Cardiorenal syndrome: Pathophysiology as a key to the therapeutic approach in an under‐diagnosed disease

FIGURE 1. Pathophysiology of CRS‐1. Interaction between heart and kidney in cardiorenal syndrome type 1. ACE‐I, angiotensin‐converting enzyme inhibitor; ald, aldosterone; ang II, angiotensin II; ANP, atrial natriuretic peptide; BNP, B‐type natriuretic peptide; CVP, central venous pressure; GFR, glomerular filtration rate; IAP, intra‐abdominal pressure; KIM‐1, kidney injury molecule‐1; L‐FABP, liver‐type fatty acid‐binding protein; RAAS, renin‐angiotensin‐aldosterone system; RBF, renal blood flow; SNS, sympathetic nervous system

FIGURE 2. Pathophysiology of CRS‐3. Interaction between heart and kidney in cardiorenal syndrome type 3. CO, cardiac output; GRF, glomerular filtration rate; RAAS, renin‐angiotensin‐aldosterone system; SNS, sympathetic nervous system

FIGURE 3. Pathophysiology of CRS‐2. Interaction between heart and kidney in cardiorenal syndrome type 2. ACE‐I, angiotensin‐converting enzyme inhibitor; ADHF, acute decompensated heart failure; ANP, atrial natriuretic peptide; BNP, B‐type natriuretic peptide; CVP, central venous pressure; GFR, glomerular filtration rate; IAP, intra‐abdominal pressure; LVH, left ventricular hypertrophy; RBF, renal blood flow; RAAS, renin‐angiotensin‐aldosterone system; SNS, sympathetic nervous system

FIGURE 4. Pathophysiology of CRS‐4. Interaction between heart and kidney in cardiorenal syndrome type 4. Ca, calcium; EPO, erythropoietin; LVH, left ventricular hypertrophy; PBUTs, protein‐bound uremic toxins; Phos, phosphorus; RAAS, renin‐angiotensin‐aldosterone system; SNS, sympathetic nervous system

FIGURE 5. Pathophysiology of CRS‐5. Interaction between systemic disease, heart and kidney in cardiorenal syndrome type 5. DIC, disseminated intravascular coagulation; LPS, lipopolysaccharide; RAAS, renin‐angiotensin‐aldosterone system; ROS, reactive oxygen species; SNS, sympathetic nervous system; SVR, system vascular resistance

FIGURE 6. Therapeutic management of CRS‐1. BP, blood pressure; CO, cardiac output; CVP, central venous pressure; GDMT, guideline‐directed medical therapy; HD, hemodynamic; HF, heart failure; IAP, intra‐abdominal pressure; ICU, intensive care unit; IV, intravenous; MCS, mechanical circulatory support; NSAIDS, non‐steroidal anti‐inflammatory drugs; TTE, transthoracic echocardiography; WRF, worsening of renal function

FIGURE 7. Therapeutic management of CRS‐3. AHF, acute heart failure; AKI, acute kidney injury; CKD, chronic kidney disease; RRT, renal replacement therapy

FIGURE 8. Therapeutic management of CRS‐2. CRT, cardiac resynchronization therapy; FU, follow‐up; GFR, glomerular filtration rate; HD, hemodynamic; ICU, intensive care unit; MCS, mechanical circulatory support; NSAIDS, non‐steroidal anti‐inflammatory drugs; RAAS, renin–angiotensin–aldosterone system; RAASi, renin–angiotensin–aldosterone system inhibitor; Scr, serum creatinine; SGLT2, sodium–glucose co‐transporter 2

FIGURE 9. Therapeutic management of CRS‐4. ACE‐I, angiotensin‐converting enzyme inhibitor; ARBs, angiotensin receptor blockers; BB, beta blockers; CKD, chronic kidney disease; MRA, antimineralocorticoid; NSAIDs, non‐steroidal anti‐inflammatory drugs; RAAS, renin–angiotensin–aldosterone system; RRT, renal replacement therapy

FIGURE 10. Therapeutic management of CRS‐5. RAAS, renin–angiotensin–aldosterone system; QoL, quality of life