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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
Disclosures
Supported by the Netherlands Heart Institute (ICIN) and a HFA
Research Grant
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
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
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
CKD and prognosis
Smith et al Circulation 2005
CKD and prognosis
Heywood et al J Card Fail 2007, Blair et al Eur Heart J 2011
ADHERE EVEREST
CKD and Prognosis
Damman et al Eur Heart J 2014
Overall OR: 2.39 , 95% CI 2.25 to 2.54 (N=812139)
CKD and Prognosis
CKD present in 40 – 70% of (selected) AHF patients
Baseline CKD associated with strongly increased mortality
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
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
Pathophysiology
Damman, Tang, Testani, McMurray Eur Heart J 2014
Renal Hemodynamics
Heart failure + ACEi/Diuretic
RVP ↑↑
RVP ↑↑RVP ↓
RVP ↑↑
Damman et al Progr Cardiovasc Dis 2011
Renal Hemodynamics
Mullens et al JACC 2011
Relative Importance CI/CVP
WRF and Prognosis
Damman et al Eur Heart J 2014
Overall OR: 1.75 , 95% CI 1.47to 2.08
Predictors of WRF
Damman et al Eur Heart J 2014
Predictors of WRF
Damman et al Eur Heart J 2014
Not all WRF equal
Testani et al AJC 2010, Metra et al Circ HF 2012
Any change (no) residual congestion
Not all WRF equal
Valente et al Eur Heart J 2014
Uncoupling between WRF,Diuretic Response and mortality
CKD and Diuretic Response
Singh J Card Fail 2014
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
Terminology
Damman, Tang, Testani, McMurray Eur Heart J 2014
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
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
(Pseudo) WRF and AKI
Damman and Testani Eur Heart J 2015
Approach to (Pseudo) WRF
Damman and Testani Eur Heart J 2015
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
Ultrafiltration
Bart et al NEJM 2012 CARRESS-HF study
Consider Paracentesis
Mullens et al JACC 2008 and J Card Fail 2008
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
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
