CORRESPONDENCE: LETTER TO THE EDITOR
Renal Venous Congestion and Renal Function in Congestive Heart Failure
Jaap A. Joles, DVM, PhD,
Lennart G. Bongartz, MD,
Carlo A. Gaillard, MD, PhD and
Branko Braam, MD, PhD*
* Division of Nephrology and Immunology, University of Alberta Hospital, Clinical Science Building 11-107, 8440 112 Street, Edmonton, Alberta T6G 2G3, Canada
Jessup and Constanzo (1) recently proposed mechanisms explaining the reported inverse relationship between central venous pressure (CVP) and glomerular filtration rate (GFR) in congestive heart failure (CHF) (2,3). Their figure, depicting the impact of venous congestion, seems implausible because efferent arteriolar pressure exceeds afferent arteriolar pressure. Understanding how increased CVP relates to decreased GFR is important because both variables predict mortality (4).
If the renal vascular bed was rigid, elevated venous pressure would increase pressure all along the renal vascular tree and cause increased net ultrafiltration pressure. Normally, this is corrected by autoregulation (5). In a diseased kidney, with failing autoregulation, glomerular pressure could indeed increase.
Regarding the interstitial and tubular compartments, elevated renal venous pressure will increase interstitial hydrostatic pressure (Pint). If Pint exceeds tubular hydrostatic pressure, tubules will collapse. Consequently, increasing tubular hydrostatic pressure (6) will oppose filtration and decrease net ultrafiltration pressure. This mechanism is supported by experimental data showing a linear decrease in GFR upon increases in renal venous pressure, in particular during volume expansion (7). How CVP, intra-abdominal pressure, and accumulation of renal interstitial fluid and adipose tissue affect interstitial compliance and Pint is complex.
Furthermore, elevated angiotensin II constricts both afferent and efferent arterioles and decreases renal blood flow. Fortunately, and different from the view in the editorial comment (1), the renin-angiotensin system has an internal brake whereby angiotensin II inhibits renin release to prevent the positive feedback proposed by the authors.
Therefore, the contribution of renal venous congestion to low GFR in CHF is extremely complex. Note that we have neglected the tubuloglomerular feedback system, colloid osmotic pressure, and neurohormonal systems. A systematic analysis of mechanisms that contribute to decreasing GFR in CHF is warranted.
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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. 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] 3. 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] 4. Damman K, Navis G, Voors AA, et al. Worsening renal function and prognosis in heart failure: systematic review and meta-analysis J Card Fail 2007;13:599-608.[CrossRef][Web of Science][Medline] 5. Cupples WA, Braam B. Assessment of renal autoregulation Am J Physiol Renal Physiol 2007;292:F1105-F1123.[Abstract/Free Full Text] 6. Boberg U, Persson AE. Tubuloglomerular feedback during elevated renal venous pressure Am J Physiol 1985;249:F524-F531.[Web of Science][Medline] 7. Burnett Jr. JC, Knox FG. Renal interstitial pressure and sodium excretion during renal vein constriction Am J Physiol 1980;238:F279-F282.[Web of Science][Medline]
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- Maria Rosa Costanzo and Mariell Jessup
J. Am. Coll. Cardiol. 2009 54: 1632-1633.
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