ckd and chf
DESCRIPTION
CHF with reduced EF and CKD guidelinesTRANSCRIPT
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HFrEF and CKD: what do the guidelines say?
Prof. Adriaan Voors, CardiologistUniversity Medical Center Groningen
The Netherlands
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Disclosures• AAV received consultancy fees and/or research grants
from: Alere, AstraZeneca, Bayer, Cardio3Biosciences, Celladon, Merck/MSD, Novartis, Servier, Torrent, Trevena, Vifor.
• AAV was a member of the ESC 2012 Guidelines Committee
• AAV is supported by a grant from the European Commission: FP7-242209-BIOSTAT-CHF
• AAV is Clinical Established Investigator and supported by other grants of the Dutch Heart Foundation
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ESC 2012 HF Guidelines: General Statements
• The GFR is reduced in most patients with HF, especially if advanced, and renal function is a powerful independent predictor of prognosis in HF.
• Consider Causes:• Renal artery stenosis• Sodium and water depletion and hypotension• Volume overload, right heart failure, and renal venous congestion• Prostatic obstruction• Other drugs (e.g. NSAID, trimethoprim, gentamicin)• Use of RAAS-blockers• Use of thiazide and/or loop diuretics
McMurray et al. ESC-HF Guidelines; EJHF 2012
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• Contraindicated in known bilateral renal artery stenosis• Caution when significant renal dysfunction (creatinine
>221 μmol/L [>2.5 mg/dL] or eGFR <30 mL/min/1.73 m2)• In case of Worsening Renal Function:
• Creatinine ↑ ≤ 50% or 266 μmol/L (3 mg/dL)/eGFR <25 mL/min/1.73 m2, is acceptable
• Consider stopping nephrotoxic drugs or triamterene/amiloride and, if no signs of congestion, reducing the dose of diuretic
• Greater rises in creatinine: ½ dose RAAS-blockers• If creatinine ↑ by >100% or to >310 μmol/L (3.5 mg/dL)/eGFR
<20 mL/min/1.73 m2, stop RAAS-blocker
RAAS-blockers and CKD (appendix C and E)
McMurray et al. ESC-HF Guidelines; EJHF 2012
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• Significant renal dysfunction (creatinine >221 μmol/L [>2.5 mg/dL] or eGFR <30 mL/min/1.73 m2)–may be made worse by diuretic or patient may not respond to diuretic (especially thiazide diuretic)
• Worsening Renal function; • Hypovolaemia/dehydration? • Nephrotoxic agents, e.g. NSAIDs, trimethoprim? • Withhold MRA and/or thiazide? • Reduce dose of ACE inhibitor/ARB? • Haemofiltration/dialysis?
Loop diuretics and CKD (appendix F)
McMurray et al. ESC-HF Guidelines; EJHF 2012
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• Insufficient diuretic response/diuretic resistance: • Check compliance and fluid intake• Increase dose of diuretic• Consider switching from furosemide to bumetanide or
torasemide• Add MRA/increase dose of MRA • Combine loop diuretic and thiazide/metolazone• Consider short-term i.v. infusion of loop diuretic; • Consider ultrafiltration
Loop diuretics and CKD (appendix F)
McMurray et al. ESC-HF Guidelines; EJHF 2012
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WRF WHF Mortality re-Hosp0
5
10
15
20
25
30
Q1: GoodQ2Q3Q4Q5: Poor
Diuretic Response in AHFPROTECT: 2033 AHF patients;
Diuretic Response = kg weight loss/40 mg furosemide
*
*
**
*p<0.001
Valente et al. EHJ 2014
%
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ESC HF Guidelines 2012
McMurray et al. ESC-HF Guidelines; EJHF 2012
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CARESS-HF: primary endpoint
Bart et al. NEJM 2012
96 hours after randomization
N=188 ADHF pts with WRF
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ROSE-AHF: low dose dopamine in AHF
72 hour Urine volume
01,0002,0003,0004,0005,0006,0007,0008,0009,000
10,000
placebo
Urin
ary
Out
put (
L)
P=0.59
dopamine
Change in Cystatin C
0
0.02
0.04
0.06
0.08
0.1
0.12
0.14
placebo
dopamine
P=0.72
Mg/
dL
N=360 AHF patients with eGFR 15-60 ml/min
Chen et al. JAMA 2013
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• CKD and WRF often occur in HF• Always consider cause of WRF• RAAS-inhibitors: mild increase in creatinine allowed;
excessive increase: stop RAAS-blocker• Loop diuretic; less response in CKD• WRF: reduce stop loop diuretic, NSAIDs, trimethoprim,
MRA, thiazide, ACEi/ARB• Diuretic resistance: poor outcome• Ultrafiltration: as yet not proven to be effective• No benefit of low dose dopamine
Conclusions