الفهرس 
Pathophysiology of Cardiorenal SyndromeOnly 14 pages are availabe for public view
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Abstract
Combined heart and kidney dysfunction is common.
A disorder of one of these two organs often leads to
dysfunction or injury to the other. This is the
pathophysiological basis for the clinical entity defined
cardiorenal syndrome (CRS). Generally defined as a
condition characterized by the initiation and/ or progression
of renal insufficiency secondary to heart failure, the term
CRS should also be used to describe conditions of renal
dysfunction leading to heart dysfunction (renocardiac
syndrome).
Evolutionary mechanisms designed to maintain
constant blood volume and organ perfusion under
continuously changing conditions are clearly responsible
for CRS. Unfortunately, when primary cardiac or renal
dysfunction develops; the renin-angiotensin-aldosterone
system (RAAS), pressure sensing baroreceptors, cellular
signaling, and sympathetic nervous system mechanisms
turn from friend to enemy. Attempting to understand the
nature of these normal physiological mechanisms is a key
to developing a multimodal approach to preserving
function in both organs.
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Cardiorenal syndrome being classified into five
subtypes as follows:
Type 1 or acute CRS is characterized by an acute
heart disorder leading to acute kidney injury (AKI).
Type 2 or chronic CRS is characterized by chronic
abnormalities in cardiac function causing progressive
chronic kidney disease.
Type 3 CRS or acute renocardiac syndrome is
characterized by an abrupt and primary worsening of renal
function (e.g. AKI, ischemia or glomerulonephritis) which
then causes or contributes to acute cardiac dysfunction (e.g.
heart failure, arrhythmia, ischemia).
Type 4 CRS or chronic renocardiac syndrome is
characterized by a primary CKD condition leading to
decreased cardiac function, ventricular hypertrophy,
diastolic dysfunction and/or increased risk of adverse
cardiovascular events.
Type 5 or secondary CRS is characterized by the
presence of combined cardiac and renal dysfunction due to
systemic disorders.
A detailed and accurate history is crucial to aid in
diagnosing the type of CRS and in determining its
Summary
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subsequent treatment. A detailed history and a physical
examination in combination with routine laboratory tests,
chest X-ray, bedside ultrasound and biomarkers are useful
in making a correct diagnosis. In an acute setting,
biomarkers can contribute to integrate the diagnosis of
renal dysfunction with that of HF.
Three criteria are required for a biomarker to be
clinically useful. First, the assay should be precise,
accurate, and rapidly available to the clinician at a
relatively low cost. Second, the biomarker should provide
additional information that is not obvious from clinical
evaluation. Lastly, the absolute measured value should help
in clinical decision-making.
Most patients admitted to hospital for AHFS present
with systemic and/or pulmonary congestion associated with
normal-to-high systolic blood pressure. Treatments for this
group of patients primarily target congestion (increased
pulmonary capillary wedge pressure, PCWP).
Pharmacologic agents that are commonly used in this
setting include diuretics, vasodilators (e.g., nitroglycerin,
nitroprusside, nesiritide), and intravenous ACE inhibitors.
Therapeutic approaches to patients with chronic heart
failure (CHF) are complex and include pharmacological
and non-pharmacological management. Increasing survival
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88
remains the key endpoint and major goal in clinical trials
coupled with therapies directed towards improvement in
quality of life. Non-pharmacological management of CHF
includes symptom recognition, adherence to treatment,
lifestyle changes regarding nutrition and diet, exercise
training, education and smoking.