Diuretic therapy in heart failure: current controversies and new approaches for fluid removal

Abstract

Hospitalization for heart failure is a major health problem with high in-hospital and postdischarge mortality and morbidity. Non-potassium-sparing diuretics (NPSDs) still remain the cornerstone of therapy for fluid management in heart failure despite the lack of large randomized trials evaluating their safety and optimal dosing regimens in both the acute and chronic setting. Recent retrospective data suggest increased mortality and re-hospitalization rates in a wide spectrum of heart failure patients receiving NPSDs, particularly at high doses. Electrolyte abnormalities, hypotension, activation of neurohormones, and worsening renal function may all be responsible for the observed poor outcomes. Although NPSD will continue to be important agents to promptly resolve signs and symptoms of heart failure, alternative therapies such as vasopressine antagonists and adenosine blocking agents or techniques like veno-venous ultrafiltration have been developed in an effort to reduce NPSD exposure and minimize their side effects. Until other new agents become available, it is probably prudent to combine NPSD with aldosterone blocking agents that are known to improve outcomes.

Ultrasound evaluation of the inferior vena cava collapsibility index in congestive heart failure patients treated with intravenous diuretics: new insights about its relationship with renal function: An observational study

“…the patients with the lowest eGFR values. This finding also is in line with the data of other studies (32)(33)(34)(35), where a higher dose of diuretics is usually given to CHF patients who have a more compromised renal function at baseline. According to several Authors (36), in these patients a higher diuretic dosing may be appropriate because the delivery of furosemide to the renal tubules positively depends on renal function in CHF patients and considering that a creatinine clearance of 15 mL/ min parallels a tubular secretion of furosemide five-to ten-fold lower than that in normal subjects (37).…”

RETRACTED: Vasopressin Receptor Antagonists for the Correction of Hyponatremia in Chronic Heart Failure: An Underutilized Therapeutic Option in Current Clinical Practice?

“…Particularly, hyponatremia is likely to be mostly favored or provoked by erroneous and/or overzealous diuretic therapy [5,6]. Therefore, further impairment in effective arterial circulating volume has frequently been blamed on overly drastic or inappropriate diuretic therapy, resulting in the worsening of renal perfusion and fall in glomerular filtration rate (GFR) [7]. Both decreased GFR and stimulation of the thirst mechanism by angiotensin II may favor the development of hyponatremia.…”

Renoprotective effect of small volumes of hypertonic saline solution in chronic heart failure patients with marked fluid retention: results of a case-control study

“…It is subsequently maintained by a massive release of renin [8]. In other words, in the case of diuretic therapy generating or further enhancing a marked activation of RAAS, as typically seen in CHF patients after sodium and/or volume depletion, the diuretic action of furosemide and torsemide appears to be lost [9,10,11]. To effectively antagonize the reduction in intravascular volume and renal blood supply, some compounds capable of exercising an osmotic attraction on the plasmatic water from extravascular to intravascular fluid compartments have been proposed, such as mannitol [12], dextran and other plasma expanders [13,14,15], as well as hypertonic saline solution (HSS) [16,17,18,19].…”