A mainstay of therapy for congestive heart failure has been the use of potent diuretic agents, such as furosemide, that target the kidney to enhance sodium and water excretion. Although furosemide is widely used to treat the symptoms of acute decompensated heart failure (ADHF), the consequent activation of the renin-angiotensin-aldosterone system may limit the natriuretic response by reducing the glomerular filtration rate. In addition, excessive diuresis may reduce cardiac preload and result in systemic hypotension, which reduces renal perfusion pressure and prerenal azotemia and raises levels of blood urea nitrogen. In order to preserve and/or enhance renal function in ADHF, especially with agents such as conventional diuretics and vasodilators, an understanding of intrarenal factors that may protect the kidney may provide a direction for optimal use of current therapies and also lead to newer therapeutic strategies. Vasodilators, especially those that are linked to cGMP activation, may provide an alternative approach.
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