Diuretic Resistance

Problem

Mechanism

Solution

Limits active transport of diuretics into proximal tubular fluid, reducing inhibitory effect at a more distal intraluminal membrane site

Reduced renal blood flow

Use of large doses of a diuretic and appropriate dosing interval to achieve a therapeutic tubular drug concentration

Limits absolute amount of sodium filtered

Reduced glomerular filtration rate

Use loop diuretics with steep dose response curve and/or block multiple sites of sodium reabsorption: loop diuretic with thiazide-like diuretic

Sodium recaptured at late distal tubule and collecting duct

Secondary hyperaldosteronism

Addition of a potassium-sparing diuretic to above, to maintain urine sodium/potassium ratio > 1

Diuretic resistance. Diuretic resistance may result from patient noncompliance, impaired bioavailability in an edematous syndrome, impaired diuretic secretion by the proximal tubule, protein binding in the tubule lumen (eg, nephrotic syndrome), reduced glomerular filtration rate, or enhanced sodium chloride reabsorption [7,8]. Resultant fluid retention will attenuate the effectiveness of most anti-hypertensive drugs. Renal mechanisms, problems, and solutions are provided in this table [6,8,9].

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