In the loop of Henle, the thick ascending limb (TAL) is impermeable to water. Furosemide, a loop diuretic, blocks NKCC2 in the TAL. The consequence on the renal medullary interstitial gradient is:

• A Medullary osmolality decreases (gradient is 'washed out') because NaCl is no longer pumped from TAL into the interstitium; tubular fluid is delivered to the collecting duct hypotonically with reduced capacity for concentration ✓
• B Medullary osmolality increases as more NaCl accumulates in the interstitium
• C Medullary gradient is maintained by urea trapping even without NaCl contribution
• D Furosemide has no effect on medullary gradient as the thin descending limb compensates

Explanation

The renal medullary concentration gradient (up to ~1200 mOsm/kg at the papilla) depends on the countercurrent multiplication system. The TAL actively reabsorbs NaCl (via NKCC2) without water (impermeable), making the interstitium hyperosmotic and tubular fluid hypotonic. This is the 'single effect' multiplied by countercurrent flow. Furosemide blocking NKCC2 abolishes NaCl reabsorption in the TAL, collapsing the medullary osmolality gradient ('gradient washout'). Even if ADH is present, the collecting duct cannot concentrate urine because the driving osmotic gradient for water reabsorption is absent. Urea contributes ~40–50% of medullary gradient but cannot compensate for loss of NaCl component. This mechanism explains why furosemide causes profound diuresis.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.