[5] Cardiorenal Syndrome is characterized by the dysfunction of both the cardiac and renal systems, resulting in a range of clinical manifestations.

Many patients will have volume overload and therefore may show clinical signs such as jugular venous distension, generalized swelling of the abdomen and/or the lower legs, and difficulty breathing.

[6] Patients with Type 1 CRS, have a rapid worsening of cardiac function leading to Acute Kidney Injury, which may manifest as oliguria or anuria.

[9] In addition, 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 heart failure patients.

These include increased formation of reactive oxygen species, endothelin, arginine vasopressin, and excessive sympathetic activity which can result in myocardial hypertrophy and necrosis.

Recently, research has found several biomarkers that can be used for early detection of acute kidney injury before serious loss of organ function may occur.

Several of these biomarkers include neutrophil gelatinase-associated lipocalin (NGAL), N-acetyl-B-D-glucosaminidase (NAG), Cystatin C, and kidney injury molecule-1 (KIM-1) which have been shown to be involved in tubular damage.

[11] Ronco et al. first proposed a five-part classification system for CRS in 2008 which was also accepted at ADQI consensus conference in 2010.

[1] These include: The distinction between CRS type 2 and CRS type 4 is based on the assumption that, also in advanced and chronic disease, two different pathophysiological mechanisms can be distinguished, whereas both CKD and HF often develop due to a common pathophysiological background, most notably hypertension and diabetes mellitus.

[15] One study shows how ACE inhibitors and angiotensin II receptor antagonists have been found to prevent nephropathy in patients who have diabetes.