CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Mariell Jessup, MD* and
Maria Rosa Costanzo, MD
* University of Pennsylvania, Heart Failure/Transplant, 6 Penn Tower, 3400 Spruce Street, Philadelphia, Pennsylvania 19104 (Email: jessupm{at}uphs.upenn.edu).
We appreciate the opportunity to answer the thoughtful letter of Drs. Maqsood and Szerlip, who raised the issues of the role of vigorous diuresis in the patients discussed in the article by Mullens et al. (1), and the activation of the renin-angiotensin-aldosterone system (RAAS) after ultrafiltration (2).
Our interpretation of the study by Mullens et al. (1) is that the central venous pressure decrease in the worsening renal function (WRF) group was not significantly different from that of the non-WRF group, approximately 35%. Nevertheless, the central venous pressure remained significantly (p = 0.04) higher in the WRF group. We think this supports the hypothesis proposed by Mullens et al. (1) about the important role of venous congestion in contributing to WRF.
Our suggestion about the differing activation of the RAAS with diuretics and ultrafiltration is derived from an elegant study done over a decade ago. In 1994, Agostoni et al. (3) demonstrated that in heart failure patients treated with either ultrafiltration or diuretics to achieve equivalent fluid removal, sustained hemodynamic and neurohormonal benefit occurred only in the ultrafiltration group. Compared with the diuretic group, patients treated with ultrafiltration had lower norepinephrine, plasma renin, and aldosterone levels for up to 90 days. Lower RAAS activation was associated with sustained improvement in objective measures of functional capacity. The rate of 14 to 15 ml/min for interstitial fluid mobilization was outlined still earlier by Fauchald and Fauchald (4), as recently reviewed by Schrier (5).
The conclusions of Rogers et al. (6) about the impact of diuretics and ultrafiltration on renal function might or might not be verified in larger trials. However, we feel strongly that the important outcomes in subsequent studies involving patients hospitalized with heart failure remain focused on a reduction of cardiovascular mortality and heart failure rehospitalizations, rather than on the more specific end point of renal function. This is where we propose that new tactics are needed.
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References
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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. 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] 3. Agostoni P, Marenzi G, Lauri G, et al. Sustained improvement in functional capacity after removal of body fluid with isolated ultrafiltration in chronic cardiac insufficiency: failure of furosemide to provide the same result Am J Med 1994;96:191-199.[CrossRef][Web of Science][Medline] 4. Fauchald P, Fauchald P. Effects of ultrafiltration on body fluid volumes and transcapillary colloid osmotic gradient in hemodialysis patients Contrib Nephrol 1989;74:170-175.[Medline] 5. Schrier RW. Blood urea nitrogen and serum creatinine: not married in heart failure Circ Heart Fail 2008;1:2-5.[Free Full Text] 6. Rogers HL, Marshall J, Bock J, et al. A randomized, controlled trial of the renal effects of ultrafiltration as compared to furosemide in patients with acute decompensated heart failure J Card Fail 2008;14:1-5.[CrossRef][Web of Science][Medline]
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