Effects of Glucocorticoids in Potentiating Diuresis in Heart Failure Patients With Diuretic Resistance

- There is no evidence supporting the notion that glucocorticoids could cause renal sodium and water retention in heart failure.
- In the kidney, glucocorticoids improve renal responsiveness to atrial natriuretic peptide by increasing the density of natriuretic peptide receptor A in the renal inner medullary collecting duct.
- The short-term use of glucocorticoids, when added to maximum conventional therapy, can potentiate renal responsiveness to diuretic therapy in patients with heart failure.
- The short-term use of glucocorticoids with minimal mineralocorticoid action in patients with heart failure, when indicated for the treatment of other acute comorbid conditions, eg, acute gout, is safe and perhaps even advantageous.

Diuretic resistance in heart failure is defined as a state in which diuretic response is diminished or lost before the therapeutic goal of relief from congestion has been reached. Diuretic resistance is very common and is associated with poor outcomes. Over the past decade, several new drugs and devices targeting decongestion and improvement in renal function in patients with heart failure have failed to show benefit in randomized clinical trials. Glucocorticoids had been used to manage diuretic resistance before the advent of loop diuretics. More recent evidence appears to confirm that glucocorticoids may also help to overcome resistance to loop diuretics. This review tries to summarize the available evidence and potential mechanisms related to glucocorticoid therapy in patients with heart failure and its effect on diuretic resistance.