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European Journal of Heart Failure 2007 9(9):872-878; doi:10.1016/j.ejheart.2007.05.010
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© 2007 European Society of Cardiology

Decreased cardiac output, venous congestion and the association with renal impairment in patients with cardiac dysfunction

Kevin Dammana, Gerjan Navisb, Tom D.J. Smildea, Adriaan A. Voorsa, Wim van der Bijc, Dirk J. van Veldhuisena and Hans L. Hillegea,d,*

a Department of Cardiology, University Medical Center Groningen, University of Groningen Groningen, The Netherlands
b Department of Nephrology, University Medical Center Groningen, University of Groningen Groningen, The Netherlands
c Department of Pulmonary Diseases, University Medical Center Groningen, University of Groningen Groningen, The Netherlands
d Department of Epidemiology, University Medical Center Groningen, University of Groningen Groningen, The Netherlands

* Corresponding author. Hanzeplein 1, PO 30001, 9700 RB Groningen, The Netherlands. Tel.: +31503618066; fax: +31503618062. E-mail address: h.hillege{at}tcc.umcg.nl


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Study limitations
 6. Conclusion
 Acknowledgments
 References
 
Background: Renal failure in heart failure is related to decreased cardiac output. However, little is known about its association with venous congestion.

Aims: To investigate the relationship between venous congestion and glomerular filtration rate (GFR) in patients with cardiac dysfunction.

Methods and results: Right atrial pressure (RAP) and cardiac index (CI) were determined by right heart catheterisation in 51 patients with cardiac dysfunction, secondary to pulmonary hypertension. GFR and renal blood flow (RBF) were measured as 125I-Iothalamate and 131I-Hippuran clearances, respectively. Mean age was 40±11 years and 69% of patients were female. GFR was 73±19 ml/min/1.73 m2 with a CI of 2.1±0.7 l/min/m2. In multivariate analysis, RBF (r=0.664, p<0.001) and RAP (r<0.367, p=0.020) were independently associated with GFR. In patients in the lower ranges of RBF, venous congestion was an important determinant of renal function.

Conclusion: RBF is the main factor determining GFR in patients with cardiac dysfunction. Venous congestion, characterised by an increased RAP, adjusted for RBF is also related to GFR. Treatment to preserve GFR should not only focus on improvement of renal perfusion, but also on decreasing venous congestion.

Key Words: Heart failure • Renal function • Kidney • Haemodynamics • Venous congestion

Received November 29, 2006; Revised April 2, 2007; Accepted May 16, 2007


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 5. Study limitations
 6. Conclusion
 Acknowledgments
 References
 
Impaired renal function independently increases the risk of death, cardiovascular death and hospitalisation for worsening heart failure in patients with chronic heart failure (CHF) [1-3]. The main determinant of renal function in CHF is renal blood flow (RBF) [4]. Reduction in cardiac output (CO) results in a disproportionate reduction in renal perfusion, which consequently leads to a diminished glomerular filtration rate (GFR).

CHF is not only characterised by decreased cardiac output and subsequent decreased organ perfusion, but also by increased venous congestion. However, most previous reports have studied the interrelationship between reduced cardiac output, renal function and prognosis in CHF of different aetiologies, including the impact of right ventricular function on mortality [5,6].

There are very few data on the association between venous congestion and indices of renal function. One very small study suggested a relationship between venous congestion and RBF in CHF [7]. The authors showed an inverse relationship between RBF and venous pressure. However, the association between venous congestion and GFR, remains to be elucidated.

Patients with pulmonary hypertension often have decreased cardiac output in combination with elevated right sided filling pressures and signs of congestion. Therefore, from a haemodynamic point of view, these patients are a suitable cohort to investigate the relationship between venous congestion and GFR in patients with cardiac dysfunction.

The aim of the present study was therefore to investigate the relative contribution of decreased renal perfusion and determinants of venous congestion on renal function in patients with cardiac dysfunction secondary to pulmonary hypertension.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 5. Study limitations
 6. Conclusion
 Acknowledgments
 References
 
2.1. Patients
The study enrolled consecutive patients diagnosed with pulmonary hypertension who were potential candidates for lung transplantation. All patients underwent right heart catheterization and clearance measurements of renal haemodynamic parameters as a part of the work up for transplantation. Patients with idiopathic pulmonary arterial hypertension, as well as secondary pulmonary hypertension, were included. The study protocol was approved by the institutional ethics committee. All patients gave written informed consent.

2.2. Right heart catheterization
Right sided cardiac catheterisation data included measurements of mean arterial pressure (MAP, mm Hg), right atrial pressure (RAP, mm Hg), mean pulmonary artery pressure (MPAP, mm Hg), pulmonary capillary wedge pressure (PCWP, mm Hg), systemic vascular resistance (SVR, dyne.sec.cm– 5) and pulmonary vascular resistance (PVR, dyne.s.cm– 5). Cardiac output (CO, l/min) was determined using the method of thermodilution. Systemic blood flow was used as measurement of cardiac output in patients with intracardiac shunting. Cardiac index (CI, l/min/m2) was calculated as CO divided by body surface area (BSA). Cardiac catheterisation measurements were obtained from the patient at rest.

2.3. Renal function measurement by 125I-Iothalamate and 131I-Hippuran clearances
GFR and effective renal plasma flow (ERPF) were measured by constant infusion of radiolabelled tracers, 125I-Iothalamate and 131I-Hippuran. The clearances were calculated as (U.V)/P and (I.V)/P, respectively. U.V represents the urinary excretion of the tracer, I.V represents the infusion rate of the tracer; P represents the tracer value in plasma at the end of each clearance period. GFR was measured as U.V/P for 125I-Iothalamate, and corrected for voiding errors by the ratio of (I.V/P)/(U.V/P)131I-Hippuran as described previously. RBF was calculated as ERPF/1-haematocrit. The filtration fraction (FF) was calculated as the ratio of GFR and ERPF and expressed as a percentage. GFR and ERPF were expressed per 1.73 m2 of BSA.

2.4. Relative contributions of RAP and RBF
In order to assess and visualise relative contributions of RBF and RAP, RBF was dichotomised (= 400 versus > 400 ml/min/1.73 m2) and subsequently ranked to low and high RAP within both subgroups. This stratification is based on the haemodynamic renal response in a setting of reduced perfusion when RBF declines below approximately 400 ml/min/1.73 m2 [4,8]. It considers a potential relationship between RBF and venous congestion and allows a within-group comparison of patients with and without venous congestion, who have comparable RBF [4].

2.5. Statistical analysis
Results are expressed as means±SD unless otherwise indicated. All variables were normally distributed. Pearson correlation coefficients were calculated to determine which variables had a significant univariate association with GFR. Stepwise multivariate linear regression analysis was used to determine the independent relationships between univariately associated variables with GFR. Subjects with missing data were excluded from multivariate analysis. In a secondary analysis, the multivariate regression analysis was repeated after imputing missing values using expectation maximization as estimation method. To examine all possible interactions of the effects of various variables, a secondary analysis was performed including interaction terms. Differences between the different groups of low versus high RBF or RAP were carried out using Student's T-tests. All reported probability values are 2-tailed, and a p value<0.05 was considered statistically significant. Statistical analyses were performed using SPSS, Chicago version 12.

The investigation conforms with the principles outlined in the Declaration of Helsinki.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 5. Study limitations
 6. Conclusion
 Acknowledgments
 References
 
3.1. Patient characteristics
In total 51 consecutive patients were included (Table 1). Twenty eight patients (55%) had idiopathic pulmonary arterial hypertension. Secondary pulmonary hypertension was mostly due to pulmonary embolism (n=9) and atrial septum defect (n=7). Both left ventricular ejection fraction (52±14%) and right ventricular ejection fraction (42±11%) were mildly impaired. Mean MPAP (60±16 mm Hg) and RAP (11±6 mm Hg) were elevated and the cardiac index was decreased (2.1±0.7 l/min/m2, normal range 2.5-4.0 l/min/m2). GFR was mildly impaired (73±19 ml/min/1.73 m2) in combination with an increased filtration fraction. No differences in baseline characteristics were found between patients with idiopathic and secondary pulmonary hypertension.


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  		Table 1 Patient characteristics (n=51)

 
3.2. Relationship between haemodynamic parameters and GFR
Univariate analysis showed that RBF was strongly associated with GFR (r=0.797, p<0.001). Next to RBF, RAP was inversely related to GFR (r=– 0.616, p<0.001). Other variables related to renal function were CI (r=0.404, p=0.007) and PVR (r=– 0.298, p=0.040). In multivariate regression analysis, including all univariately associated variables (p<0.1), only RBF and RAP remained significant and independent predictors of GFR (Table 2). Addition of diuretic treatment or ACE-inhibition to the model did not interfere with these results. Also beta-blocker therapy was not a mediator of the relationship with GFR.


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  		Table 2 Regression analysis for GFR

 
Analysis of interaction terms between the different variables revealed no significant interaction on a continuous scale. We further analyzed possible interactions between the two variables in the multivariate model, when both were dichotomised by the median. The interaction term of these dichotomised variables showed a trend toward significance (p 0.095). The multivariate analysis showed, after imputing of missing values, similar results.

Fig. 1 illustrates the relative contributions of RBF and RAP to GFR when dichotomised to high versus low values. The effect of increased RAP appears to reside solely among patients with already reduced RBF. Characteristics of these groups are shown in Table 3. Lowest GFR was seen in patients with a relatively high RAP and low RBF. The highest GFR was present in patients with high RBF and low RAP; in these patients GFR was almost similar when compared to the group of patients with a high RAP (p=0.736). In patients with a low RBF, a high RAP was associated with a significantly lower GFR when compared to patients with normal RBF and/or normal RAP (p<0.001 and p<0.01, respectively). Both RBF and RAP differed significantly between high and low subgroups. Both groups with low RBF had higher RAP than the groups with high RBF.


Figure 01
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  		Fig. 1 Relative contributions of right atrial pressure (RAP) and renal blood flow (RBF) to glomerular filtration rate (GFR). Error bars represent 95% confidence interval. * p<0.001 for difference with High RAP, Low RBF. {dagger} p<0.01 for difference with Low RAP, Low RBF.

 


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  		Table 3 Characteristics of the different subgroups

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
5. Study limitations
 6. Conclusion
 Acknowledgments
 References
 
In the present study we show that GFR is not only determined by reduced cardiac output, but also by venous congestion, characterised by an increased RAP in patients with cardiac dysfunction, secondary to pulmonary hypertension. The association between RAP and renal function was primarily present in patients with a reduced RBF.

4.1. Relationship between venous congestion and renal function in CHF
In a substudy of the SOLVD, Drazner et al. established the prognostic implication of jugular venous pressure in patients with CHF [9]. Elevated jugular venous pressure was associated with adverse outcomes. Furthermore, patients with increased venous pressure had a significantly higher serum creatinine level (115±27 versus 106±27 µmol/l). This suggests an important relationship between renal dysfunction and venous congestion in patients with cardiac dysfunction.

The main determinant of GFR in CHF is RBF [4]. However, we recently showed that increased levels of atrial and brain natriuretic peptides (ANP, BNP respectively) are associated with renal dysfunction in patients with CHF [10]. Both peptides are secreted when volume overload causes ventricular stretch, while ANP is also released in response to volume overload in the atria. This could indicate that not only reduced renal perfusion but also volume overload is related to renal dysfunction, again suggesting a relation between venous congestion and renal impairment.

4.2. Independent component of venous congestion in pathophysiology of reduced GFR
In a multivariate analysis we found that both RAP and RBF were independent determinants of GFR. Both parameters are reflections of cardiac status and are mutually associated. Renal venous pressure is closely related to RBF in certain pathophysiological states, such as CHF [11]. Therefore, it is to be expected that it influences GFR. Ljungman showed that even during decreased RBF, the kidney can preserve GFR by increasing filtration fraction in CHF [4]. Below a certain threshold value (400 ml/min/1.73 m2) of RBF, GFR declines. To address this in our population we dichotomised RBF to low and high values, and then assessed the relationship between RAP in the patients with low and high RBF. We observed an association between venous pressure and GFR independent of RBF. Furthermore, we showed that in the lower regions of RBF, there is an additive effect on GFR between increased RAP and decreased RBF, which is absent in the higher regions of RBF. This suggests that the independent contribution of RAP is mainly relevant in the low ranges of renal perfusion. While RAP is less elevated in the high RBF group with high RAP, this could also imply that the effect of venous congestion on GFR is limited to higher levels of RAP.

The specific circulatory physiology underlying this direct link between increased venous pressure and GFR is unclear, but there are a number of possibilities as shown in Fig. 2. Renal venous pressure rises, in response to increased central venous pressure and causes an increase in renal interstitial pressure [11-13]. This may lead to impairment of GFR induced by an hypoxic state similar to the mechanism by which hepatic congestion leads to liver failure in CHF [14], or by an increase in hydrostatic pressure in Bowman's capsule [13]. Furthermore, with increasing renal venous pressure, not only intrarenal but also systemic, angiotensin II concentrations increase [13,15]. This will lead to a further fall in GFR [16,17], either directly or by modulation of the sympathetic nervous system (SNS) [18,19]. Increased SNS activity will influence GFR by changing the filtration-coefficient [20,21]. Furthermore, increased SNS activity triggers angiotensin II release, increasing the effect on GFR [21]. Finally, the effect of ANP on preserving GFR by decreasing sensitivity of the tubuloglomerular feedback mechanism is blunted in CHF, thereby compromising GFR [22]. In addition, both SNS-activation and angiotensin II are mediators of the blunted response to ANP observed in CHF [23,24].


Figure 02
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  		Fig. 2 Pathophysiology of the relation between venous congestion and reduced glomerular filtration rate (GFR). ANP; Atrial Natriuretic Peptide, SNS; Sympathetic Nervous System, RAAS; renin-angiotensin aldosterone system. Numbers in circles represent the targets for specific therapies, as follows: 1. Ultrafiltration, diuretics, sodium and water restriction and arginine vasopressin receptor antagonists [36,37,39]. 2. Ultrafiltration, diuretics and sodium and water restriction [36,37]. 3. ACE-inhibitors and angiotensin II receptor blockers. 4. Statin therapy [38]. 5. Beta-blocker therapy. 6. Angiotensin II receptor blockers. 7. Neutral endopeptidase inhibitors [41]. 8. Urodilatin [40].

 
The combination of both decreased cardiac output and increased venous congestion in CHF was introduced in a model of four clinical profiles by Stevenson et al. [25,26]. These profiles were defined as the presence or absence of venous congestion (wet or dry) in combination with adequacy of perfusion (warm or cold). These clinical profiles were shown to correlate strongly with outcome [27]. Those patients who not only suffered from hypoperfusion but also had clinical signs of venous congestion had the worst prognosis. The recent ESCAPE trial investigated whether treatment directed at lowering invasively measured RAP and PCWP, was superior to treatment guided by clinical assessment [28]. No difference was observed in clinical outcome between the treatment groups. However, in the group tailored to filling pressures, renal function did not worsen when RAP was actively lowered, while it did worsen in the group tailored by clinical assessment. More recently, Stevenson argued that haemodynamic goals are (still) important in the treatment of CHF and that worsening of renal function is not solely attributable to a fall in cardiac output [29]. The current study indicates that venous congestion could be one of these additional factors.

4.3. Clinical profiles and relation to renal function
The profiles provided by Stevenson can now be extended, in light of our findings of a combined effect of decreased perfusion and venous congestion on renal function (Figs. 1 and 3). In the ‘warm’ profiles, GFR is mainly characterised by a relatively preserved RBF. However, there are patients with preserved RBF who experience increased RAP. Possibly, in these patients increased RAP reflects adaptation to reduced cardiac function by the Frank-Starling mechanism [30]. The dependency on renal perfusion rather than RAP indicates that the contribution of increased venous pressure on GFR is limited. We therefore hypothesize that therapy to reduce venous congestion and/or filling pressures in these patients will have little impact on GFR. This profile might reflect the haemodynamic state of patients with heart failure and preserved systolic function. Interestingly, in this patient group, renal impairment is associated with greater mortality than observed in patients with systolic dysfunction [31]. In addition, these patients (compared to the dry-warm profile) are at risk for accelerated renal function loss when renal perfusion is compromised, shifting to the ‘wet-cold’ profile. Therefore, reducing venous congestion in this patient group will result in a shift towards the more favourable ‘dry-warm’ profile, with subsequent improved survival [27].


Figure 03
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  		Fig. 3 Different haemodynamic profiles. Schematic representation of haemodynamic profiles, as adapted from Stevenson [25].

 
In contrast, when renal perfusion is compromised (‘cold’), especially patients in the ‘wet’ profile have trouble preserving GFR. While RBF is closely related to reduced cardiac output, these profiles represent more advanced stages of cardiac dysfunction [4,32]. The observation that in the presence of reduced RBF, increased RAP can also be absent, indicates that at least a subgroup of patients is able to adapt to reduced renal perfusion and reduced cardiac output, without increasing filling pressures.

4.4. Clinical implications for therapy
Therapy to preserve GFR is especially warranted in profiles with reduced RBF. First line therapy to improve RBF consists of ACE inhibitors and ARBs [33,34]. In addition to improved renal perfusion, this will also lead to improvement of GFR by targeting one of the mechanisms by which venous congestion reduces GFR. This interaction and the targets for other therapies are shown in Fig. 2. Diuretics are prescribed frequently in patients with CHF who are fluid overloaded, mainly to relieve symptoms. Concerns have been raised about whether aggressive diuresis in patients in the ‘wet-cold’ profile leads to further renal impairment [35]. However, our present data suggest that when diuretic therapy is tailored to decrease venous congestion, it may benefit GFR and subsequently improve prognosis. Future therapeutic options include ultrafiltration which is a promising therapy to reduce venous congestion [36,37]. In addition, beta-blockers can impact on the relationship between venous congestion and renal function, by blocking SNS activation. Also, as observed in a study of experimental heart failure [38], statins can indirectly influence SNS activation by down-regulation of angiotensin II receptor expression. Other new therapies to preserve renal function and to reduce venous congestion have effects on the cardiorenal interaction. Arginine vasopressin antagonists inhibit water reabsorption in the distal tubule [39]. Urodilatin is a recombinant ANP which increases natriuresis and improves symptoms in acute heart failure [40], while neutral endopeptidase inhibitors reduce breakdown of ANP, thereby increasing the bioavailability of ANP resulting in delayed onset of sodium retention [41]. The safety and efficacy of these therapies is still under investigation, but they may be potential candidates for renal-protective therapy in patients with reduced renal perfusion and venous congestion.


   5. Study limitations
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Study limitations
6. Conclusion
 Acknowledgments
 References
 
The present analysis was conducted in a cross sectional design. Therefore, a cause and effect relationship from venous congestion to renal dysfunction can not be demonstrated, while decreased renal function leads to increased water and salt retention, thereby increasing venous congestion. Furthermore, although patients with pulmonary hypertension provide unique data on the relationship between cardiac dysfunction, venous congestion and renal haemodynamics, they have secondary heart problems due to increased pulmonary pressure, instead of primary cardiac illness. On the other hand, in this population use of ACE-inhibitors, that can confound the interrelationships between systemic and renal haemodynamics, was limited. The current analysis was conducted in a small cohort with a specific cause for cardiac dysfunction, future research to assess the relationship between venous congestion and renal function in a broader cohort of patients with different aetiologies of cardiac dysfunction, is now required.


   6. Conclusion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Study limitations
 6. Conclusion
Acknowledgments
 References
 
Renal function is not only related to decreased renal perfusion, but also to increased venous congestion in patients with cardiac dysfunction secondary to pulmonary hypertension. Differentiation between haemodynamic profiles may be useful in tailoring treatment for preservation of GFR in CHF, by not only focussing on improvement of RBF, but also on alleviation of venous congestion.


   Acknowledgments
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Study limitations
 6. Conclusion
 Acknowledgments
References
 
K. Damman and A.A. Voors are supported by the Netherlands Heart Foundation (grants 2006B157 and 2006T37, respectively).


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Study limitations
 6. Conclusion
 Acknowledgments
 References
 

  1. Dries D.L., Exner D.V., Domanski M.J., Greenberg B., Stevenson L.W. The prognostic implications of renal insufficiency in asymptomatic and symptomatic patients with left ventricular systolic dysfunction. J Am Coll Cardiol (2000) 35:681–689.[Abstract/Free Full Text]
  2. Hillege H.L., Nitsch D., Pfeffer M.A., et al. Renal function as a predictor of outcome in a broad spectrum of patients with heart failure. Circulation (2006) 113:671–678.[Abstract/Free Full Text]
  3. Al Ahmad A., Rand W.M., Manjunath G., et al. Reduced kidney function and anemia as risk factors for mortality in patients with left ventricular dysfunction. J Am Coll Cardiol (2001) 38:955–962.[Abstract/Free Full Text]
  4. Ljungman S., Laragh J.H., Cody R.J. Role of the kidney in congestive heart-failure — relationship of cardiac index to kidney-function. Drugs (1990) 39:10–21.[CrossRef][Web of Science][Medline]
  5. Ghio S., Gavazzi A., Campana C., et al. Independent and additive prognostic value of right ventricular systolic function and pulmonary artery pressure in patients with chronic heart failure. J Am Coll Cardiol (2001) 37:183–188.[Abstract/Free Full Text]
  6. Zornoff L.A.M., Skali H., Pfeffer M.A., et al. Right ventricular dysfunction and risk of heart failure and mortality after myocardial infarction. J Am Coll Cardiol (2002) 39:1450–1455.[Abstract/Free Full Text]
  7. Kos T., Pacher R., Wimmer A., et al. Relationship between kidney function, hemodynamic variables and circulating big endothelin levels in patients with severe refractory heart failure. Wien Klin Wochenschr (1998) 110:89–95.[Web of Science][Medline]
  8. Smilde T.D.J., Harst P., van Veldhuisen D.J., et al. Reduced renal blood flow is the main determinant of GFR in heart failure. (2005) Abstract.
  9. Drazner M.H., Rame J.E., Stevenson L.W., Dries D.L. Prognostic importance of elevated jugular venous pressure and a third heart sound in patients with heart failure. N Engl J Med (2001) 345:574–581.[Abstract/Free Full Text]
  10. Smilde T.D., Hillege H.L., Navis G., et al. Impaired renal function in patients with ischemic and nonischemic chronic heart failure: association with neurohormonal activation and survival. Am Heart J (2004) 148:165–172.[CrossRef][Web of Science][Medline]
  11. Maxwell M.H., Breed E.S., Schwartz I.L. Renal venous pressure in chronic congestive heart failure. J Clin Invest (1950) 29:342–348.[CrossRef][Web of Science][Medline]
  12. Fiksen-Olsen M.J., Romero J.C. Renal effects of prostaglandin inhibition during increases in renal venous pressure. Am J Physiol (1991) 260:525–529.
  13. Fiksen-Olsen M.J., Strick D.M., Hawley H., Romero J.C. Renal effects of angiotensin II inhibition during increases in renal venous pressure. Hypertension (1992) 19:137–141.[Web of Science]
  14. Seeto R.K., Fenn B., Rockey D.C. Ischemic hepatitis: clinical presentation and pathogenesis. Am J Med (2000) 109:109–113.[CrossRef][Web of Science][Medline]
  15. Kastner P.R., Hall J.E., Guyton A.C. Renal hemodynamic responses to increased renal venous pressure: role of angiotensin II. Am J Physiol (1982) 243:F260–F264.[Web of Science][Medline]
  16. Blantz R.C., Konnen K.S., Tucker B.J. Angiotensin II effects upon the glomerular microcirculation and ultrafiltration coefficient of the rat. J Clin Invest (1976) 57:419–434.[Web of Science][Medline]
  17. Tucker B.J., Mundy C.A., Maciejewski A.R., et al. Changes in glomerular hemodynamic response to angiotensin II after subacute renal denervation in rats. J Clin Invest (1986) 78:680–688.[CrossRef][Web of Science][Medline]
  18. Taddei S., Favilla S., Duranti P., Simonini N., Salvetti A. Vascular renin-angiotensin system and neurotransmission in hypertensive persons. Hypertension (1991) 18:266–277.[Abstract/Free Full Text]
  19. DiBona G.F. Nervous kidney. Interaction between renal sympathetic nerves and the renin-angiotensin system in the control of renal function. Hypertension (2000) 36:1083–1088.[Abstract/Free Full Text]
  20. DiBona G.F., Kopp U.C. Neural control of renal function. Physiol Rev (1997) 77:75–197.[Abstract/Free Full Text]
  21. Kon V., Yared A., Ichikawa I. Role of renal sympathetic nerves in mediating hypoperfusion of renal cortical microcirculation in experimental congestive heart failure and acute extracellular fluid volume depletion. J Clin Invest (1985) 76:1913–1920.[Web of Science][Medline]
  22. Morsing P., Stenberg A., Casellas D., et al. Renal interstitial pressure and tubuloglomerular feedback control in rats during infusion of atrial natriuretic peptide (ANP). Acta Physiol Scand (1992) 146:393–398.[CrossRef][Web of Science][Medline]
  23. De Leon H., Garcia R. Regulation of glomerular atrial natriuretic factor receptor subtypes by renal sympathetic nerves. Am J Physiol (1991) 260:R1043–R1050.[Web of Science][Medline]
  24. Charloux A., Piquard F., Doutreleau S., Brandenberger G., Geny B. Mechanisms of renal hyporesponsiveness to ANP in heart failure. Eur J Clin Invest (2003) 33:769–778.[CrossRef][Web of Science][Medline]
  25. Stevenson L.W., Perloff J.K. The limited reliability of physical signs for estimating hemodynamics in chronic heart failure. JAMA (1989) 261:884–888.[Abstract/Free Full Text]
  26. Stevenson L.W. Design of therapy for advanced heart failure. Eur J Heart Fail (2005) 7:323–331.[Abstract/Free Full Text]
  27. Nohria A., Tsang S.W., Fang J.C., et al. Clinical assessment identifies hemodynamic profiles that predict outcomes in patients admitted with heart failure. J Am Coll Cardiol (2003) 41:1797–1804.[Abstract/Free Full Text]
  28. Binanay C., Califf R.M., Hasselblad V., et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial. JAMA (2005) 294:1625–1633.[Abstract/Free Full Text]
  29. Stevenson L.W. Are hemodynamic goals viable in tailoring heart failure therapy? Hemodynamic goals are relevant. Circulation (2006) 113:1020–1027.[Free Full Text]
  30. Reddi B.A., Carpenter R.H. Venous excess: a new approach to cardiovascular control and its teaching. J Appl Physiol (2005) 98:356–364.[Abstract/Free Full Text]
  31. Ahmed A., Rich M.W., Sanders P.W., et al. Chronic kidney disease associated mortality in diastolic versus systolic heart failure: a propensity matched study. Am J Cardiol (2007) 99:393–398.[CrossRef][Web of Science][Medline]
  32. Leithe M.E., Margorien R.D., Hermiller J.B., Unverferth D.V., Leier C.V. Relationship between central hemodynamics and regional blood flow in normal subjects and in patients with congestive heart failure. Circulation (1984) 69:57–64.[Abstract/Free Full Text]
  33. Creager M.A., Halperin J.L., Bernard D.B., et al. Acute regional circulatory and renal hemodynamic—effects of converting-enzyme inhibition in patients with congestive heart-failure. Circulation (1981) 64:483–489.[Abstract/Free Full Text]
  34. Hillege H.L., van Gilst W.H., van Veldhuisen D.J., et al. Accelerated decline and prognostic impact of renal function after myocardial infarction and the benefits of ACE inhibition: the CATS randomized trial. Eur Heart J (2003) 24:412–420.[Abstract/Free Full Text]
  35. Weinfeld M.S., Chertow G.M., Stevenson L.W. Aggravated renal dysfunction during intensive therapy for advanced chronic heart failure. Am Heart J (1999) 138:285–290.[CrossRef][Web of Science][Medline]
  36. Costanzo M.R., Guglin M.E., Saltzberg M.T., et al. Ultrafiltration versus intravenous diuretics for patients hospitalized for acute decompensated heart failure. J Am Coll Cardiol (2007) 49:675–683.[Abstract/Free Full Text]
  37. Bart B.A., Boyle A., Bank A.J., et al. Ultrafiltration versus usual care for hospitalized patients with heart failure: the relief for acutely fluid-overloaded patients with decompensated congestive heart failure (RAPID-CHF) trial. J Am Coll Cardiol (2005) 46:2043–2046.[Abstract/Free Full Text]
  38. Gao L., Wang W., Li Y.L., et al. Simvastatin therapy normalizes sympathetic neural control in experimental heart failure: roles of angiotensin II type 1 receptors and NAD(P)H oxidase. Circulation (2005) 112:1763–1770.[Abstract/Free Full Text]
  39. Costello-Boerrigter L.C., Smith W.B., Boerrigter G., et al. Vasopressin-2-receptor antagonism augments water excretion without changes in renal hemodynamics or sodium and potassium excretion in human heart failure. Am J Physiol Renal Physiol (2006) 290:F273–F278.[Abstract/Free Full Text]
  40. Mitrovic V., Seferovic P.M., Simeunovic D., et al. Haemodynamic and clinical effects of ularitide in decompensated heart failure. Eur Heart J (2006) 27:2823–2832.[Abstract/Free Full Text]
  41. Martin F.L., Stevens T.L., Cataliotti A., et al. Natriuretic and antialdosterone actions of chronic oral NEP inhibition during progressive congestive heart failure. Kidney Int (2005) 67:1723–1730.[CrossRef][Web of Science][Medline]

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