A 58-year-old man is evaluated in the hospital for worsening renal function. He was admitt… — USMLE Step 3

A $58$ -year-old man is evaluated in the hospital for worsening renal function. He was admitted $3$ days ago for fever, confusion, and abdominal pain. He has a history of alcohol-associated cirrhosis. On admission, diagnostic paracentesis revealed an ascitic fluid absolute neutrophil count of $600/\text{mm}^3$ . He was appropriately started on intravenous cefotaxime, and his home regimen of spironolactone and furosemide was discontinued.

Despite resolving fever and improving mental status over the past $48$ hours, his urine output has decreased to $300$ mL/day. Vital signs today show a temperature of $37.1^\circ\text{C}$ ( $98.8^\circ\text{F}$ ), blood pressure of $88/52$ mmHg, and heart rate of $94/\text{min}$ . Physical examination reveals scleral icterus, spider angiomas, and tense ascites without peripheral edema.

Laboratory results:
Sodium: $130$ mEq/L
Potassium: $4.8$ mEq/L
Blood urea nitrogen: $68$ mg/dL (was $22$ mg/dL on admission)
Creatinine: $3.2$ mg/dL (was $1.1$ mg/dL on admission)
Urine sodium: $8$ mEq/L
Urinalysis: No red blood cells, white blood cells, or casts.

A volume expansion trial with intravenous albumin ( $1$ g/kg/day for $2$ days) was completed, but his repeat serum creatinine today is $3.4$ mg/dL. Renal ultrasound reveals normal-sized kidneys with no hydronephrosis.

Which of the following is the most appropriate next pharmacologic intervention for this patient's renal failure?

A
Intravenous hydrocortisone
B
Intravenous furosemide
Intravenous terlipressinCevap
D
Oral lisinopril
E
Intravenous dopamine

Cevap

Intravenous terlipressin

The correct answer is a splanchnic vasoconstrictor. The patient's clinical presentation of progressive acute kidney injury in the setting of decompensated cirrhosis, oliguria, very low urine sodium, absence of intrinsic renal disease, and failure to improve after a

48

-hour albumin challenge confirms the diagnosis of hepatorenal syndrome-acute kidney injury (HRS-AKI). The fundamental pathophysiology of HRS is severe splanchnic arterial vasodilation, which triggers compensatory but deleterious intense renal vasoconstriction. The most appropriate pharmacologic intervention is a splanchnic vasoconstrictor, such as intravenous terlipressin, alongside continued albumin administration. Terlipressin counteracts the splanchnic vasodilation, improving effective arterial blood volume and restoring renal perfusion.

Adım Adım Çözüm

Analyze the patient's clinical and laboratory trajectory.

The patient has advanced cirrhosis and developed severe acute kidney injury (creatinine from 1.1 to 3.4 mg/dL) with oliguria and profound sodium retention (urine sodium < 10 mEq/L).

Tracking renal function changes identifies the severity and phenotype of the acute kidney injury.

Rule out intrinsic and post-renal causes of acute kidney injury.

Urinalysis is bland (no casts or cells) and renal ultrasound is normal, ruling out acute tubular necrosis and obstructive uropathy.

Establishing a pre-renal or functional etiology is required before diagnosing hepatorenal syndrome.

Evaluate the response to fluid resuscitation.

The patient failed to improve after a 48-hour challenge with intravenous albumin.

Failure to respond to albumin withdrawal confirms the diagnosis of Hepatorenal Syndrome-Acute Kidney Injury (HRS-AKI).

Determine the appropriate pharmacologic mechanism to reverse HRS-AKI.

Select a splanchnic vasoconstrictor to counteract the profound splanchnic vasodilation driving the syndrome.

Intravenous terlipressin (often in combination with albumin) is the standard-of-care pharmacologic intervention to restore effective arterial blood volume and renal perfusion.

Anahtar Kavram

Diagnosis and pharmacologic management of Hepatorenal Syndrome (HRS-AKI) using splanchnic vasoconstrictors.

Soru

Cevap

Adım Adım Çözüm

Anahtar Kavram

Sık Yapılan Hatalar

Konular

Bu konudan daha fazla soru