Cardiorenal syndrome Domina Petric, MD.

Cardiorenal syndrome Domina Petric, MD

Introduction Cardiorenal syndrome (CRS) commonly occurs during treatment of acute decompensated heart failure (ADHF) and is associated with poor clinical outcome. The pathophysiology of CRS entails a complex interaction between hemodynamic alterations, including reduced renal perfusion, increased venous pressure and activation of multiple neurohormonal systems.

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Definition Cardiorenal syndromes (CRSs) are broadly defined as disorders of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other. PowerPlugs Templates for PowerPoint Preview

Classification Type Inciting event Secondary disturbances Example I-acute CRS Abrupt worsening of heart function Kidney injury Acute cardiogenic shock or acute decompensation of chronic heart failure II-chronic CRS Chronic abnormalities in heart function Progressive chronic kidney disease Chronic heart failure III-acute renocardiac syndrome Abrupt worsening of kidney function Acute cardiac disorder (heart failure, abnormal heart rhythm or pulmonary edema) Acute kidney failure, glomerulonephritis PowerPlugs Templates for PowerPoint Preview

Classification IV-chronic renocardiac syndrome Chronic kidney disease Decreased cardiac function, cardiac hypertrophy and/or increased risk of adverse cardiovascular events Chronic glomerular disease V-secondary CRS Systemic condition Both heart and kidney dysfunction Diabetes mellitus, sepsis, lupus PowerPlugs Templates for PowerPoint Preview

Epidemiology Worsening renal function (WRF) is most commonly defined as an absolute increase in serum creatinine of ≥0,3 mg/dl (26,5 mmol/l). Between 14 and 34% of patients with ADHF develop WRF. PowerPlugs Templates for PowerPoint Preview

Predictors of cardiorenal syndrome
Reduced baseline renal function Age Hypotension Anemia Diabetes Hypertension Combination of loop diuretics and thiazides Hyponatremia Severe diastolic dysfunction Secondary pulmonary hypertension Right ventricular dysfunction Marked functional tricuspid or mitral regurgitation Previous heart failure hospitalizations History of acute kidney injury with previous acute decompensated heart failure episodes History of ultrafiltration of transient dialysis ! PowerPlugs Templates for PowerPoint Preview

BUN Although serum creatinine is most often used to define baseline renal function and WRF in ADHF, both baseline and increasing blood urea nitrogen (BUN) have been shown to be more powerful markers of clinical outcomes than serum creatinine! PowerPlugs Templates for PowerPoint Preview

Tubular markers Kidney injury molecule-1, N-acetyl-β-D- glucosaminidase and neutrophil gelatinase- associated lipocalin (NGAL) are novel urinary biomarkers that were initially identified and evaluated in patients with acute kidney injury (AKI). They predominantly indicate tubular injury and are earlier and more sensitive indicators of AKI than plasma creatinine. PowerPlugs Templates for PowerPoint Preview

Tubular markers NGAL has been shown to be associated with the h development of type I CRS in patients with ADHF. PowerPlugs Templates for PowerPoint Preview

Reduced cardiac output! Increased intra-abdominal pressure!
Mechanisms of CRS Reduced cardiac output! Venous congestion! Increased intra-abdominal pressure! PowerPlugs Templates for PowerPoint Preview

Neurohormonal activation
HF involves activation of the sympathetic nervous system and enhanced release of vasoconstricting and sodium-retaining neurohormones, such as angiotensin II, norepinephrin, endothelin-1 and arginine vasopressin. These neurohormonal systems are central to both the pathophysiology of HF and the regulation of multiple aspects of renal function. Excessive neurohormonal activation is thought to be an important mediator of CRS. PowerPlugs Templates for PowerPoint Preview

Therapy ADHF is associated with hypervolemia and nearly always with a significant increase in filling pressures. Ongoing volume overload in patients with ADHF is poorly tolerated and is a frequent cause of hospital readmission. Loop diuretics are the mainstay and an integral component of current treatment for congestive symptoms. PowerPlugs Templates for PowerPoint Preview

Too aggressive diuresis may worsen kidney function!
Therapy Too aggressive diuresis may worsen kidney function! PowerPlugs Templates for PowerPoint Preview

Therapy When the initial diuretic response is inadequate despite continued increases in intravenous boluses or infusions of loop diuretics with the addition of metolazone, diuresis may frequently be enhanced by positive inotropic agents (including dopamine, dobutamine, phosphodiesterase inhibitors and levosimendan) with short- term improvement in urine output. PowerPlugs Templates for PowerPoint Preview

Therapy Multiple studies have shown that hyponatremia in patients with heart failure and acute coronary syndrome is an independent predictor of mortality and repeated hospitalizations for decompensation. Hyponatremia is frequently evident in patients with multiple hospitalizations for congestion, with diuresis interrupted each time by decreasing serum sodium levels. PowerPlugs Templates for PowerPoint Preview

Therapy In the EVEREST trial, patients treated with the vasopressin V2-receptor antagonist tolvaptan exhibited improved physician and patient- assessed symptoms, increased serum sodium levels, reductions in bodyweight and furosemide use without serious adverse effect. PowerPlugs Templates for PowerPoint Preview

Therapy Adenosine is an important intrarenal mediator of both WRF and diuretic resistance. ATP hydrolysis releases free adenosine into the extracellular space, which in turn acts on adenosine A1 receptors in the afferent arterioles and causes local constriction, reducing renal blood flow and glomerular filtration rate and stimulating the release of renal renin. A1 receptor activation increases sodium reabsorption in the proximal and distal tubules, leading to sodium and water retention. PowerPlugs Templates for PowerPoint Preview

Therapy The adenosine A1 receptor antagonist rolofylline enhanced diuresis in patients with ADHF and increased GFR and renal plasma flow in ambulatory patients with chronic HF in small studies. PowerPlugs Templates for PowerPoint Preview

Ultrafiltration The proposed advantages of ultrafiltration as compared with diuretics in fluid-overloaded HF patients include: Rapid removal of fluid and improvement in symptoms. Higher mass clearance of sodium for similar volumes of fluid removal. Lower risk of electrolyte abnormality (hypokalemia). Lack of neurohormonal activation. Potential restoration of responsiveness to diuretics. Shortened length of stay for HF-related hospitalizations and decreased rate of readmissions for HF. Decreased risk of WRF. HF-heart failure

Literature Aronson D. Cardiorenal Syndrome in Acute Decompensated Heart Failure. Expert Rev Cardiovasc Ther. 2012;10(2): Ronco C, McCullough SD. Cardio-renal syndromes: Reports from the consensus conference of the acute dialysis quality initiative. European Heart Journal ;31(6): PowerPlugs Templates for PowerPoint Preview

Literature Gheorghiade M, Konstam MA, Burnett JC Jr et al. Short-term clinical effects of tolvaptan, an oral vasopressin antagonist, in patients hospitalized for heart failure: the EVEREST Clinical Status Trials. JAMA 2007;297: Givertz MM, Massie BM, Fields TK, Pearson LL, Dittrich HC. The effects of KW-3902, an adenosine A1-receptor antagonist,on diuresis and renal function in patients with acute decompensated heart failure and renal impairment or diuretic resistance. J. Am. Coll. Cardiol. 2007;50: PowerPlugs Templates for PowerPoint Preview

Literature Kazory A, Ross EA. Contemporary trends in the pharmacological and extracorporeal management of heart failure: a nephrologic perspective. Circulation 2008;117: Costanzo MR, Guglin ME, Saltzberg MT et al. Ultrafiltration versus intravenous diuretics for patients hospitalized for acute decompensated heart failure. J. Am. Coll. Cardiol. 2007;49: PowerPlugs Templates for PowerPoint Preview

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