comorbidities in AHF Kidney disease
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Transcript of comorbidities in AHF Kidney disease
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Comorbidities in Acute Heart Failure
Kidney DiseaseHow to protect the kidney ?
Kevin Damman, MD, PhDUniversity Medical Center Groningen
Groningen, The Netherlands
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Disclosures
Supported by the Netherlands Heart Institute (ICIN) and a HFA
Research Grant
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Background
Chronic Kidney Disease (CKD) is one of the most prevalent
comorbidities in acute (and chronic) Heart Failure
Presence of an impaired renal function / reduced glomerular
filtration rate (GFR) is strongly associated with worse outcomes
Pathophysiology of impaired renal function multifactorial, and
probably slightly different form chronic HF
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BackgroundEVEREST
(2007)VERITAS(2009)
PROTECT(2010)
ASCEND-HF(2011)
RELAX(2012)
N 4133 1448 2033 7141 1161
Age (years) 66 70 70 67 72
Male (%) 74 61 67 66 62
Creatinine (μmol/L) 124 118 124 106 NA
eGFR (mL/min/1.73m2) NA 57 50 62 53
CKD (%) 53 37 67 52 72
WRF (%) 14 20 18 13 NA
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Background
EVEREST(2007)
VERITAS(2009)
PROTECT(2010)
ASCEND-HF(2011)
RELAX(2012)
CKD (%) 53 37 67 52 72
Hypertension (%) 71 80 79 72 87
Diabetes (%) 40 48 46 41 47
COPD (%) 10 NA 20 NA 15
AF (%) 43 37 56 38 52
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CKD and prognosis
Smith et al Circulation 2005
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CKD and prognosis
Heywood et al J Card Fail 2007, Blair et al Eur Heart J 2011
ADHERE EVEREST
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CKD and Prognosis
Damman et al Eur Heart J 2014
Overall OR: 2.39 , 95% CI 2.25 to 2.54 (N=812139)
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CKD and Prognosis
CKD present in 40 – 70% of (selected) AHF patients
Baseline CKD associated with strongly increased mortality
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Cardiorenal Syndrome
Ronco et al JACC
“Cardiorenal Syndrome type I”
Classification based on epidemiology
Great for:- Creating Awareness- Popular term- Hype
However:- Does not help for
treatment- “CRS type I” very diverse
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Pathophysiology
GFR ↓
RBF ↓Cardiac Output↓
CVP ↑
Salt and water retention ↑
• Interplay between: Comorbid organ dysfunction: Hypertension Diabetes CKD Peripheral artery disease
Hemodynamics: Reduced Cardiac Output Reduced Renal Blood Flow Increased Central Venous Pressure Increased Renal Venous Pressure
Intra-abdominal pressure
Therapy (Inotropes, vasodilators, diuretics)
Damman et al Progr Cardiovasc Dis 2011
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Pathophysiology
Damman, Tang, Testani, McMurray Eur Heart J 2014
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Renal Hemodynamics
Heart failure + ACEi/Diuretic
RVP ↑↑
RVP ↑↑RVP ↓
RVP ↑↑
Damman et al Progr Cardiovasc Dis 2011
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Renal Hemodynamics
Mullens et al JACC 2011
Relative Importance CI/CVP
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WRF and Prognosis
Damman et al Eur Heart J 2014
Overall OR: 1.75 , 95% CI 1.47to 2.08
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Predictors of WRF
Damman et al Eur Heart J 2014
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Predictors of WRF
Damman et al Eur Heart J 2014
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Not all WRF equal
Testani et al AJC 2010, Metra et al Circ HF 2012
Any change (no) residual congestion
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Not all WRF equal
Valente et al Eur Heart J 2014
Uncoupling between WRF,Diuretic Response and mortality
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CKD and Diuretic Response
Singh J Card Fail 2014
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AKI ≠ WRF
• Acute kidney injury is a condition in nephrology/intensive
care/shock
• Often intrinsic renal ‘hit’
• Very large increases in serum creatinine
• Associated with azotemia
• WRF can deteriorate in AKI
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Terminology
Damman, Tang, Testani, McMurray Eur Heart J 2014
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TerminologySuggested Definition
Serum Creatinine / eGFR Additional Criteria
Chronic HF (WRF)*
≥26.5 μmol/L and ≥ 25% increase in sCr#
OR
≥ 20% decrease in eGFR
over 1 to 26 weeks
Deterioration in HF status but
not leading to hospitalization
Acute HF (WRF/AKI)*
Increase 1.5 - 1.9 times baseline sCr within 1-7
days before or during hospitalization
OR
≥ 26.5 μmol/L increase in sCr# within 48 hours
OR
Urine output < 0.5 mL/kg/h for 6-12 hours
Deterioration in HF status or failure to
improve
OR
Need for inotropes, ultrafiltration or renal
replacement therapy
Damman, Tang, Testani, McMurray Eur Heart J 2014
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Pseudo WRF
• ‘Unprovoked’ WRF associated with poor outcome
• WRF that occurs in patients with good Diuretic Response:
Often transient
No association with poor outcome
Could be called “Pseudo WRF”
Damman, Tang, Testani, McMurray Eur Heart J 2014
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(Pseudo) WRF and AKI
Damman and Testani Eur Heart J 2015
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Approach to (Pseudo) WRF
Damman and Testani Eur Heart J 2015
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Dopamine
Chen JAMA 2013 ROSE-AHF study
Placebo Dopamine P-value
N 119 122
Urine volume (72h, mL) 8296 8524 0.59
Change in Cystatin C (mg/L) 0.11 0.12 0.72
Change in Creatinine (µmol/L) 1.8 0 0.78
WRF (%) 22 22 0.88
Sodium excretion (72h, mmol) 540 527 0.75
Weight change (72h, kg) -3.5 -3.3 0.82
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Ultrafiltration
Bart et al NEJM 2012 CARRESS-HF study
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Consider Paracentesis
Mullens et al JACC 2008 and J Card Fail 2008
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Renal Spectrum in AHFDecreased Renal Blood Flow
Increased (Renal) Venous Pressure
Decreased GFR and renal reserve
Tubular and glomerular injury
Worsening Renal Function and Diuretic Resistance
Acute Kidney Injury / Azotemia
Renal Replacement Therapy / Ultrafiltration
Death
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CKD/WRF in AHF• CKD at baseline strongly prevalent in AHF (50-70%)
• During admission, up to 20% experience WRF
However, WRF not always an omnious sign: Pseudo WRF
Risk stratify on WRF and diuretic response/efficiency
AKI is not the same as WRF
• Pathophysiology of both CKD and WRF is multifactorial
Decreased renal perfusion and increased renal venous pressure
Including abdominal hypertension (ascites)
• Treat the Heart – Don’t mind the Kidneys!*
(up to certain limits, and only if diuretic response is good)
* Ruggenenti et al Eur J Heart Fail 2011
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