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Cardiorenal syndrome : Overview



Cardiorenal syndrome (CRS) is an umbrella term utilized in the medical field that defines disorders of the guts and kidneys whereby “acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other”. The guts and therefore the kidneys are involved in maintaining hemodynamic stability and organ perfusion through an intricate network. These two organs communicate with one another through a variety of pathways in an interdependent relationship. CRS was defined as a condition where treatment of congestive heart failure is limited by decline in kidney function. This definition has since been challenged repeatedly but there still remains little consensus over a universally accepted definition for CRS. At a consensus conference of the Acute Dialysis Quality Initiative (ADQI), the CRS was classified into five subtypes based upon the organ that initiated the insult also as the acuity of disease.


Risk factors

The following risk factors have been associated with increased incidence of CRS.


·         Older age

·         Comorbid conditions (diabetes mellitus, uncontrolled hypertension, anemia)

·         Drugs (anti-inflammatory agents, diuretics, ACE inhibitors, ARBs)

·         History of heart failure with impaired left ventricular ejection fraction

·         Prior myocardial infarction

·         Elevated New York Heart Association (NYHA) functional class

·         Elevated cardiac troponins

·         Chronic kidney disease (reduced eGFR, elevated BUN, creatinine, or cystatin)



The pathophysiology of CRS are often 
attributed to 2 broad categories of "hemodynamic factors" like low flow , elevation of both intra-abdominal and central venous pressures, and non-hemodynamic factors or "cardiorenal connectors" like neurohormonal and inflammatory activation. It had been previously believed that low flow in coronary failure patients end in decreased blood flow to the kidneys which can lead to progressive deterioration of kidney function. As a result, diuresis of those patients will end in hypovolemia and pre-renal azotemia. However, several studies didn't find an association between kidney dysfunction and flow or other hemodynamic parameters. Additionally, CRS has been observed in patients with diastolic dysfunction who have normal left ventricular systolic function.


Therefore, there must be additional mechanisms involved within the progression of CRS. Elevated intra-abdominal pressures resulting from ascites and abdominal wall edema may be associated with worsening kidney functions in heart failure patients. Several studies have shown that as a result of this increased intra-abdominal pressure there is increased central venous pressure and congestion of the kidneys' veins, which can lead to worsening kidney function.


Additionally, many neurohormonal and inflammatory agents are implicated within the progression of CRS. These include increased formation of reactive oxygen species, endothelin, arginine vasopressin, and excessive sympathetic activity which may end in myocardial hypertrophy and necrosis. Other cardiorenal connectors include renin-angiotensin-system activation, nitric oxide/reactive oxygen species imbalance, inflammatory factors and abnormal activation of the sympathetic systema nervosum , which may cause structural and functional abnormalities in both heart and/or the kidney. There is an in depth interaction within these cardiorenal connectors also as between these factors and therefore the hemodynamic factors which makes the study of CRS pathophysiology complicated.



It is critical to diagnose CRS at an early stage so as 
to realize optimal therapeutic efficacy. However, unlike markers of heart damage or stress like troponin, creatine kinase, natriuretic peptides, reliable markers for acute kidney injury are lacking. Recently, research has found several biomarkers which will be used for early detection of acute kidney injury before serious loss of organ function may occur. Several of those biomarkers include neutrophil gelatinase-associated lipocalin (NGAL), N-acetyl-B-D-glucosaminidase (NAG), Cystatin C, and kidney injury molecule-1 (KIM-1) which is shown to be involved in tubular damage. Other biomarkers that have been shown to be useful include BNP, IL-18, and fatty acid binding protein (FABP). However, there is great variability in the measurement of these biomarkers and their use in diagnosing CRS must be assessed.



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