypokalemia, hyponatremia, hypocalcemia, hypomagnesemia) - **Hyperuricemia** → gout risk - **Ototoxicity** → high-dose IV furosemide (especially with aminoglycosides) - **Alkalosis** → contraction metabolic alkalosis - **Electrolyte losses** → K^+^, Na^+^, Ca^2+^, Mg^2+^ wasting [cite:KD Tripathi 8e Ch 18]