Renal failure occurring in the setting of acute decompensated heart failure (ADHF) is traditionally believed to be due to renal hypoperfusion from poor “forward flow”. This mechanism has intuitive appeal, and appears to be borne out by our clinical experience of improvement in urine output following the introduction of inotrope support in such cases. However, objective testing using pulmonary artery catheterization does not support the “forward-flow” model: degree of renal dysfunction does not correlate with cardiac index, and improvement in cardiac index isn’t associated with improvement in renal function either. This has been observed in many trails, but most notably in the recent ESCAPE trial. So, what then is the explanation?
Evidence is mounting for elevated renal venous pressure and intra-abdominal pressure (IAP) as being prime movers in causing renal dysfunction patients with ADHF. Consider the following:
- In the ESCAPE trial, the only measure that was associated with serum creatinine was right atrial pressure, suggesting that renal congestion is more important than previously believed.
- Studies in dogs show that the kidney stops producing urine at venous pressures of 20-25 mmHg.
- Extrinsic pressure of the kidney to similar levels also causes significant renal dysfunction via increases in venous pressure in modern animal models, as well being frequently observed clinically in cases of the abdominal compartment syndrome.
- Reduction of elevated IAP, irrespective of the mechanism (intensive medical therapy, paracentesis, or ultrafiltration) improved renal function in a study of volume-overloaded patients admitted with ADHF.
- Changes in IAP correlate better with changes in renal function than any other hemodynamic variable.
Reduction in central venous pressure is a far more satisfying explanation for improvement in renal function with diuresis than any putative movement onto a more favorable portion of the Frank-Starling curve, as Nate previously observed.