Cardiorenal syndrome type 2 (CRS-2)

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What is Cardiorenal syndrome type 2 (CRS-2)?

Cardiorenal syndrome type 2 is characterized by chronic abnormalities in cardiac function leading to kidney injury or dysfunction.

Chronic Kidney Disease has been observed in 45% to 63% of congestive heart failure (CHF) patients.

What are the main pathophysiologic pathways involved in Cardiorenal syndrome type 2?

Intrinsic to its definition, Cardiorenal syndrome type 2 is characterized by CKD onset or progression in HF patients, but two fundamental features are proposed: CHF and CKD are found simultaneously, and CHF is the cause of the CKD or responsible for its progression.

Examples of Cardiorenal syndrome type 2 include cyanotic nephropathy occurring in patients with congenital heart disease, when heart disease clearly precedes kidney involvement or acute coronary syndrome leading to left ventricular dysfunction and the onset or progression of coexisting CKD.

The pathophysiological mechanisms of Cardiorenal syndrome type 2 include:

• Neurohormonal activation

• Kidney hypoperfusion

• Venous congestion

• Inflammation

• Atherosclerosis

• Oxidative stress

These mechanisms are operative in recurrent episodes of acute heart and kidney decompensation associated with HF and CKD progression.

Is there a pathophysiological role for the RAAS?

Patients with decompensated HF and venous congestion often have significant RAAS activation without decreased circulating volume.

Kidneys of HF patients release renin, which increases angiotensin II production. Persistent RAAS and sympathetic nervous system (SNS) activation could contribute to CKD progression.

Angiotensin II production and aldosterone release increase sodium reabsorption leading to increased blood pressure and volume overload. Increased aldosterone levels also contribute to glomerular fibrosis due to the up-regulation of transforming growth factor-β (TGF-β) and increased fibronectin.

Persistent inflammation triggered by cardiac decompensation also promotes CKD progression in CHF.

What about new biomarkers for the diagnosis of Cardiorenal syndrome type 2?

Assessment of kidney injury in chronic HF patients previously has been limited to creatinine, estimated glomerular filtration rate (eGFR), and urinary protein excretion.

Recently, novel kidney biomarkers (cystatin C, NGAL, kidney injury molecule-1 and N-acetylbeta-glucosamidase) have been evaluated in CHF patients, and may eventually become effective prognostic markers for CKD and cardiovascular outcomes.

Is there a diagnostic role for ultrasound?

In Cardiorenal syndrome type 2, the kidney ultrasound shows a reduction of cortical thickness, reduced cortico-medullary ratio, and increased parenchymal echogenicity.

Echocardiography may show:

  • • High atrial volumes and areas as indices of volume overload
  • • Normal or decreased ejection fraction (EF)
  • • Right chamber dilation
  • • Increased pulmonary arterial pressure
  • • Pericardial effusion
  • • Valvular disease (calcific disease)

How is Cardiorenal syndrome type 2 treated?

In the treatment of Cardiorenal syndrome type 2, the main issues are:

  • • Preventing new-onset kidney dysfunction, emerging in a setting of CHF
  • • Counteract kidney dysfunction once it has developed

Special attention should be paid to several CHF drugs that may worsen kidney function. Diuresis-associated hypovolemia, the early introduction of RAAS blockade, and drug-induced hypotension may all contribute to the genesis or aggravation of Cardiorenal syndrome type 2.

In patients with a poor response to oral loop diuretics, a number of strategies can be employed to improve urine output. Loop diuretics can be switched to intravenous (IV) infusions.

This removes the problem of erratic bioavalability found in furosemide. Often HF patients require nearly continuous exposure to a diuretic in order to achieve adequate diuresis. This can be achieved through increased frequency or a continuous infusion. Adding thiazide diuretics to block distal sodium resorption can enhance loop diuretic activity. High doses of IV loop diuretics in patients with signs and symptoms of HF adequately controlled should be lowered because of the side effects:

  • • Hypokalemia
  • • Hypotension
  • • Dysnatremia
  • • Marked neurohormonal activation
  • • Kidney impairment

These iatrogenic influences may often account for kidney damage as much as the congestive nephropathy itself.

Ultrafiltration for cardiorenal syndrome type 2

Isolated ultrafiltration (IUF) in the setting of Cardiorenal syndrome type 2 allows rapid correction of fluid overload when standard management (high-dose IV diuretics with or without inotrope support) has failed.

Current American Heart Association/American College of Cardiology and the European Society of Cardiology treatment guidelines establish that IUF is an option (class IIa, level of evidence B and C) if all diuretic strategies have failed. IUF does not affect electrolytes or significantly reduce urea levels like dialysis or hemofiltration.

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