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    Cardiorenal Syndrome

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    Andy McCullough
    Cardiorenal syndrome describes the interaction between heart and kidney diseases where acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. There are five subtypes depending on which organ is primarily involved and the time-course of involvement. Worsening kidney function is common in heart failure and associated with higher mortality. The pathophysiology involves reduced cardiac output, neurohormonal activation of the RAAS and sympathetic nervous systems, and other factors which can induce a vicious cycle of further organ dysfunction. Effective therapies aim to interrupt the cycle through approaches such as RAAS blockade, diuresis, and management of anemia.

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    Cardiorenal Syndrome

    Uploaded by

    Andy McCullough
    100 views21 pages
    Cardiorenal syndrome describes the interaction between heart and kidney diseases where acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. There are five subtypes depending on which organ is primarily involved and the time-course of involvement. Worsening kidney function is common in heart failure and associated with higher mortality. The pathophysiology involves reduced cardiac output, neurohormonal activation of the RAAS and sympathetic nervous systems, and other factors which can induce a vicious cycle of further organ dysfunction. Effective therapies aim to interrupt the cycle through approaches such as RAAS blockade, diuresis, and management of anemia.

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    Cardiorenal syndrome describes the interaction between heart and kidney diseases where acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. There are five subtypes depending on which organ is primarily involved and the time-course of involvement. Worsening kidney function is common in heart failure and associated with higher mortality. The pathophysiology involves reduced cardiac output, neurohormonal activation of the RAAS and sympathetic nervous systems, and other factors which can induce a vicious cycle of further organ dysfunction. Effective therapies aim to interrupt the cycle through approaches such as RAAS blockade, diuresis, and management of anemia.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    100 views21 pages

    Cardiorenal Syndrome

    Uploaded by

    Andy McCullough
    Cardiorenal syndrome describes the interaction between heart and kidney diseases where acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. There are five subtypes depending on which organ is primarily involved and the time-course of involvement. Worsening kidney function is common in heart failure and associated with higher mortality. The pathophysiology involves reduced cardiac output, neurohormonal activation of the RAAS and sympathetic nervous systems, and other factors which can induce a vicious cycle of further organ dysfunction. Effective therapies aim to interrupt the cycle through approaches such as RAAS blockade, diuresis, and management of anemia.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    of 21

    Cardiorenal Syndrome

    Andy McCullough

    The coexistence of heart failure and renal insufficiency

    FIVE TYPES (Mumbo-Jumbo)


    1. Acute worsening of cardiac function leads to renal dysfunction 2. Chronic Abnormalities in cardiac function lead to renal dysfunction 3. Acute worsening of renal function leads to cardiac dysfunction 4. Chronic abnormalities in renal function lead to cardiac disease 5. Systemic conditions cause dysfunction in both systems

    Epidemiology of Cardiorenal syndrome


    20%-40% of patients with acute decompensated heart failure have chronic RI or elevated baseline creatinine 30% of patients with heart failure exacerbations have chronic RI and 20% have baseline Cr>2.0 (ADHERE) 27%-45% of patients hospitalized with acute decompensated heart failure develop an acute worsening in renal function (Cr >0.3) Better to use EGFR, and when one does, most have CKD Stage 3

    Effect on Prognosis
    PRIME-II: EGFR strongest predictor of mortality, including functional status and ejection fraction. ADHERE: Admission creatinine and BUN: 2/3 strongest independent risk factors for in-hospital mortality. Worsening renal function=Poorer prognosis
    Cr increasing >0.3 during admission 81% sensitive and 62% specific for in-hospital mortality in 1002 patients admitted for ADHF.

    PRIME-II

    Pathophysiology

    Diminished Renal Perfusion


    Pump Failure -> Low CO and Cardiogenic Shock Neurohormonal Activation
    Fluid Retention Increased CVP (>19 -> decreased GFR, FeNa) Increased Vasoconstriction

    ABDOMINAL PRESSURE! NSAIDS/ACEIs/ARBs all WORSEN this problem


    Though initially thought to worsen Cr, and thus prognosis, ACEIs/ARBs actually renoprotective

    Neurohormonal activation
    Increased circulating components of the RAAS in patients with HF RAAS
    Renal Hypoxia Renal vasoconstriction Intraglomerular Hypertension Glomerulosclerosis Fibrosis of Renal Tubules Proteinurea

    Sympathetic Activation
    Proliferation of intrarenal vascular smooth muscle cells

    NO/ROS Imbalance
    Furthers Sympathetic dysfunction -> Afferent Vasoconstriction

    ALL OF THESE DECREASE BONE MARROW SENSITIVITY TO EPO, CAUSING ANEMIA, WHICH WORSENS THE PROBLEM!

    RI adversely effects on Cardiac Function


    VICIOUS CYCLE! Neurohormonal activation produced by kidneys in an effort to maintain a normal GFR. Hormones cause:
    Increased Volume and Pressure on the failing heart Decreased myocardial oxygen supply Deleterious cardiac remodeling Accelerates atherosclerosis (NFkB pathway)

    IMPLICATIONS FOR THERAPY

    Diuretics
    Higher doses independently associated with pump failure and death
    SOLVD trial (RR-1.31, 95% CI 1.09-1.57, P=0.0004) PRAISE TRIAL
    Total Mortality HR=1.37 Pump Failure Death HR=1.51

    Aggressive diuresis in conjunction with ACE inhibitor use worsens renal function DIURETICS INCREASE NEUROHORMONAL ACTIVITY!
    Volume Contraction Prevent Na Uptake into the Macula Densa Stimulate renal prostacyclin production (and thus renin)

    RAAS Blockade
    Though serum creatinine increases with use of an ACE inhibitor or ARB, their benefits for survival in HF are well documented, and increases in creatinine should NOT preclude their use. Aldosterone Antagonists
    Well documented mortality benefit in HF (RALES) Greater antiproteinuric effect than losartan or placebo in hypertensive diabetic nephropathy

    Ionotropes
    Improve short term hemodynamics but worsen mortality
    ESCAPE Trial
    Ionotropes associated with increased:
    Death HR 1.57, P=0.032 Death Plus Rehospitalization HR=2.12, P<0.001

    Vasodilators
    Nitrates + low dose diuresis relieve pulmonary congestion more effectively than high dose diuresis PROBLEMS:
    Inappropriate use can worsen sympathetic outflow and RAAS activation Tolerance develops within 24-48 hours

    Anemia Management
    EPO therapy in heart failure associated with mean increases in Hb from 10.2 to 12.1 associated with:
    Increased NYHA functional class Increased LVEF Reduced the need for diuretic therapy

    STAMINA-HeFT
    Darbopoeitin- vs. placebo did NOT increase:
    Exercise duration NYHA Class Quality of Life score

    Conclusions
    Cardiorenal syndrome is highly prevalent, associated with increased mortality, and is a poor prognostic indicator Complex interactions involving:
    RAAS Sympathetic Nervous System Inflammation NO and ROS balance

    References
    Adams KF, Jr, Fonarow GC, Emerman CL, et al.: Characteristics and outcomes of patients hospitalized for heart failure in the United States: rationale, design, and preliminary observations from the first 100,000 cases in the Acute Decompensated Failure National Registry (ADHERE). Am Heart J 2005, 149:209216. Domanski M, Norman J, Pitt B, et al.: Diuretic use, pro- gressive heart failure, and death in patients in the studies of left ventricular dysfunction (SOLVD). J Am Coll Cardiol 2003, 42:705708. Dries DL, Exner DV, Domanski MJ, et al.: The prognostic implications of renal insufficiency in asymptomatic and symptomatic patients with left ventricular systolic dysfunction. J Am Coll Cardiol 2000, 35:681689. Firth JD, Raine AE, Ledingham JG: Raised venous pressure: a direct cause of renal sodium retention in oedema? Lancet 1988, 1:10331035. Francis GS, Benedict C, Johnstone DE, et al.: Comparison of neuroendocrine activation in patients with left ventricular dysfunction with and without congestive heart failure. A substudy of the Studies of Left Ventricular Dysfunction (SOLVD). Circulation 1990, 82:17241729. Gottlieb SS, Abraham W, Butler J, et al.: The prognostic importance of different definitions of worsening renal function in congestive heart failure. J Card Fail 2002, 8:136 141. Heywood JT: The cardiorenal syndrome: lessons from the ADHERE database and treatment options. Heart Fail Rev 2004, 9:195201. Nitta K. Pathogenesis and therapeutic implications of cardiorenal syndrome. Clin Exp Nephrol. 2011 Apr;15(2):187-94. Packer M, Lee WH, Kessler PD, et al.: Prevention and reversal of nitrate tolerance in patients with congestive heart failure. N Engl J Med 1987, 317:799804. Rastogi A, Fonarow GC. The cardiorenal connection in heart failure. Curr Cardiol Rep. 2008 May;10(3):190-7.

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