Why ESRD patient still take furosemide???

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Why ESRD patient still take furosemide???

I know that furosemide can increase urine output, but if the patient is on HD or peritoneal dialysis, is it really need to take this drug?

moreover, someone said using this drug in this case is to challenge the kidneys to see if there is any renal function left. is it reasonable?

besides, some friend said CHF is easily to get in ESRD patient, this drug is used in this case is to prevent and relieve CHF. is it reasonable?

help me pls. it is sosososo difficult.>

Specializes in Critical Care, Hospice, Picc LInes.

Ok - I just read this excellent article which explains why diuretics a in ESRD patients. Here is the link: http://www.advancesinpd.com/adv14/115-119_Kumra.pdf

Ok - I just read this excellent article which explains why diuretics a in ESRD patients. Here is the link: http://www.advancesinpd.com/adv14/115-119_Kumra.pdf

Excerpts (number refer to the articles in the bib at the end of the article):

Loop diuretics are the drug of choice in patients with end-stage renal disease (ESRD) because they are thought to be effective to some degree at low GFR (3). However, a reduction in GFR results in less tubular transport of the diuretic to the lumen of the nephron (the site of action), which limits the maximum achievable diuretic effect. In fact, in patients with a GFR below 15 mL/min, secretion of the loop diuretic into tubular fluid is only 10% – 20% of that seen in individuals with normal renal function (4). To overcome that difference, a sufficiently high dose (that is, 160 – 200 mg intravenous furosemide) might be needed to attain effective diuresis or maximal natriuresis (approaching 20% of the filtered Na+ load) (4,5). In patients with a GFR below 10 mL/min and a daily urine volume below 100 mL, the effect of diuretics might be minimal (6).

Thiazide diuretics block the Na+·Cl co-transporterin the distal tubule. Hydrochlorothiazide,metolazone, indapamide, and chlorthalidone belongto this class of diuretics. As in the case of loop diuretics,decreased delivery of thiazide diuretics tothe nephron lumen requires that sufficiently highdoses be given in the context of diminishing GFR.Using hydrochlorothiazide as an example, 50 –100 mg daily might have to be prescribed in mildto-moderaterenal failure and 100 – 200 mg daily insevere renal failure (5). Still, even at those highdoses, hydrochlorothiazide, because of its low potencyand limited natriuresis, is not typically effectivein severe renal failure (4). To achieve effectivediuresis with a thiazide diuretic in patients with aGFR below 30 mL/min, the more common approachis to give it in combination with a loop diuretic (7,8).The combination generates additive natriuresis inthe setting of loop diuretic resistance and can allowfor lower doses of the latter drug to be administered.

Potassium-sparing diuretics act in the distal renaltubule. Spironolactone, amiloride, and triamterene areexamples of this drug class. Spironolactone competeswith aldosterone for receptor sites and increases sodium,chloride, and water excretion while conservingpotassium. Amiloride and triamterene block epithelialsodium channels that inhibit sodium reabsorption,decrease the function of the Na–K pump, and leadto potassium retention. True to their name, they cancause hyperkalemia (especially in patients with diabetes)and should be used with caution (7).Other less commonly used classes of diuretics areosmotic diuretics (mannitol) and carbonic anhydraseinhibitors (acetazolamide).
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