Decongestive Therapy and Renal Function in Acute Heart Failure
Time for a New Approach?
Outcomes after admission for acute heart failure (AHF) remain extremely poor, especially for patients with decreased renal function or those in whom worsening renal function (WRF) develops during treatment. The Table shows the baseline estimated glomerular filtration rate (GFR) with 30- and 60-day mortality from the Dose Optimization Strategies Evaluation trial in acute Heart Failure (DOSE HF), the CArdioRenal REScue Study in acute Heart Failure (CARRESS HF), and the Renal Optimization Strategies Evaluation trial in acute Heart Failure (ROSE HF).1–3 GFR at randomization in each of these trials was significantly decreased, and the 60-day mortality of 14.7% in CARRESS HF (the only study to date requiring documentation of WRF before randomization) is one of the highest yet reported.
WRF may have many causes in the setting of AHF.4 These include underdiuresis (which may lead to persistent increases in central venous pressure, thereby adversely affecting GFR), direct renal damage from the effects of drugs or procedures, progression of underlying disease, and overdiuresis leading to volume depletion with the subsequent engagement of baroreflex mechanisms and, as a result, a reduction in renal blood flow, GFR, and a fall in cardiac output. WRF may also be caused by a transient reduction in intravascular volume such that the rate at which intravascular volume is replenished from the extravascular space (the so-called plasma refill rate) is exceeded. This can occur despite persistent systemic congestion, as suggested by the results from CARRESS HF in which serum creatinine increased further during treatment with ultrafiltration, despite clinical evidence of ongoing congestion. Regardless of cause, outcomes …