In the proximal tubule, secondary to the activation of angiotensin II and Norepinephrine.1, 5 Increased tubular sodium reabsorption associated with the diuretic braking phenomenon may occur at different segments of the nephron: This problem is often due to increased tubular sodium reabsorption in nephron segments other than the loop of Henle with the chronic use of diuretics (the diuretic braking phenomenon). The fourth factor is that some patients with diuretic resistance have decreased natriuresis, despite adequate urinary delivery of the diuretic.The third and one of the important causes of diuretic resistance is the use of nonsteroidal anti-inflammatory drugs, which reduce the synthesis of prostaglandins, which will affect diuretic responsiveness. ![]() In addition, the filtered albumin in the urine secondary to high venous pressure may bind loop diuretics in the tubular lumen and interfere with its action. Secondary to this hypoalbuminemia the degree of diuretic - protein binding is reduced, which will result in a larger extravascular space of distribution of the diuretic with a slower rate of delivery to the kidney, and then reduced diuresis. Hypoalbuminemia may occur in CHF if albumin is filtered in the urine secondary to high venous pressure. It is also well known that loop diuretics are highly (≥95 percent) protein bound, which keeps the diuretic within the intravascular space, which will ensure good delivery of the diuretic to the kidney. 2 In case of CHF, renal perfusion and tubular blood supply is decreased due to decreased cardiac output, which decrease the delivery of diuretics to their site of action causing insignificant effect. Diuretic efficacy is mainly related to urinary excretion rates of the drug, rather than to its plasma concentrations. After that loop diuretics inhibit the Na-K-2Cl carrier in the luminal membrane of the thick ascending limb of the loop of Henle, which will reduce NaCl reabsorption. An important step in the mechanism of action of loop diuretics is that they enter the tubular lumen by secretion in the proximal tubule, not by glomerular filtration. Second factor that may contribute to refractory edema is decreased loop diuretic secretion.First factor is high salt intake which prevents net fluid loss even with adequate therapeutic doses of diuretics.Many factors are involved in the development of refractory edema, and the decreased response to the usual diuretic regimen. Keywords: refractory edema, congestive heart failure, furosemide-albumin infusion Abbreviations ![]() How to Monitor Response and Side Effects of IV Diuretic Therapy? All these questions are answered in the review article. ![]() To use intermittent Intravenous Bolus versus Continuous IV Infusion Diuretic Therapy, which is better, which is safest? What is Single IV Effective Dose of Loop Diuretics What is Maximum IV Effective Dose of Loop Diuretics? If IV Furosemide is Ineffective, Can I Switch to Equivalent IV Dose of Bumetanide or Torsemide? When to Add Thiazide Diuretic? When to Add Spironolactone? IV High-Dose Furosemide and Hypertonic Saline Solutions, The new ERA. Some pre-diuresis precautions, lab and imaging procedures are mandatory to ensure good effect of management. Many factors are involved in the development of refractory edema, and the decreased response to the usual diuretic regimen, during management of diuretic resistance all these factors must be in consideration. Diuretic resistance means failure to decrease the extracellular fluid volume despite the using of diuretics. Generalized edema occurs secondary to many clinical disorders the usual management of edema is the using of diuretics.
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