Correlation of Venous Congestion to Kidney Function in Patients with Decompensated Heart Failure
Sara Mohammed MohammedAmr;
Abstract
Cardiorenal syndrome has been defined as the simultaneous dysfunction of both the heart and the kidney. In the setting of acute decompensated heart failure (ADHF), worsening renal function (WRF) is a common finding and is due to complex, multifactorial, and not fully understood processes involving hemodynamic (renal arterial hypoperfusion and renal venous congestion) and nonhemodynamic factors. Despite its high prevalence, WRF still represents a diagnostic, prognostic, and therapeutic challenge and has been associated with worse outcome.
Decompensated heart failure is predominantly a disease of fluid overload and high venous pressure in the presence of low cardiac output state. As such, the primary therapeutic objective is fluid removal and decrease of the central venous pressure which is predominantly account for the renal dysfunction in such cases rather than low cardiac output as it was previously thought.
In This study we enrolled 30 consecutive subjects (according to eligible criteria) aged (51.6 ± 9.3) presented with DHF. Overall, 10 patients (33.3%) with eGFR> 60 ml/min, 14 patients (46.7%) with eGFR 30 – 59 ml/min and patients (20%) with eGFR< 30 ml/min calculated by MDRD on admission. overall, 46.7% of the patients had Hypertension, 46.7% had Ischemic Heart Disease, 40% had Diabetes Mellitus. All subjects were followed up for 7 days, decongestive therapy was started with intravenous or oral loop diuretics while continuing and other needed medication (angiotensin-converting enzyme inhibitors, beta-blockers, and spironolactone) as tolerated. At follow up, 11 (36.7%) subjects developed WRF and 19 (63.3%) did not.
We have noticed thatthe mean baseline CVP was significantly greater in subjects who developed WRF versus those who did not. Furthermore, there was an incremental risk in WRF with increasing categories of baseline CVP, As it appears to be a near linear relationship, as if the baseline CVP reached >19 or > 24 cmH2O, we observed a sharp increase in the incidence of WRF approaching 51% and 71%, respectively.
During treatment for DHF, persistent venous congestion also posed a very high risk for the development of WRF. Indicating that venous congestion evaluated by high central venous pressure is the most important hemodynamic factor driving WRF in patients with decompensated heart failure rather than EF.
We have also noticed that baseline EF was significantly lower in subjects who developed WRF versus those who did not but it has limited contribution on the pattern of changes in eGFR on follow up which is correlated significantly with CVP.
We also noticed that percentage of subjects with Diabetes Mellitus were significant in those who developed WRF versus who did not, while there was a weak association between history of Hypertension or IHD and WRF during decongestion therapy.
We noticed also that dose of furosemide was significantly higher in patients who developed WRF versus who did not. The mean doses of furosemideon admission were similar in both groups (298.2 ± 119.1 vs 260.0 ± 123.1, p=NS). However, on follow up the mean dose of furosemide was increased significantly in patients who developed WRF. It may be contributed to be having lower (eGFR), however multiple facets of renal physiology contribute to diuretic resistance, only one of which is captured by GFR and decongestion often comes at the expense of deterioration in renal function.
We also noticed that Subjects who developed WRF were more likely to have lower eGFR at baseline (41.7 ± 24.9 vs 53.7 ± 13.7, p = 0.03), had also greater serum creatinine at baseline (2.1 ± 0.8 mg/dl vs. 1.4 ± 0.4 mg/dl, p=0.03) in relation to subjects who did not. Overall, 66% of the subjects presented with baseline eGFR< 30 ml/min developed worsening renal function on follow up, 35% of subjects with baseline eGFR 30-59ml/min also developed WRF and only 20% of the subjects with baseline eGFR≥ 60ml/min developed WRF on follow up.
We have also noticed that greater drop of Mean Arterial Pressure was significant in patients who developed WRF, although there was no significant correlation between MAP neither at baseline nor at the end of the study period between subjects who developed WRF and who did not.
Gradual improvement of venous congestion and decrease of CVP will improve kidney function (GFR), with exclusion of the cases that had WRF during the duration of the study. Incidence of WRF approaching (11- 40 %) During treatment for ADHF, This substantial difference may be explained not only by different patient populations but also by differences in the definition and assessment of WRF. In addition, low BP in combination with high CVP might also indicate potential therapy resistance and explain the comparable observed association of high CVP with WRF in our study. Clearly, this could simply be interpreted as a “sicker” patient population with more advanced disease states that might be reflected by higher CVP.
Our results may also add to some data that implicate ‘‘kidney congestion’’ rather than poor forward flow, as the principal etiologic factor for renal dysfunction in patients with decompensated heart failure. However, this is not to imply that low cardiac output itself does not contribute to WRF, as we acknowledge that patients with progressive pump failure or cardiogenic shock may progress to renal impairment as a result of impaired organ perfusion or indirectly through “backward failure” and venous congestion and also increased intra-abdominal pressure caused by visceral edema or ascites. However, prolonged increases in plasma volume or CVP will attenuate several vascular reflexes, leading to an impaired arterial responsiveness, thereby further impairing the effective renal blood flow. In our small study, the reported correlation might be only modest and of questionable clinical relevance (though of value for hypothesis generating). Thus, we believe that recruitment of more patients would not alter our main results substantially.
In conclusion, our study showed that in the setting of decompensated heart failure,venous congestion (high CVP) is the most important driving factor of changes in kidney function rather than low cardiac output which has a little contribution on that changes and that also the drop of MAP is considered a risk factor for WRF during treatment of decompensated heart failure.
Decompensated heart failure is predominantly a disease of fluid overload and high venous pressure in the presence of low cardiac output state. As such, the primary therapeutic objective is fluid removal and decrease of the central venous pressure which is predominantly account for the renal dysfunction in such cases rather than low cardiac output as it was previously thought.
In This study we enrolled 30 consecutive subjects (according to eligible criteria) aged (51.6 ± 9.3) presented with DHF. Overall, 10 patients (33.3%) with eGFR> 60 ml/min, 14 patients (46.7%) with eGFR 30 – 59 ml/min and patients (20%) with eGFR< 30 ml/min calculated by MDRD on admission. overall, 46.7% of the patients had Hypertension, 46.7% had Ischemic Heart Disease, 40% had Diabetes Mellitus. All subjects were followed up for 7 days, decongestive therapy was started with intravenous or oral loop diuretics while continuing and other needed medication (angiotensin-converting enzyme inhibitors, beta-blockers, and spironolactone) as tolerated. At follow up, 11 (36.7%) subjects developed WRF and 19 (63.3%) did not.
We have noticed thatthe mean baseline CVP was significantly greater in subjects who developed WRF versus those who did not. Furthermore, there was an incremental risk in WRF with increasing categories of baseline CVP, As it appears to be a near linear relationship, as if the baseline CVP reached >19 or > 24 cmH2O, we observed a sharp increase in the incidence of WRF approaching 51% and 71%, respectively.
During treatment for DHF, persistent venous congestion also posed a very high risk for the development of WRF. Indicating that venous congestion evaluated by high central venous pressure is the most important hemodynamic factor driving WRF in patients with decompensated heart failure rather than EF.
We have also noticed that baseline EF was significantly lower in subjects who developed WRF versus those who did not but it has limited contribution on the pattern of changes in eGFR on follow up which is correlated significantly with CVP.
We also noticed that percentage of subjects with Diabetes Mellitus were significant in those who developed WRF versus who did not, while there was a weak association between history of Hypertension or IHD and WRF during decongestion therapy.
We noticed also that dose of furosemide was significantly higher in patients who developed WRF versus who did not. The mean doses of furosemideon admission were similar in both groups (298.2 ± 119.1 vs 260.0 ± 123.1, p=NS). However, on follow up the mean dose of furosemide was increased significantly in patients who developed WRF. It may be contributed to be having lower (eGFR), however multiple facets of renal physiology contribute to diuretic resistance, only one of which is captured by GFR and decongestion often comes at the expense of deterioration in renal function.
We also noticed that Subjects who developed WRF were more likely to have lower eGFR at baseline (41.7 ± 24.9 vs 53.7 ± 13.7, p = 0.03), had also greater serum creatinine at baseline (2.1 ± 0.8 mg/dl vs. 1.4 ± 0.4 mg/dl, p=0.03) in relation to subjects who did not. Overall, 66% of the subjects presented with baseline eGFR< 30 ml/min developed worsening renal function on follow up, 35% of subjects with baseline eGFR 30-59ml/min also developed WRF and only 20% of the subjects with baseline eGFR≥ 60ml/min developed WRF on follow up.
We have also noticed that greater drop of Mean Arterial Pressure was significant in patients who developed WRF, although there was no significant correlation between MAP neither at baseline nor at the end of the study period between subjects who developed WRF and who did not.
Gradual improvement of venous congestion and decrease of CVP will improve kidney function (GFR), with exclusion of the cases that had WRF during the duration of the study. Incidence of WRF approaching (11- 40 %) During treatment for ADHF, This substantial difference may be explained not only by different patient populations but also by differences in the definition and assessment of WRF. In addition, low BP in combination with high CVP might also indicate potential therapy resistance and explain the comparable observed association of high CVP with WRF in our study. Clearly, this could simply be interpreted as a “sicker” patient population with more advanced disease states that might be reflected by higher CVP.
Our results may also add to some data that implicate ‘‘kidney congestion’’ rather than poor forward flow, as the principal etiologic factor for renal dysfunction in patients with decompensated heart failure. However, this is not to imply that low cardiac output itself does not contribute to WRF, as we acknowledge that patients with progressive pump failure or cardiogenic shock may progress to renal impairment as a result of impaired organ perfusion or indirectly through “backward failure” and venous congestion and also increased intra-abdominal pressure caused by visceral edema or ascites. However, prolonged increases in plasma volume or CVP will attenuate several vascular reflexes, leading to an impaired arterial responsiveness, thereby further impairing the effective renal blood flow. In our small study, the reported correlation might be only modest and of questionable clinical relevance (though of value for hypothesis generating). Thus, we believe that recruitment of more patients would not alter our main results substantially.
In conclusion, our study showed that in the setting of decompensated heart failure,venous congestion (high CVP) is the most important driving factor of changes in kidney function rather than low cardiac output which has a little contribution on that changes and that also the drop of MAP is considered a risk factor for WRF during treatment of decompensated heart failure.
Other data
| Title | Correlation of Venous Congestion to Kidney Function in Patients with Decompensated Heart Failure | Other Titles | تقييم العلاقة بين الاحتقان الوريدي وتأثيره على وظائف الكلى في المرضى الذين يعانون فشل لاتعويضي في وظائف القلب | Authors | Sara Mohammed MohammedAmr | Issue Date | 2015 |
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