Cardiorenal syndrome is a bidirectional pathophysiological interaction between the heart and kidneys1
It occurs because of acute or chronic dysfunction in one organ leading to dysfunction in the other. Underlying mechanisms include arterial under-filling, neurohormonal activation, venous congestion and endothelial dysfunction.1
It is associated with increased mortality among patients with heart failure2
Around 60% of patients with decompensated heart failure have chronic kidney disease (CKD) with an estimated glomerular filtration rate (eGFR) of less than 60 mL/min/1.73 m2.2 Patients with heart failure and CKD have a 27% increase in mortality, compared with patients with heart failure and normal renal function. A decrease in eGFR by 10 mL/min/1.73 m2 increases mortality by 15%.2
Patients with cardiorenal syndrome should be treated with angiotensin-converting-enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs)1
These agents reduce risk of death and prolong time to end-stage kidney disease.1 Both ACE inhibitors and ARBs should be titrated to the maximum tolerated dose, provided that the patient has no symptomatic hypotension or hyperkalemia.3 Although angiotensin receptor–neprilysin inhibitors can be used in place of ACE inhibitors or ARBs for heart failure, their renal protective effects are unknown.
Sodium–glucose cotransporter-2 (SGLT2) inhibitors should be added to ACE inhibitors or ARBs for renal and cardiovascular protection1,4
Once a patient’s eGFR is stable (> 20 mL/min/1.73 m2) for 3 months on an ACE inhibitor or an ARB, an SGLT2 inhibitor should be started, such as empagflozin (10 mg/d). Independent of diabetes, SGLT2 inhibitors reduce the risk of renal failure progression by 37%.4
Patients with cardiorenal syndrome benefit from guideline-directed medical therapy5
Patients with an eGFR of less than 60 mL/min/1.73 m2 or with an estimated 5-year risk of kidney failure greater than 5% are at high risk for worsening kidney disease and referral to nephrology should be considered. Engaging primary care physicians, transitional care at hospital discharge and multidisciplinary clinic follow-up may increase uptake of guideline-directed medical therapy.5
Footnotes
Competing interests: Bourne Auguste has received speaking honoraria from Amgen and Baxter Healthcare. No other competing interests were declared.
This article has been peer reviewed.
This is an Open Access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY-NC-ND 4.0) licence, which permits use, distribution and reproduction in any medium, provided that the original publication is properly cited, the use is noncommercial (i.e., research or educational use), and no modifications or adaptations are made. See: https://creativecommons.org/licenses/by-nc-nd/4.0/
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- Cardiorenal syndrome is a bidirectional pathophysiological interaction between the heart and kidneys1
- It is associated with increased mortality among patients with heart failure2
- Patients with cardiorenal syndrome should be treated with angiotensin-converting-enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs)1
- Sodium–glucose cotransporter-2 (SGLT2) inhibitors should be added to ACE inhibitors or ARBs for renal and cardiovascular protection1,4
- Patients with cardiorenal syndrome benefit from guideline-directed medical therapy5
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