CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Maria Rosa Costanzo, MD and
Mariell Jessup, MD*
* Cardiology Division, Department of Medicine, University of Pennsylvania School of Medicine, 2 East Perelman Center, 3400 Civic Center Boulevard, Philadelphia, Pennsylvania 19014 (Email: jessupm{at}uphs.upenn.edu).
We greatly appreciate the letter from Dr. Joles and colleagues regarding our editorial comment (1).
We completely agree that the mechanisms in heart failure by which renal venous congestion contributes to a decrease in the glomerular filtration rate (GFR) are extremely complex and are influenced by many factors including renal autoregulation, tubuloglomerular feedback, and the renin-angiotensin-aldosterone system. The main intent of the example depicted in our figure is to underscore to clinicians that in heart failure, worsening renal function is not always due to volume contraction. In fact, in the majority of patients with heart failure, a decreased GFR is due to increased congestion. Unfortunately, the elegant studies of Winton (2) and Firth et al. (3) have largely been ignored until recent analyses showed that both renal dysfunction and congestion independently predict poor outcomes in heart failure patients (4,5).
To stress the effects of increased central venous pressure on GFR, we simplified the example shown in our editorial with the assumption that the forces opposing filtration, hydrostatic pressure in the Bowman's capsule and oncotic pressure in the glomerular capillaries, remain constant. In a normal patient, net filtration pressure will be approximately 14 mm Hg:
In patients with heart failure, assuming there is a small decrease in systemic arterial pressure from a decreased cardiac output and a small increase in central venous pressure, subtraction of the same forces opposing filtration from the arterial and venous sides of the circulation will result in a decrease in net filtration pressure:
We agree that understanding how an increase in central venous pressure affects a decrease in GFR is important because of the impact of both variables on outcomes in patients with heart failure. The complexity of the relationship between volume overload and renal function in heart failure emphasizes to us the critical importance of a close collaboration between cardiologists and nephrologists to thoroughly evaluate how increased cardiac filling pressures alter renal pathophysiology.
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1. Jessup M, Costanzo MR. The cardiorenal syndrome: do we need a change of strategy or a change of tactics? J Am Coll Cardiol 2009;53:597-599.[Free Full Text]2. Winton F. The influence of venous pressure on the isolated mammalian kidney J Physiol 1931;72:49-61.[Free Full Text] 3. Firth JD, 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. Damman K, van Deursen VM, Navis G, Voors AA, van Veldhuisen DJ, Hillege HL. Increased central venous pressure is associated with impaired renal function and mortality in a broad spectrum of patients with cardiovascular disease J Am Coll Cardiol 2009;53:582-588.[Abstract/Free Full Text] 5. Hillege HL, Girbes ARJ, de Kam PJ, et al. Renal function, neurohormonal activation, and survival in patients with chronic heart failure Circulation 2000;102:203-210.[Abstract/Free Full Text]
Related Article
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Renal Venous Congestion and Renal Function in Congestive Heart Failure
- Jaap A. Joles, Lennart G. Bongartz, Carlo A. Gaillard, and Branko Braam
J. Am. Coll. Cardiol. 2009 54: 1632.
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