Cardiorenal syndrome

Cardiorenal syndrome

Description, Causes and Risk Factors:

Abbreviation: CRS.

The term cardiorenalsyndrome increasingly has been used without a consistent or well-accepted definition. To include the vast array of interrelated derangements, and to stress the bidirectional nature of heart-kidney interactions, we present a new classification of the CRS with 5 subtypes that reflect the pathophysiology, the time-frame, and the nature of concomitant cardiac and renal dysfunction. CRS can be generally defined as a pathophysiologic disorder of the heart and kidneys whereby acute or chronic dysfunction of 1 organ may induce acute or chronic dysfunction of the other.

Cardiorenal syndrome

Fundamentally, the heart and the kidneys are the organs which are richly vascular (the kidneys are more vascular than the heart). In addition, both organs are supplied by sympathetic and parasympathetic innervations. These two organs are acting in tandem to regulate blood pressure, vascular tone, diuresis, natriuresis, intravascular volume homeostasis, peripheral tissue perfusion, and oxygenation. They have endocrine functions with interdependent physiological hormonal actions regulated by arterial natriuretic peptide, a vasodilator secreted from the heart, and renninangiotensin-aldosterone system (RAAS). Also, vitamin D3, erythropoietin, and renalase are all secreted from the kidneys and are capable of cellular and humoral signaling. Dysfunction of either of the two organs can cause dysfunction of the other. Changes in the RAAS, the imbalance between nitric oxide (NO) and reactive oxygen species (ROS), the sympathetic nervous system, and inflammation are the cardiorenal connectors to develop cardiorenal syndrome. These connectors together decrease the sensitivity of erythropoietin and are responsible for renal anemia that also aggravates the clinical conditions of cardiac failure.


    Type 1 CRS reflects an abrupt worsening of cardiac function (e.g., acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury.

  • Type 2 CRS comprises chronic abnormalities in cardiac function (e.g., chronic congestive heart failure) causing progressive chronic kidney disease.

  • Type 3 CRS consists of an abrupt worsening of renal function (e.g., acute kidney ischemia or glomerulonephritis) causing acute cardiac dysfunction (e.g., heart failure, arrhythmia, ischemia).

  • Type 4 CRS describes a state of chronic kidney disease (e.g., chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy, and/or increased risk of adverse cardiovascular events.

  • Type 5 CRS reflects a systemic condition (e.g., sepsis) causing both cardiac and renal dysfunction.

To date, little is known regarding the pathophysiology of CRS. A reduced cardiac output (CO) in CHF resulting in decreased renal perfusion could be an easy explanation for the worsening renal function. Interestingly, worsening renal function has been demonstrated in patients with ADHF (acute decompensated heart failure) even though left ventricular EF is preserved. This decline in renal function, despite a presumed preservation of blood flow to the kidneys, has led to the search for other mechanisms of CRS, including the role of the renin-angiotensin-aldosterone system (RAAS), various chemicals (nitric oxide [NO], prostaglandins, natriuretic peptides, endothelins, etc), oxidative stress and sympathetic overactivity.

Cardiorenal syndrome, a poorly understood clinical entity, needs more widely accepted definition and pathogenesis, and its challenging management needs to be looked into. Yet it has remained a source of debate.


Cardiorenal syndrome is an interdependentinvolvement of both the heart and the kidneyin a spiral fashion leading to volume overload,diuretic resistance, and further involvement ofall systems in which clinical condition will likelyworsen before they get better. Decrease in GFR orcreatinine clearance in patients with decompensatedheart failure involves longer hospital stay andmore utilization of hospital resources, but still theprognosis is grave.


While making a diagnosis of CRS, it should be kept in mind that there is no correlation between serum creatinine and GFR (glomerular filtration rate). Relative to a decline in EF (ejection fraction), a fall in GFR is more important regarding the prognosis in heart failure patients. In addition, measurements of serum creatinine alone could also be misleading in terms of prognosis. Approximately two-thirds of patients admitted for acute exacerbations of CHF have decreased GFR or creatinine clearance, despite many of them having relatively normal levels of serum creatinine.

The estimation of GFR should be a part of the initial evaluation because GFR provides a general sense of prognosis. Moreover, GFR is helpful in the evaluation for planning a management strategy (use of ACE inhibitors, angiotensin receptor antagonists and radiocontrasts for diagnostic tests, etc). Because serum creatinine level is a relatively insensitive indicator of CRS, true GFR is calculated, although cumbersome, using the Cockcroft-Gault formula (by calculating creatinine clearance) or the Modification of Diet in Renal Disease equation.

The CO is also not a reliable indicator to assess the severity of CRS. More often, CO will be normal in cases of CRS. Nevertheless, the presence of low filling pressures, a low cardiac index or even reduced renal perfusion is not necessary to identify CRS.


Clinical management of the patient with cardiorenal syndrome includes the challenge of diuretic resistance, which may involve correcting the underlying cause, combination diuretics or diuretic infusions. The key to improved outcome is the optimization of proven heart failure therapies. The use of vasodilator therapy is the current mainstay of treatment. Nesiritide, or recombinant B-type natriuretic peptide, has courted controversy regarding its role in cardiorenal syndrome. However, data are emerging that low doses appear to be renal-protective. Other more recent strategies include ultrafiltration, vasopressin antagonists and adenosine antagonists. All of these newer modalities promise more rapid volume removal, but their ultimate impact on survival or preservation of renal function is unknown at the present time.

Because of the complex nature of these patients, and the compromised outcome, it is important that cardiologists, nephrologists and internists all work together toward the common goal of protecting the patient with cardiorenal syndrome, and use the best available evidence for management.

NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.


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