A 54-year-old man comes to the emergency department due to progressively worsening shortness of breath, lower extremity swelling, and decreased urine output for the past week. Medical history includes heart failure with reduced ejection fraction. Medications include metoprolol succinate, lisinopril, spironolactone, and furosemide. The patient has been taking the same doses of these medications for the past 6 months but admits that he "misses some doses now and then." Temperature is 36.9 C (98.4 F), blood pressure is 112/64 mm Hg, pulse is 90/min, and respirations are 20/min. Oxygen saturation is 93% on room air. Physical examination shows jugular venous distension. S1 and S2 are normal, and there are no murmurs. An S3 is heard. Crackles are heard at the bilateral lung bases. The abdomen is distended, and there is 2+ pitting lower extremity edema bilaterally. Laboratory results (current and from 3 weeks ago) are as follows:
| Current | Previous | |
| Blood urea nitrogen | 46 mg/dL | 20 mg/dL |
| Serum creatinine | 2.2 mg/dL | 1.3 mg/dL |
Urinalysis is unremarkable. Which of the following is the most likely cause of this patient's acute kidney injury?
Prerenal acute kidney injury | |
Etiology |
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Clinical features |
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Treatment |
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EABV = effective arterial blood volume; NSAID = nonsteroidal anti-inflammatory drug. | |
This patient has acute kidney injury (AKI) with an elevated blood urea nitrogen/creatinine ratio (>20:1) and unremarkable urinalysis, suggesting a prerenal cause. Although prerenal AKI usually results from total body volume depletion, it can also occur in volume-overloaded states that involve reduced effective arterial blood volume (EABV). This patient has volume overload due to an acute heart failure exacerbation, and the AKI is most likely due to cardiorenal syndrome.
Cardiorenal syndrome involves mutually detrimental interactions between the heart and the kidneys. Left ventricle failure with reduced cardiac output leads to decreased renal perfusion followed by activation of the renin-angiotensin-aldosterone system (RAAS). The increase in RAAS activity causes vasoconstriction and volume retention, which increase the load on the left ventricle and further reduce renal perfusion.
Elevated central venous pressure is likely the major driver of AKI in cardiorenal syndrome. The elevated central venous pressure leads to elevated renal venous pressure and congestion. This reduces the glomerular capillary filtration gradient, possibly due to interstitial edema (from venous congestion) increasing Bowman capsule hydrostatic pressure; the result is a reduction in the glomerular filtration rate (GFR). Decreased renal perfusion due to reduced cardiac output also has a role in the reduced GFR. Diuretics are usually the most effective therapy for AKI due to cardiorenal syndrome; the resulting reduction in renal venous pressure restores the glomerular capillary filtration gradient and improves GFR.
(Choice B) Glomerular hyperfiltration occurs in the early stages of diabetic nephropathy and is recognized by a temporary increase in GFR (leading to a decrease in serum creatinine).
(Choice C) Low blood oncotic pressure occurs in nephrotic syndrome, but it is not typical of heart failure. Nephrotic syndrome involves total body volume overload with intravascular volume depletion, and prerenal AKI can occur due to reduced EABV.
(Choice D) Left ventricular preload, or end-diastolic volume, is increased in heart failure. Patients with prerenal AKI due to volume depletion (eg, dehydration) have reduced left ventricular preload.
(Choice E) Patients with bilateral renal artery stenosis (RAS) typically have a maintained GFR thanks to angiotensin II–mediated efferent arteriole constriction; in these patients, starting an ACE inhibitor (eg, lisinopril) or an angiotensin receptor blocker removes angiotensin II activity and can cause AKI. This patient has been on lisinopril and had normal kidney function just 3 weeks ago, making bilateral RAS highly unlikely.
Educational objective:
Prerenal acute kidney injury (AKI) can occur in volume-overloaded states. Prerenal AKI in an acute heart failure exacerbation is most likely due to cardiorenal syndrome, which involves elevated central venous and renal venous pressures leading to a reduction in glomerular filtration.