Cardiorenal syndrome

Domina Petric, MD
Cardiorenal syndrome

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.
Introduction

Definition
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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

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

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.

Predictors of cardiorenal syndrome
• 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
• Reduced baseline
renal function
• Age
• Hypotension
• Anemia
• Diabetes
• Hypertension
• Combination of loop
diuretics and thiazides
• Hyponatremia

BUN

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.

Tubular markers
NGAL has been shown to
be associated with the 48-
72 h development of type I
CRS in patients with ADHF.

Mechanisms of CRS
Reduced
cardiac output!
Venous
congestion!
Increased intra-
abdominal
pressure!

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.

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.

Therapy
Too aggressive
diuresis may
worsen kidney
function!

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.

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.

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.

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.

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.

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 20

Literature
• Aronson D. Cardiorenal Syndrome in Acute
Decompensated Heart Failure. Expert Rev
Cardiovasc Ther. 2012;10(2):177-189.
• Ronco C, McCullough SD. Cardio-renal
syndromes: Reports from the consensus
conference of the acute dialysis quality
initiative. European Heart Journal.
2010;31(6):703-711.

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;297:1332-1343.
• 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;50:1551-1560.

Literature
• Kazory A, Ross EA. Contemporary trends in the
pharmacological and extracorporeal management
of heart failure: a nephrologic
perspective. Circulation 2008;117:975-983.
• 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;49:675-683.

Cardiorenal syndrome

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