Continuing intravenous diuretic therapy is the most appropriate next step in management. In acute decompensated heart failure, elevated renal venous pressure can cause distended renal venules with increased tubular fluid pressure and backleak, leading to venous congestion and cardiorenal syndrome (CRS). This patient has CRS, defined as a change in function of either the heart or kidneys that may influence the function of the other organ system. CRS is categorized into five types: 1) acute heart failure leading to acute kidney injury (AKI) (CRS1), 2) chronic heart failure leading to chronic kidney disease (CKD), 3) AKI leading to acute heart failure, 4) CKD leading to cardiac dysfunction (heart failure, coronary artery disease, arrhythmias), and 5) systemic conditions leading to simultaneous heart and kidney dysfunction (such as sepsis). Management of CRS may be challenging because treatment of one organ system may cause worsening of the other. In patients with heart failure–related CRS, treatment is directed toward improving cardiac function and fluid balance, which may optimize kidney function. However, it is common to see mild to moderate worsening of kidney function associated with treatment of volume overload until fluid balance is achieved. In general, diuresis in heart failure should be maintained until fluid retention (as seen by elevated central venous pressure and peripheral edema) is resolved, even if this results in asymptomatic mild to moderate decreases in kidney function that are followed closely.

Nesiritide, a recombinant human B-type natriuretic peptide that acts as a vasodilator, is available for treatment of selected patients with acute decompensated heart failure. However, there is no evidence that nesiritide improves kidney function when used in this setting and is therefore an inappropriate addition to therapy for this purpose.

Ultrafiltration, or the removal of plasma water through an extracorporeal circuit, has been used in patients unresponsive to diuretics; however, this patient has responded to diuretic therapy, and ultrafiltration is not indicated at present.

Excessive concern about precipitating kidney failure can lead to underutilization of diuretics and persistent volume overload, which may reduce the efficacy of ACE inhibitors and increase the risk of carvedilol-induced decompensated heart failure.