How to optimize the use of diuretics in patients with heart failure?

Abstract

Considering the pathophysiology and clinical presentation of heart failure, using diuretics or drugs with diuretic properties is indispensable for adequate management of heart failure patients. However, in clinical practice, fluid expansion is often undiagnosed, and diuretic therapy is not always adequately titrated. Today, several drug classes with diuretic properties are available in addition to classical thiazides, thiazide-like, and loop diuretics. The purpose of this short review is to discuss different ways to optimize diuretic therapy using currently available drugs. Several approaches are considered, including a combination of diuretics to obtain a sequential nephron blockade, use of a drug combining a blocker of the renin-angiotensin system (RAS) and an inhibitor of the metabolism of natriuretic peptides (ARNI), prescription of potassium binders to maintain and up-titrate RAS blockers and mineralocorticoid antagonists, and finally use of inhibitors of renal reabsorption of glucose through the sodium-glucose cotransporter 2 system. Optimal use of these various drug classes should improve the quality of life and reduce the need for hospital admissions and mortality in heart failure patients.

Prevalence of increased intra-abdominal pressure and its impact on renal function in acute decompensated heart failure: A prospective pilot study

“…We believe that in this type of kidney dysfunction, the compromised function of renal tubules causes the residual capacity for water absorption to remain, even if sodium absorption deteriorates. Further, the effect of IAP on water and sodium handling in current ADHF patients varies due to the pharmacological blockade of the renin-angiotensin-aldosterone system, sodium-glucose transport protein 2 inhibitors, and the administration of loop diuretics, which are cornerstones of HF therapy, whereas the observed satisfactory natriuresis may indicate correct dosing [26,27]. Moreover, the number of osmotically active compounds in the final urine that affects its volume goes well beyond sodium, and observed alterations in the final urine may be the result of heightened dietary salt intake, metabolic alkalosis, and dyselectrolytemia, overactivation of the sympathetic nervous system, or individualized patterns of fluid redistribution and intravascular filling which restrict aquaresis [28,29].…”