What condition can cause prerenal acute kidney injury (AKI) through both systemic vasodilation and renal vasoconstriction?

Cirrhosis Causes Prerenal AKI Through Both Systemic Vasodilation and Renal Vasoconstriction

Cirrhosis is the correct answer because it uniquely causes prerenal acute kidney injury through the dual mechanism of splanchnic/systemic vasodilation combined with compensatory renal vasoconstriction, a pathophysiologic hallmark of hepatorenal syndrome. 1

Pathophysiologic Mechanism in Cirrhosis

The fundamental hemodynamic abnormality in cirrhosis involves:

• Splanchnic and systemic vasodilation that decreases effective arterial blood volume despite total body fluid overload 1
• Compensatory activation of vasoconstrictor systems (renin-angiotensin-aldosterone system, sympathetic nervous system, arginine vasopressin) in response to the perceived hypovolemia 1
• Intense renal arteriolar vasoconstriction resulting from these activated vasoconstrictor pathways, which reduces kidney blood flow and impairs glomerular filtration rate 1

This creates a paradoxical situation where the kidneys are vasoconstricted while the systemic circulation is vasodilated—the defining feature of hepatorenal syndrome-AKI (HRS-AKI). 1

Why the Other Options Are Incorrect

Sepsis

While sepsis causes AKI and involves complex hemodynamic alterations, it does not follow the prerenal pattern of combined systemic vasodilation with renal vasoconstriction. 2, 3

• Sepsis-induced AKI can occur with normal or even increased renal blood flow in resuscitated hyperdynamic patients 2, 3, 4
• The pathogenesis involves inflammatory mechanisms, microcirculatory dysfunction, and tubular epithelial cell injury rather than the prerenal hemodynamic pattern 3, 5, 4
• Renal vascular resistance may be increased, but this occurs alongside systemic inflammatory injury, not as a compensatory response to systemic vasodilation 2, 4

Congestive Heart Failure

CHF causes prerenal AKI through decreased cardiac output and forward flow, not through systemic vasodilation. 1

• The mechanism is reduced renal perfusion from inadequate cardiac output 1
• This represents true hypoperfusion rather than the effective arterial underfilling seen in cirrhosis 1

Contrast Media

Contrast-induced AKI is primarily a direct nephrotoxic injury causing acute tubular necrosis, not a prerenal hemodynamic process. 1

• The injury mechanism involves direct tubular toxicity and oxidative stress 1
• While contrast can cause transient renal vasoconstriction, it does not cause systemic vasodilation 1

Clinical Recognition and Management Implications

The diagnosis of HRS-AKI requires recognition of this unique dual pathophysiology:

• Patients have ascites and signs of portal hypertension (systemic vasodilation) 1
• AKI develops without response to volume expansion with albumin (1 g/kg/day for 2 days, maximum 100 g/day) 1
• Absence of structural kidney injury (no proteinuria >500 mg/day, no hematuria, bland urine sediment) 1
• Vasoconstrictor therapy (terlipressin, norepinephrine, or octreotide/midodrine) plus albumin is the specific treatment that counteracts the splanchnic vasodilation 1

Critical Pitfall to Avoid

Do not confuse the term "prerenal" with simple hypovolemia requiring fluid administration. 6, 7 In cirrhosis with HRS-AKI, indiscriminate fluid administration can cause life-threatening pulmonary edema because these patients already have total body fluid overload despite effective arterial underfilling. 1 The treatment requires vasoconstrictors to counteract splanchnic vasodilation, not additional volume. 1