Cardiorenal

Question 1

What is Type 1 Cardiorenal syndrome?

Answer 1

Acute cardiorenal Heart failure leading to AKI

Acute coronary syndrome leading to acute heart and kidney failure

Question 2

What is Type 2 Cardiorenal syndrome?

Answer 2

Chronic cardiorenal Chronic heart failure leading to CKD Chronic heart failure

Question 3

What is Type 3 Cardiorenal syndrome?

Answer 3

Acute nephrocardiac AKD leading to acute heart failure AKI related uremic

Question 4

What is type 4 cardiorenal syndrome?

Answer 4

Chronic nephrocardiac CKD leading to heart failure Left ventricular hypertrophy and diastolic heart failure due to CKD

Question 5

What is type 5 cardiorenal syndrome?

Answer 5

Secondary Systemic disease leading to heart and kidney failure Sepsis, vasculitis, diabetes mellitus, amyloidosis

Question 6

How common is Type 1 CRS?

Answer 6

Type 1 CRS occurs in about 25% of patients hospitalized for acute decompensated heart failure (ADHF). Among these patients, underlying chronic kidney disease (CKD) is quite common and contributes to acute kidney injury (AKI) in 60% of all cases studied. AKI is an independent mortality risk factor in acute decompensated heart failure patients, including those with acute myocardial infarction (AMI) and/or reduced left ventricular ejection fraction

Question 7

Definition of Type 1 CRS? Pathophysiology?

Answer 7

Type 1 CRS (acute cardio- renal syndrome) is characterized by acute worsening of cardiac function leading to AKI5, in the setting of active cardiac disease such as ADHF.

Hemodynamic mechanisms play a major role in type 1 CRS in presence of ADHF leading to decreased renal arterial flow and a consequent fall in glomerular filtration rate(GFR). Once hemodynamics have been restored, renal and cardiac parameters come back to normal

Question 8

What are the two hemodynamic patterns seen in type 1 CRS? What is a nonhemodynamic potential pathophysiology?

Answer 8

Different hemodynamic profiles have been proposed: in “cold” pattern patients, reduction in effective circulation fluid volume (ECFV) represents the main hemodynamic change, while there is a marked increase in central venous pressure (CVP) in “wet” pattern patients.

“Cold” patients also present with decrease in renal blood flow related to the renin angiotensin-aldosterone system (RAAS) and systemic nervous system activation causing afferent vasoconstriction, decreased renal blood flow and decreased effective glomerular perfusion pressure. Patients who present with a “wet” hemodynamic profile display increased pulmonary and/or systemic congestion. In these patients, high CVP directly affects renal vein and kidney perfusion pressure; CVP increase also results in increased interstitial pressure with tubular’ collapse and progressive decline in GFR.

“Warm and wet” patients represent the most frequent profile in acute and chronic advanced heart failure. Mechanisms of increased CVP are quite similar to “cold” profile patients, but renal perfusion pressure is less affected because of higher arterial blood pressures.

Non-hemodynamic mechanisms were also proposed as involved in type 1 CRS including sympathetic nervous system (SNS) and RAAS activation, chronic inflammation and imbalance in the proportion of reactive oxygen species (ROS)/nitric oxide (NO) production. Patients with ADHF show more frequently defective regulation of monocyte apoptosis and activation of inflammatory pathways compared with healthy subjects