Cardiorenal syndrome



Cardiorenal syndrome (CRS) defines disorders of the heart and kidneys whereby  dysfunction in one organ may induce acute or chronic dysfunction of the other.



The heart and the kidneys are involved in maintaining hemodynamic stability and organ perfusion.



The  CRS is classified into five subtypes primarily based upon the organ that initiated the insult as well as the acuity of disease.



Acute cardiac impairment leading to acute kidney injury is, type one. 



Chronic cardiac impairment leading to kidney impairment, is type2



Type 3 is acute kidney injury leading to cardiac impairment.



Type 4 is chronic kidney disease leading to cardiac impairment.



Type 5 is systemic conditions leading to both cardiac and kidney impairment.



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: hemodynamic factors such as low cardiac output, elevation of both intra-abdominal and central venous pressures, and non-hemodynamic factors such as neurohormonal and inflammatory activation.



Studies do not find an association between kidney dysfunction and cardiac output or other hemodynamic parameters.



CRS has been observed in patients with diastolic dysfunction who have normal left ventricular systolic function.



Elevated intra-abdominal pressures resulting from ascites and abdominal wall edema may be associated with worsening kidney functions in patients with heart failure, due to increased central venous pressure and congestion of the kidneys’ veins.



Worsening CRS occurs with neurohormonal and inflammatory agent changes and  include increased formation of reactive oxygen species, endothelin, arginine vasopressin, excessive sympathetic activity which can result in myocardial hypertrophy and necrosis, renin-angiotensin-system activation, nitric oxide/reactive oxygen species imbalance, and inflammatory factors, causing structural and functional abnormalities in both heart and/or the kidney. 



Reliable markers for acute kidney injury are lacking. 



Types of CrSx.



Type 1 (acute CRS) Abrupt worsening of heart function kidney injury acute cardiogenic shock or acute decompensation of chronic heart failure



Type 2 (chronic CRS) Chronic abnormalities in heart function progressive chronic kidney disease chronic heart failure



Type 3 (acute renocardiac syndrome)


Abrupt worsening of kidney function, acute cardiac disorder (e.g. heart failure, abnormal heart rhythm, or pulmonary edema) acute kidney failure or glomerulonephritis



Type 4 (chronic renocardiac syndrome)


Chronic kidney disease, decreased cardiac function, cardiac hypertrophy and/or increased risk of adverse cardiovascular events chronic glomerular disease



Type 5 (secondary CRS) Systemic condition of both heart and kidney dysfunction, diabetes mellitus, sepsis, lupus.



Others define  the CRS as a pathophysiological condition in which combined heart and kidney dysfunction amplifies progression of failure of the individual organs, by inducing similar pathophysiological mechanisms. 



The same neurohormonal systems are activated causing accelerated cardiovascular disease, and progression of damage and failure of both organs. 



Medical management of patients with CRS is difficult as treatment of one organ may have worsening outcome on the other. 



Diuretic use in the treatment of heart failure must be carefully dosed to prevent kidney injury. 



The use of ACE inhibitors have long term protective effect on kidney and heart tissue. 



The combined use of statin and an ACEI improves clinical outcome more than a statin alone and considerably more than ACE inhibitor alone.



Adenosine is responsible for constriction of afferent arteriole and reduction in GFR. 



Ultrafiltration can improve kidney function.



Kidney failure is very common in patients suffering from congestive heart failure, and it complicates one-third of all hospital admissions for heart failure.



About 44% of deaths in patients with end-stage kidney failure (ESKF) are due to cardiovascular disease.



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