Introduction
Congestive heart failure (CHF) continues to be a serious medical concern despite significant breakthroughs in diagnosis and therapy over the last decade. The prognosis of heart failure patients remains poor.The relationship between heart failure, chronic kidney failure, and anemia is known as the cardio-renal anemia syndrome. The cycle of these three diseases deteriorates cardiac and renal function and promotes anemia. Each of the three can initiate or be initiated by the others.
What Is the Classification of Cardio-Renal Anemia Syndrome?
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Type I - Acute Cardio-Renal Anemia Syndrome:It is caused by a sudden deterioration in heart function due to cell signaling, neurohormonal, and hemodynamic anomalies.
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Type II - Chronic Cardio-Renal Anemia Syndrome: It results in gradual and irreversible chronic kidney disease due to the hyperactivation of neurohormones over time.
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Type III - Acute Renocardiac Syndrome: It occurs due to acute deterioration of kidney function induced by the inflammatory surge, volume overload, or metabolic abnormalities leading to an acute cardiac condition such as acute heart failure, arrhythmia (irregular heartbeat), or ischemia, acute volume overload, hyperkalemia (increase in the level of potassium), and acidosis.
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Type IV - Chronic Renocardiac Syndrome: It leads to impaired heart function, such as cardiac hypertrophy, or a higher risk of unfavorable cardiovascular events, such as chronic hypertension, volume overload, and metabolic or micronutrient imbalances.
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Type V - Secondary Cardio-Renal Anemia Syndrome: This occurs when a systemic disorder such as liver cirrhosis or diabetes mellitus can cause a decrease in both heart and kidney function.
How Does Anemia Affect People With Congestive Heart Failure (CHF)?
According to research, a significant proportion of patients treated with the highest prescribed doses of ACE inhibitors, Aldospirone, beta blockers, nitrates, Digoxin, and Furosemide developed severe fluid retention, acute exhaustion, and shortness of breath. The vast majority of these patients were also severely anemic, indicating that anemia is more common and the severity of congestive heart failure (CHF) increases. Anemia also increases the risk of cardiovascular events, including stroke. It is also linked to left ventricular dilatation and hypertrophy (increase in heart muscles). Anemia may also hasten the decline of renal function in patients with chronic kidney failure (CKD) and therefore progress to renal failure.
What Is the Mechanism of Cardio-Renal Anemia Syndrome?
The cardio-renal anemia syndrome is a correlation between congestive heart failure, chronic kidney disease, and anemia, which forms a vicious cycle. The mechanism by which anemia can cause cardiac and renal damage has been gradually explored since the early times. Severe anemia, however, has been demonstrated to be a risk factor for cardiac and renal disease in people with no history of basic heart disease. Anemia causes a lack of oxygen supply to the tissues (tissue hypoxia), which causes peripheral vasodilation and decreased vascular resistance, thus lowering blood pressure. In order to maintain sufficient blood pressure, the sympathetic nervous system is engaged, resulting in the following:
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Increased heart rate (tachycardia).
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Increased stroke volume (blood pumped out of the left ventricle of the heart).
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Peripheral vasoconstriction (constriction of blood vessels).
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Renal vasoconstriction (constriction of blood vessels of the kidney).
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Reduced renal blood flow.
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Reduced glomerular filtration rate (GFR) (filtration process done by the kidney)
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Renal ischemia (reduced or restricted blood supply).
Reduced renal blood flow activates the renin-angiotensin-aldosterone system (RAAS) and antidiuretic hormone, resulting in further renal vasoconstriction and salt and water retention. The resulting renal insufficiency may also result in anemia due to decreased erythropoietin (produces red blood cells) production and bone marrow activity.
How Does Cardio-Renal Anemia Syndrome Cause Congestive Heart Failure?
Fluid retention induces plasma volume expansion, which produces stress on an already strained heart muscle. The resulting left ventricular enlargement causes necrosis and death of myocardial cells, as well as myocardial fibrosis and cardiomyopathy (enlargement of heart muscles), which results in CHF. Furthermore, high amounts of renin, angiotensin, and aldosterone directly injure cardiac cells, aggravating the damage already done. TNFa (tumor necrosis factor-alpha) levels are elevated in CHF, and there is evidence that cardiac cells release this cytokine (increases inflammation) in response to injury, further damaging the heart. This increased cytokine production has also been linked to the development of chronic illness anemia and may aggravate anemia in CHF patients, resulting in a vicious loop of disease progression.
How Is Cardio-Renal Anemia Syndrome Diagnosed?
The American College of Cardiology Foundation suggests routine anemia screening in all patients with congestive heart failure. Similarly, the kidney disease global outcomes recommendation suggests regular hemoglobin level testing in CKD patients. In order to determine the likely cause of anemia and rule out absolute iron deficiency, the following tests are performed:
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Complete blood cell count.
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Serum ferritin levels.
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Absolute reticulocyte count.
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Serum vitamin B12 and folate levels.
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Serum transferrin saturation.
How Is Cardio-Renal Anemia Syndrome Managed?
Management of cardio-renal anemia syndrome necessitates a multidisciplinary approach. Parenteral Iron is found to be appropriate for patients with simultaneous CHF and CKD, improving functional capacity and symptoms. In addition to the supplement, intravenous iron and erythropoiesis-stimulating agents (ESA) are the mainstays of treatment for treating iron shortages.
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Iron Infusion - Intravenous Iron therapy improves iron parameters in patients with heart failure and iron deficiency serum ferritin when transferrin saturation is 20 percent, with or without anemia, and whether or not they have CKD.
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Transfusions of Red Blood Cells - When ESA medication is ineffective or when quick repair of acute anemia is required, RBC transfusion (RBCT) is advised to reduce the risk of adverse outcomes. Transfusion of red blood cells should be avoided in patients with chronic CKD anemia or those eligible for organ transplants.
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Erythropoiesis-Stimulating Agents (ESA) - ESA medication is effective in many CKD and congestive HF patients and gains improvements in Hb levels at standard therapeutic ESA doses.
Conclusion
Cardiorenal syndrome (CRAS) is a group of kidney and cardiac illnesses in which loss of function in one organ contributes to impaired function in the other. Comorbid anemia frequently complicates cardiorenal syndrome, resulting in reciprocal and increasing cardiac and renal impairment. Cardiorenal anemia syndrome (CRAS) refers to the combination of heart failure, chronic kidney disease (CKD), and anemia. Anemia in CRAS patients is difficult since numerous guideline-recommended drugs are required to successfully control the loss of heart and kidney function. Proper screening and management of anemia in CRAS would enhance the clinical outcomes of patients.
