Cardiorenal syndromes

Abstract

Cardiorenal syndromes (CRS) have been subclassified as five defined entities which represent clinical circumstances in which both the heart and the kidney are involved in a bidirectional injury and dysfunction via a final common pathway of cell-to-cell death and accelerated apoptosis mediated by oxidative stress. Types 1 and 2 involve acute and chronic cardiovascular disease (CVD) scenarios leading to acute kidney injury or accelerated chronic kidney disease. Types 2 and 3 describe acute and chronic kidney disease leading primarily to heart failure, although it is possible that acute coronary syndromes, stroke, and arrhythmias could be CVD outcomes in these forms of CRS. Finally, CRS type 5 describes a simultaneous insult to both heart and kidneys, such as sepsis, where both organs are injured simultaneously. Both blood and urine biomarkers are reviewed in this paper and offer a considerable opportunity to enhance the understanding of the pathophysiology and known epidemiology of these recently defined syndromes.

Keywords: Biological biomarkers; Cardiovascular diseases; Creatinine; Heart diseases; Kidney diseases.

Figure 1

Pathophysiology and definitions of the five subtypes of cardiorenal syndromes. CVP: Central venous pressure; GFR: Glomerular filtration rate; BNP: Brain natriuretic peptide; ANP: Atrial natriuretic peptide; RAAS: Renin-angiotensin-aldosterone system ; ADHF: Acute decompensated heart failure; ACS: Acute coronary syndrome; CKD: Chronic kidney disease; CVD: Cardiovascular disease; ATN: Acute tubular necrosis; CI-AKI: Contrast-induced acute kidney injury; CSA-AKI: Cardiac surgery-associated AKI; CHF: Chronic heart failure; LVH: Left ventricular hypertrophy; EPO: Erythropoietin; LPS: Lipopolysaccharide.