Diuretic resistance – how to overcome? Review article

Main Article Content

Robert Małecki

Abstract

Diuretic therapy remains a cornerstone of therapy for patients with chronic heart failure and clearly improve symptoms and quality of life. Resistance to diuretic action is frequently encountered in the clinical setting. Diuretic resistance may be caused by decreased renal function and reduced and delayed peak concentrations of loop diuretics in the tubular fluid but chronic treatment with a diuretic results in compensatory hypertrophy of epithelial cells and consequently its diuretic effect will be blunted. Strategies to overcome diuretic resistance include restriction of sodium intake. Salt intake must be restricted in patients with heart failure to obtain a negative sodium balance. Pharmacodynamic measures include improving the underlying disease state, limiting the use of vasodilators and eliminating drugs which may modify the response to the diuretic. Concomitant administration of a more distally acting diuretic will usually result in substantial diuresis. Diuretic resistance can also be managed by increasing the frequency of loop diuretic dosing or by switching to a continuous intravenous infusion. Potassium sparing diuretics may also be able to increase the effectiveness of more proximally acting diuretics. Ultrafiltration has also been used as a nonpharmacologic strategy to treat patients who exhibit resistance to diuretics. Effective monitoring of volume status with newer modalities may allow more selective use of diuretics.

Downloads

Download data is not yet available.

Article Details

How to Cite
Małecki , R. (2007). Diuretic resistance – how to overcome?. Cardiology in Practice, 1(3), 139-143. Retrieved from https://journalsmededu.pl/index.php/kwp/article/view/1707
Section
Articles

References

1. Bard R.L. et al.: Food: An Unrecognized Source of Loop Diuretic Resistance. Pharmacotherapy 2004, 24 (5):630.
2. Kirchner K.A., Voelker J.R., Brater D.C.: Intratubular albumin blunts the response to frusemide-A mechanism for diuretic resistance in the nephrotic syndrome. J. Pharmacol. Exp. Ther. 1990, 252:1097.
3. Brater D.C.: Diuretic therapy. N. Engl. J. Med. 1998, 339:387-95.
4. Hamm L.L., Batuman V.: Edema in the Nephrotic Syndrome: New Aspect of an Old Enigma. J. Am. Soc. Nephrol. 2003, 14(12).
5. Sica D.A.: Diuretic-Related Side Effects: Development and Treatment. J. Clin. Hypertens. 2004, 6(9):532.
6. Heywood J.T.: Combining nesiritide with high-dose diuretics may increase the risk of increased serum creatinine. J. Card., Fail 2005, 11 (supl.): S154.
7. Ferreira A., Bettencourt P., Pimenta J. et al.: The renal dopaminergic system, neurohumoral activation, and sodium handling in heart failure. Am. Heart. J. 2002, 143:391-7.
8. Ungar A., Fumagalli S., Marini M. et al.: Renal, but not systemic, hemodynamic effects of dopamine are influenced by severity of congestive heart failure . Crit. Care Med. 2004, 32:1125–1129.
9. Marik P.E.: Low-dose dopamine: a systematic review. Intens. Care Med. 2002, 28:877-883.
10. Elkayam U., Tasissa G., Binanay C. et al.: Use and impact of inotropes and vasodilator therapy during heart failure hospitalization in the ESCAPE Trial. Circulation 2004, 110 (supl. 3):515.
11. Sharma A., Hermann D.D., Mehta R.L.: Clinical benefit and approach of ultrafiltration in acute heart failure. Cardiology 2001, 96:144-154.
12. Jaski B.E., Ha J., Dentys B.G. et al.: Peripherally inserted veno-venous ultrafiltration for rapid treatment of volume overloaded patients. J. Card. Fail 2003, 9:227-31.
13. Costanzo M.R. for the UNLOAD Investigators. Late-Breaking Clinical Trial presented at the 2006 American College of Cardiology Scientific 55th Annual Scientific Session. Ultrafiltration versus intravenous diuretics for patients hospitalized for acute decompensated heart failure. March 11-14, 2006. Atlanta, Georgia.
14. Levey A.S.: Assessing the effectivness of therapy to prevent the progression of renal disease. Am. J. Kidney Dis. 1993, 22(1):207-14.