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Rapid Review·Cardiovascular

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Heart Failure

T2High yield

Cardiorenal Syndrome

Focus on

Kidney function falling because the heart is failing. The driver is venous congestion (high renal venous pressure), not "low flow" — so the answer to a rising creatinine in a congested patient is more diuresis, not less, and a small creatinine bump on GDMT is not a reason to stop it.

Key takeaways

What it is

Cardiorenal syndrome

a progressive decline in renal function caused by severe cardiac dysfunction.

How common

it occurs in about 30 percent of patients with acute decompensated heart failure.
  • It is the major driver of acute kidney injury (AKI) in acute heart failure.

Pathophysiology

Renal venous congestion and acute kidney injury: (1) raised renal venous pressure (2) makes the vasa recta leak fluid, (3) tubulointerstitial edema raises the pressure inside the tubules, and (4) the higher Bowman capsule pressure shrinks the filtration gradient, so the glomerular filtration rate falls.
What this shows
Renal venous congestion and acute kidney injury: (1) raised renal venous pressure (2) makes the vasa recta leak fluid, (3) tubulointerstitial edema raises the pressure inside the tubules, and (4) the higher Bowman capsule pressure shrinks the filtration gradient, so the glomerular filtration rate falls.

The main problem is venous congestion

a high central venous pressure is transmitted to the renal veins.
  • That lowers the trans-glomerular pressure gradient and the glomerular filtration rate (GFR).

Low forward flow is the smaller contributor

reduced renal perfusion from a low cardiac output also lowers the GFR (prerenal physiology).
The cardiorenal cycle: left and right ventricular failure raises central and renal venous pressure (venous congestion) and lowers cardiac output (reduced forward flow); both lower the GFR, and the renin-angiotensin-aldosterone activation that follows drives vasoconstriction and sodium and water retention, which loads the failing heart again.
What this shows
The cardiorenal cycle: left and right ventricular failure raises central and renal venous pressure (venous congestion) and lowers cardiac output (reduced forward flow); both lower the GFR, and the renin-angiotensin-aldosterone activation that follows drives vasoconstriction and sodium and water retention, which loads the failing heart again.

Renin-angiotensin-aldosterone activation

causes salt and fluid retention, hypertension, and hypertensive nephropathy.

Diagnosis and management

Diagnosis

a falling GFR and rising creatinine that cannot be explained by underlying kidney disease.

Treat the heart failure and the renal failure together.

Intravenous diuretics (furosemide)

lower central and renal venous pressure, improve cardiac output, and so raise the GFR.
  • A congested patient with a rising creatinine needs more diuresis, not less.

Prognosis

heart failure with a reduced GFR and a creatinine over 3 mg/dL carries a poor prognosis.
A patient admitted with acute decompensated heart failure is congested and the creatinine rises from 1.4 to 2.1. Should the diuretic be stopped? Explain.

No, diuresis should continue or increase. In cardiorenal syndrome the main driver is venous congestion: high central venous pressure is transmitted to the renal veins and lowers the GFR. IV furosemide lowers that pressure and raises the GFR.

How it's tested

Admitted with decompensated HFrEF, JVD and edema; creatinine rises from 1.4 to 1.9 after two days of IV furosemide while he is still congested: cardiorenal syndrome from venous congestion — continue or increase diuresis; do not stop.

Same patient, now dry with orthostatic hypotension, creatinine 2.4 and BUN 60: over-diuresis — hold the diuretic.

Starting sacubitril/valsartan raised the creatinine 15% with a potassium of 4.9: an expected hemodynamic change — continue and recheck.

Cirrhotic with tense ascites, creatinine 3, urine sodium < 10 and no response to albumin challenge: hepatorenal syndrome — the vasodilation problem, not the congestion problem.

Go deeper

Guidelines: 2022 AHA/ACC/HFSA Heart Failure Guideline

Related Step 2 pages: Heart Failure, Approach to Shock, Approach to Fluid Replacement

High-yield images2
Renal venous congestion and acute kidney injury: (1) raised renal venous pressure (2) makes the vasa recta leak fluid, (3) tubulointerstitial edema raises the pressure inside the tubules, and (4) the higher Bowman capsule pressure shrinks the filtration gradient, so the glomerular filtration rate falls.
The cardiorenal cycle: left and right ventricular failure raises central and renal venous pressure (venous congestion) and lowers cardiac output (reduced forward flow); both lower the GFR, and the renin-angiotensin-aldosterone activation that follows drives vasoconstriction and sodium and water retention, which loads the failing heart again.
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