Case Study Furosemide Resistance

A A 26-year-old woman with nephrotic syndrome comes to your office because of worsening edema. Her medications include clonidine 0.1 mg orally twice daily and furosemide 200 mg orally twice daily. On physical examination, her blood pressure is 120/85 mm Hg, and she has generalized massive edema (anasarca). The rest of the examination is unremarkable.

Labatory Studies

Serum creatinine 1.9 mg/dL

Serum albumin 2.0 g/dL

24-hour urine protein excretion 13.0 g

24-hour urine sodium excretion 74.0 mEq

Which of the following factors may contribute to resistance to furosemide in this patient?

(A) Reduced bioavailability

(B) Reduced active tubular secretion of furosemide by the proximal tubule organic acid secretory mechanism

(C) Sequestration of furosemide by intraluminal albumin thereby reducing its inhibition of the Na-K-2Cl cotransporter

(D) Increased reabsorption of sodium downstream to the thick ascending limb of Henle's loop

(E) All of the above

E. Intestinal absorption of furosemide is reduced in patients with anasarca due to edema of the intestinal mucosa. All loop diuretics are highly protein bound; therefore the GFR of these agents is negligible. Availability at the luminal site depends on the activity of the organic acid secretory pump in the proximal tubule. In this patient, secretion of loop diuretics is limited because of reduced renal blood flow and accumulation of organic acids in renal insufficiency, which can compete with furosemide for proximal tubule secretion. In animals, albumin in the tubular fluid binds furosemide, preventing its access to the Na-K-2Cl cotransporter. After prolonged use of furosemide, hypertrophy of the distal tubule epithelial cells occurs, indicating compensatory increased reabsorptive capacity.

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