A 62-year-old man with decompensated cirrhosis and refractory ascites is admitted to the ICU on a norepinephrine infusion (MAP >65 mm Hg) with a central venous catheter in place. Over 24 hours, his serum creatinine rises acutely from 1.2 to 3.1 mg/dL, and his urine output is 0.3 mL/kg/hr despite aggressive fluid challenges. His BP is 88/52 mm Hg, HR 110 bpm, and he has significant peripheral edema. Labs show BUN 65 mg/dL and urine sodium <10 mEq/L. Which of the following best describes the primary pathophysiological mechanism of his acute kidney injury?

A 62-year-old male with a history of alcohol-related decompensated cirrhosis is admitted to the critical care unit following a variceal hemorrhage. He is now stabilized on mechanical ventilation and a low-dose norepinephrine infusion via a central venous catheter for blood pressure support. Over the past 24 hours, his urine output has decreased to less than 0.5 mL/kg/hr, and his serum creatinine has risen from a baseline of 0.9 mg/dL to 2.8 mg/dL. His urine sodium is low (<10 mEq/L), and urinalysis shows no casts or proteinuria. Despite aggressive fluid resuscitation with albumin, his renal function continues to decline. Given this patient's clinical presentation and the absence of other clear causes of acute kidney injury, which of the following sequences of pathophysiological events BEST explains the development of his renal dysfunction?

A 62-year-old man with a history of decompensated cirrhosis due to alcohol-related liver disease and refractory ascites is admitted to the medical intensive care unit. He is currently on a low-dose norepinephrine infusion through a central venous catheter to maintain a mean arterial pressure above 65 mmHg. Over the past 24 hours, his serum creatinine has risen acutely from a baseline of 1.2 mg/dL to 2.8 mg/dL, with a urine output of 200 mL over the last 12 hours despite a 1 L albumin bolus. His blood urea nitrogen is 60 mg/dL, and his sodium is 128 mEq/L. There are no signs of active gastrointestinal bleeding or recent nephrotoxic medication use. Given this presentation consistent with hepatorenal syndrome–acute kidney injury (HRS-AKI), which of the following is the most appropriate initial therapeutic strategy?

A 58-year-old man with decompensated cirrhosis is admitted to the ICU for worsening ascites and oliguria. On admission, his mean arterial pressure is 65 mm Hg, heart rate is 90 bpm, serum creatinine (SCr) is 2.8 mg/dL (baseline 1.1 mg/dL), blood urea nitrogen is 60 mg/dL, and urine output is 25 mL/h. He is diagnosed with hepatorenal syndrome–acute kidney injury (HRS-AKI) after a 1 g/kg albumin challenge fails to improve renal function. Terlipressin is started at 0.85 mg IV every 6 hours plus albumin 1 g/kg/day. On day 3, his MAP is 68 mm Hg, SCr is 2.5 mg/dL, BUN is 52 mg/dL, and urine output is 30 mL/h. Which of the following is the most appropriate modification to his pharmacotherapy?

A 62-year-old man (weight 80 kg) with decompensated alcohol-associated cirrhosis is admitted to the ICU for acute respiratory failure. He is intubated and receiving a norepinephrine infusion at 0.2 mcg/kg/min via a central venous catheter to maintain a mean arterial pressure of 60 mm Hg. Over the past 24 hours his urine output has fallen to 0.3 mL/kg/hr, and his serum creatinine has risen from 1.2 to 2.8 mg/dL. Laboratory studies show a urine sodium of 8 mEq/L and urine osmolality of 650 mOsm/kg. There is no history of nephrotoxic drug exposure or recent contrast administration. Which of the following is the MOST appropriate initial pharmacologic management?

A 62-year-old man with decompensated cirrhosis in the ICU is diagnosed with hepatorenal syndrome–acute kidney injury (HRS-AKI). He is receiving a continuous norepinephrine infusion at 0.2 μg/kg/min via a central line to maintain a MAP ≥65 mmHg. Over the past 24 hours, his serum creatinine rose from 1.0 to 2.8 mg/dL, and urine output is <0.5 mL/kg/hr. Other causes of AKI have been excluded. In the US setting where terlipressin is available, which is the most appropriate initial pharmacologic intervention for HRS-AKI?

A 62-year-old man with decompensated cirrhosis from alcohol-associated liver disease is admitted to the ICU with acute hypoxic respiratory failure (intubated on assist-control ventilation) and hypotension on a continuous norepinephrine infusion via central line. Over 48 hours, his serum creatinine has risen from 1.0 to 2.8 mg/dL, and he has produced 200 mL of urine in the past 12 hours despite a 1 L albumin bolus. His MAP is 68 mmHg, HR 95 bpm, and he has significant ascites. Labs: BUN 45 mg/dL, Na⁺ 128 mEq/L, total bilirubin 12 mg/dL. There is no nephrotoxin use, recent contrast, or obstructive uropathy. Which is the MOST appropriate initial pharmacologic management strategy?

A 62-year-old man with decompensated cirrhosis from alcohol-associated liver disease has developed oliguria (<0.3 mL/kg/hr) and a rise in serum creatinine from 0.9 mg/dL to 2.8 mg/dL over 24 hours despite daily intravenous albumin. A diagnosis of hepatorenal syndrome–acute kidney injury (HRS-AKI) is made. Which initial terlipressin dosing and titration strategy is most appropriate?

A 62-year-old man with decompensated cirrhosis and ascites (weight 70 kg) is in the ICU on mechanical ventilation for acute respiratory failure and receiving a continuous norepinephrine infusion via a central venous catheter for hypotension. He was diagnosed with hepatorenal syndrome–acute kidney injury (HRS-AKI) after his serum creatinine rose from a baseline of 1.0 mg/dL to 3.5 mg/dL, with oliguria and no response to a fluid challenge. Two days ago, he was started on intravenous terlipressin and albumin (1 g/kg). This morning, he developed severe ischemic heel cyanosis and new-onset atrial fibrillation, prompting discontinuation of terlipressin. After stopping terlipressin due to these adverse effects, which of the following is the most appropriate next pharmacologic step for managing his HRS-AKI?

A 62-year-old man with decompensated cirrhosis and tense ascites is admitted to the ICU. He requires close hemodynamic monitoring and is receiving intravenous fluids via a central venous catheter. He developed acute kidney injury; on admission his serum creatinine (SCr) was 3.2 mg/dL (baseline 0.9 mg/dL). After exclusion of other causes, he was diagnosed with Type 1 hepatorenal syndrome and started on terlipressin 0.85 mg IV every 6 hours plus intravenous albumin (1 g/kg on day 1, then 20 g daily). On day 3 of therapy, his SCr is 2.6 mg/dL. His blood pressure is 95/60 mmHg, heart rate 88 bpm, and he has no new signs of ischemia. Given his renal response, which of the following is the MOST appropriate next step in managing his Type 1 HRS?