CORRESPONDENCE: LETTER TO THE EDITOR
Venous Congestion and Worsening Renal Function
Jeffrey Testani, MD*,
Martin St. John Sutton, MBBS and
James Kirkpatrick, MD
* University of Pennsylvania, Medicine, 3400 Spruce Street, 8 Gates, Philadelphia, Pennsylvania 19104 (Email: jeffrey.testani{at}uphs.upenn.edu).
We read with great interest the recent article by Mullens et al. (1) in which the investigators reported the association between invasive hemodynamic parameters and worsening renal function (WRF). Their findings demonstrate that low cardiac output is not the sole factor influencing changes in renal function during treatment of decompensated heart failure, an important contribution to this literature. We have some questions, however, regarding their conclusion that "venous congestion is the most important hemodynamic factor driving WRF in decompensated patients with advanced heart failure."
The authors cite experimental animal models of renal venous congestion to explain the mechanism for their conclusion, but the directionality of their results appears to be discordant with the cited models (2,3). In animal experiments, the degree of venous congestion is directly proportional to the severity of renal impairment. Furthermore, relief of venous congestion leads to a prompt and reproducible improvement in renal function. If right atrial pressure (RAP) is an appropriate surrogate for venous congestion, as the authors suggest, patients with high baseline RAP would be expected to have depressed baseline renal function, which should improve with the reduction in RAP. Mullens et al. (1) report that elevated RAP was not predictive of baseline renal function and that patients with the highest RAP actually had the greatest incidence of WRF despite a substantial reduction in RAP.
The robust association between RAP and WRF reported by Mullens et al. (1) is unlikely to be a chance finding, but the discordant direction of the observations with the proposed physiology makes it unlikely that venous congestion is "driving" incident WRF. There are several plausible explanations for this paradox including the well-known lack of correlation between RAP and various venous variables (4), competing pathophysiology that overshadows the effect of congestion, or a transient worsening in renal function before improvement. It would be interesting to know the degree of RAP reduction that occurred at the time of WRF, especially given the very early mean time of WRF (1 day) in their cohort.
A recent subanalysis of the ESCAPE (Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness) trial also examined the relationship between invasive hemodynamic variables and WRF (5). In this report, Nohria et al. (5) found a lack of association between WRF and baseline, or changes in hemodynamic parameters including RAP. They did report a correlation between RAP and baseline renal function, results concordant with animal experiments.
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1. Mullens W, Abrahams Z, Francis GS, et al. Importance of venous congestion for worsening of renal function in advanced decompensated heart failure J Am Coll Cardiol 2009;53:589-596.[Abstract/Free Full Text]2. Winton FR. The influence of venous pressure on the isolated mammalian kidney J Physiol 1931;72:49-61.[Free Full Text] 3. Firth JF, Raine AE, Ledingham JG. Raised venous pressure: a direct cause of renal sodium retention in oedema? Lancet 1988;1:1033-1035.[Web of Science][Medline] 4. Gelman S. Venous function and central venous pressure: a physiologic story Anesthesiology 2008;108:735-748.[Web of Science][Medline] 5. Nohria A, Hasselblad V, Stebbins A, et al. Cardiorenal interactions: insights from the ESCAPE trial J Am Coll Cardiol 2008;51:1268-1274.[Abstract/Free Full Text]
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