Hepatorenal syndrome US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Hepatorenal syndrome. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Hepatorenal syndrome US Medical PG Question 1: A 65-year-old man presents with generalized edema and dyspnea on exertion. He also complains of easy bruising and nasal bleeding. Past medical history is significant for a right-sided myocardial infarction 4 years ago. Current medications are metoprolol, aspirin, and rosuvastatin. His vital signs are as follows: blood pressure 140/90 mm Hg, heart rate 78/min, respiratory rate 17/min, and temperature 36.5℃ (97.7℉). On physical examination, the patient is pale and acrocyanotic with cold extremities. Cardiac examination shows the right displacement of the apical beat, decreased heart sounds, and the presence of an S3. Abdominal percussion reveals ascites and hepatomegaly. Which of the following hepatic cell types is most sensitive to ischemia?
- A. Pericentral hepatocytes (Correct Answer)
- B. Ito cells
- C. Ductal cells
- D. Periportal hepatocytes
- E. Sinusoidal endothelial cells
Hepatorenal syndrome Explanation: ***Pericentral hepatocytes***
- **Pericentral hepatocytes** (Zone 3) are located furthest from the hepatic arterial and portal venule blood supply, making them most vulnerable to **ischemic injury**.
- This region is primarily responsible for drug metabolism and detoxification, processes that require high oxygen demand.
*Ito cells*
- **Ito cells**, or hepatic stellate cells, are located in the **space of Disse** and are primarily involved in vitamin A storage and fibrosis upon activation.
- While important for liver function, they are not the cells most sensitive to acute ischemia.
*Ductal cells*
- **Ductal cells** line the bile ducts and are involved in bile modification and transport.
- They are generally more resistant to ischemia compared to hepatocytes.
*Periportal hepatocytes*
- **Periportal hepatocytes** (Zone 1) are closest to the incoming arterial and portal blood supply, making them the most oxygenated and last to be affected by ischemia.
- These cells are important for oxidative metabolism and gluconeogenesis, and are more vulnerable to toxicity than ischemia.
*Sinusoidal endothelial cells*
- **Sinusoidal endothelial cells** form the lining of the hepatic sinusoids and are involved in exchange between blood and hepatocytes.
- Although damage to these cells can contribute to overall liver dysfunction, they are not the primary cell type most sensitive to ischemia compared to pericentral hepatocytes.
Hepatorenal syndrome US Medical PG Question 2: A 65-year-old man with decompensated cirrhosis secondary to hepatitis C is brought to the emergency department with 2 episodes of massive hematemesis that started 2 hours ago. He is a liver transplant candidate. The blood pressure is 110/85 mm Hg in the supine position and 90/70 mm Hg after sitting for 3 minutes. The pulse is 110/min, the respirations are 22/min, and the temperature is 36.1°C (97.0°F). The physical examination shows spider angiomata, palmar erythema, and symmetric abdominal distension with positive shifting dullness. The lung and heart examination shows no abnormalities. Two large-bore intravenous lines are obtained. Saline (0.9%) is initiated. Laboratory tests are pending. The most important next step is to administer which of the following intravenous therapies?
- A. Fresh frozen plasma
- B. Octreotide (Correct Answer)
- C. Packed red blood cells (RBCs)
- D. Propranolol
- E. Pantoprazole
Hepatorenal syndrome Explanation: ***Octreotide***
- This patient's presentation with **massive hematemesis**, **decompensated cirrhosis**, and signs of portal hypertension strongly suggests **esophageal variceal bleeding**.
- **Octreotide**, a somatostatin analog, is critical in managing variceal bleeding by causing **splanchnic vasoconstriction**, which reduces portal blood flow and pressure, thereby decreasing active bleeding.
*Fresh frozen plasma*
- While patients with **cirrhosis often have coagulopathy**, administering fresh frozen plasma (FFP) without documented severe coagulopathy or active bleeding requiring immediate reversal (e.g., before an invasive procedure) is not the highest priority.
- **FFP transfusions** can paradoxically increase portal pressure and volume, potentially worsening variceal bleeding.
*Packed red blood cells (RBCs)*
- Though the patient is likely anemic due to massive hematemesis, **transfusion of RBCs** should be guided by hemoglobin levels and clinical signs of hemodynamic instability, with a goal to achieve **hemodynamic stability** rather than over-transfusing.
- While important, **stopping the bleeding** with octreotide takes precedence before optimal RBC transfusion thresholds are determined.
*Propranolol*
- **Propranolol** is a non-selective beta-blocker used for **primary and secondary prophylaxis** of variceal bleeding.
- It is **contraindicated in acute bleeding** as it can worsen hypotension and interfere with the body's compensatory mechanisms during hypovolemic shock.
*Pantoprazole*
- **Pantoprazole**, a **proton pump inhibitor (PPI)**, is used to suppress stomach acid and is beneficial in managing **peptic ulcer bleeding**.
- However, it has no direct role in controlling **variceal bleeding**, which originates from esophageal varices rather than acid-related gastric or duodenal mucosa.
Hepatorenal syndrome US Medical PG Question 3: A 67-year-old man with hypertension comes to the emergency department because of progressively worsening abdominal pain that started 1 week ago. The pain is localized to the right upper quadrant. He has also noticed yellowing of his eyes and skin during this time period. Physical examination shows jaundice, a distended abdomen, and tender hepatomegaly. There is no jugular venous distention. Laboratory studies show a hemoglobin concentration of 19.2 g/dL, aspartate aminotransferase of 420 U/L, alanine aminotransferase of 318 U/L, and total bilirubin of 2.2 mg/dL. Which of the following is the most likely cause of this patient's symptoms?
- A. Thickened pericardium
- B. Hepatic steatosis
- C. Hepatotropic viral infection
- D. Increased iron absorption
- E. Hepatic vein obstruction (Correct Answer)
Hepatorenal syndrome Explanation: ***Hepatic vein obstruction***
- The patient presents with **jaundice**, **tender hepatomegaly**, and **elevated transaminases and bilirubin** in the setting of rapidly progressive abdominal pain, suggestive of **Budd-Chiari syndrome** due to hepatic vein obstruction.
- The high **hemoglobin (19.2 g/dL)** indicates **polycythemia**, a common predisposing factor for thrombotic events like hepatic vein obstruction.
*Thickened pericardium*
- A thickened pericardium would lead to **constrictive pericarditis**, presenting with signs of right-sided heart failure like **jugular venous distention** and peripheral edema, which are absent here.
- While it can cause hepatomegaly due to passive congestion, it typically does not cause the acute, severe liver enzyme elevations or the markedly elevated hemoglobin seen in this patient.
*Hepatic steatosis*
- **Hepatic steatosis** (fatty liver) is often asymptomatic or causes mild RUQ pain, typically without significant jaundice or such acutely elevated transaminases.
- It is not associated with polycythemia or a rapid onset of severe symptoms as described.
*Hepatotropic viral infection*
- While hepatotropic viral infections (e.g., hepatitis A, B, C) can cause **jaundice**, **hepatomegaly**, and elevated liver enzymes, they are generally not associated with **polycythemia**.
- The acute, progressive nature with tender hepatomegaly and relatively low bilirubin compared to transaminase elevation might suggest a more obstructive or vascular cause rather than typical viral hepatitis.
*Increased iron absorption*
- **Increased iron absorption** (e.g., in hemochromatosis) leads to iron deposition in the liver, which can cause hepatomegaly and eventually cirrhosis.
- However, it typically has a **chronic, insidious onset** and does not present with acute, severe pain, jaundice, and marked transaminase elevation. While polycythemia can occur in some chronic liver diseases, it's not a direct consequence of iron overload itself in the acute setting described.
Hepatorenal syndrome US Medical PG Question 4: A 56-year-old woman is brought to the emergency department by her family with altered mental status. Her husband says that she complained of fever, vomiting, and abdominal pain 2 days ago. She has a history of long-standing alcoholism and previous episodes of hepatic encephalopathy. Current vital signs include a temperature of 38.3°C (101°F), blood pressure of 85/60 mm Hg, pulse of 95/min, and a respiratory rate 30/min. On physical examination, the patient appears ill and obtunded. She is noted to have jaundice, a palpable firm liver, and massive abdominal distension with shifting dullness. Which of the following is the best initial step in management of this patient's condition?
- A. Empiric antibiotics (Correct Answer)
- B. Diagnostic paracentesis
- C. Large volume paracentesis
- D. Intravenous albumin
- E. Non-selective beta-blockers
Hepatorenal syndrome Explanation: ***Empiric antibiotics***
- This patient presents with **altered mental status**, **fever**, **hypotension (85/60 mm Hg)**, **tachypnea**, and **massive ascites** in the setting of **cirrhosis**, indicating **suspected spontaneous bacterial peritonitis (SBP) with septic shock**.
- In a **hemodynamically unstable patient** with suspected SBP, **empiric antibiotics** (typically a third-generation cephalosporin like ceftriaxone or cefotaxime) should be initiated **immediately** without waiting for diagnostic paracentesis results.
- Current **AASLD and EASL guidelines** emphasize that antibiotic therapy should not be delayed in critically ill patients, as early treatment significantly reduces mortality in SBP.
- Diagnostic paracentesis should still be performed urgently but should **not delay antibiotic administration** in this unstable patient.
*Diagnostic paracentesis*
- While **diagnostic paracentesis** is the gold standard for confirming SBP and should be performed promptly, it is not the **best initial step** in a hemodynamically unstable patient.
- In this critically ill patient with septic shock, obtaining ascitic fluid can be done **simultaneously with** or **immediately after** starting antibiotics, but antibiotics take priority.
- If the patient were stable, diagnostic paracentesis before antibiotics would be appropriate to guide therapy.
*Large volume paracentesis*
- **Large volume paracentesis** is indicated for symptomatic relief of tense ascites causing respiratory compromise, not as an initial step in suspected infection.
- In the setting of suspected SBP, only diagnostic paracentesis (50-100 mL) is needed initially, not large volume removal.
*Intravenous albumin*
- **Intravenous albumin** is given as adjunctive therapy in SBP patients with **renal dysfunction** (creatinine >1 mg/dL, BUN >30 mg/dL) or **hypotension** to prevent hepatorenal syndrome.
- While this patient may benefit from albumin, it is not the **initial step**—antibiotics and fluid resuscitation take priority.
- Albumin is typically given at 1.5 g/kg within 6 hours and 1 g/kg on day 3.
*Non-selective beta-blockers*
- **Non-selective beta-blockers** (propranolol, nadolol) are used for **primary and secondary prophylaxis of variceal bleeding** in portal hypertension.
- They are **contraindicated** in patients with **hypotension** (BP 85/60 mm Hg), **sepsis**, or **SBP**, as they can worsen hemodynamic instability.
- Recent studies suggest beta-blockers may be harmful in patients with refractory ascites or SBP.
Hepatorenal syndrome US Medical PG Question 5: A 52-year-old man comes to the physician because of progressive abdominal distention and weight gain over the last 2 months. He was diagnosed with alcoholic liver cirrhosis with large ascites 1 year ago. He has congestive heart failure with a depressed ejection fraction related to his alcohol use. For the last 6 months, he has abstained from alcohol and has followed a low-sodium diet. His current medications include propranolol, spironolactone, and furosemide. His temperature is 36.7°C (98°F), pulse is 90/min, and blood pressure is 109/56 mm Hg. Physical examination shows reddening of the palms, telangiectasias on the face and trunk, and prominent blood vessels around the umbilicus. The abdomen is tense and distended; there is no abdominal tenderness. On percussion of the abdomen, there is dullness that shifts when the patient moves from the supine to the right lateral decubitus position. When the patient stretches out his arms with the wrists extended, a jerky, flapping motion of the hands is seen. Mental status examination shows a decreased attention span. Serum studies show:
Sodium 136 mEq/L
Creatinine 0.9 mg/dL
Albumin 3.6 mg/dL
Total bilirubin 1.9 mg/dL
INR 1.0
Which of the following is the most appropriate next step in treatment?
- A. Refer for liver transplantation
- B. Perform large-volume paracentesis (Correct Answer)
- C. Refer for peritoneovenous shunt
- D. Change propranolol to carvedilol
- E. Refer for transjugular intrahepatic portosystemic shunt
Hepatorenal syndrome Explanation: ***Perform large-volume paracentesis***
- The patient presents with **tense, distended ascites** refractory to diuretics and a low-sodium diet, evidenced by progressive abdominal distention and weight gain despite current management. **Large-volume paracentesis** is the most effective approach for immediate symptomatic relief
- The patient's clinical picture includes signs of **hepatic encephalopathy** (decreased attention span, asterixis) and **decompensated cirrhosis** (ascites, portal hypertension signs), but the immediate priority is to relieve the discomfort and respiratory compromise associated with large ascites.
*Refer for liver transplantation*
- While ultimately this patient may be a candidate for a **liver transplant** due to decompensated cirrhosis, it is not the immediate next step for managing **symptomatic tense ascites**.
- Liver transplantation involves extensive evaluation and a waiting period, and the acute issue needs to be addressed first.
*Refer for peritoneovenous shunt*
- **Peritoneovenous shunts** are rarely used due to high complication rates, including shunt thrombosis, infection, and disseminated intravascular coagulation.
- They are considered only in cases of **refractory ascites** where paracentesis is not feasible or effective long-term, which is not the case here as paracentesis has not been attempted for the current increase in ascites.
*Change propranolol to carvedilol*
- Both **propranolol** and **carvedilol** are non-selective beta-blockers used to reduce portal pressure, but **carvedilol** has additional alpha-1 blocking properties that may offer slightly more hemodynamic effects.
- However, switching beta-blockers will not directly address the immediate issue of **tense ascites** and could potentially worsen **hypotension** given the current blood pressure of 109/56 mm Hg.
*Refer for transjugular intrahepatic portosystemic shunt*
- A **TIPS** procedure is considered for **refractory ascites** that does not respond to repeated large-volume paracentesis and aggressive diuretic therapy.
- Given that a large-volume paracentesis has not been performed for the current exacerbation, **TIPS** would be a premature intervention and is associated with risks such as worsening hepatic encephalopathy.
Hepatorenal syndrome US Medical PG Question 6: A 57-year-old immigrant from Nigeria presents to the emergency department for sudden, severe pain and swelling in her lower extremity. She was at a rehabilitation hospital when her symptoms became apparent. The patient has a past medical history of obesity, diabetes, bipolar disorder, and tonic-clonic seizures. Her current medications include metformin, insulin, lisinopril, and valproic acid. The patient is a prominent IV drug and alcohol user who has presented to the ED many times for intoxication. On physical exam you note anasarca and asymmetric lower extremity swelling. Based on the results of a doppler ultrasound of her swollen lower extremity, heparin is started. The patient is then transferred to the general medicine floor for continued management. Laboratory studies are shown below.
Serum:
Na+: 137 mEq/L
K+: 5.5 mEq/L
Cl-: 100 mEq/L
HCO3-: 24 mEq/L
Urea nitrogen: 22 mg/dL
Ca2+: 5.7 mg/dL
Creatinine: 1.7 mg/dL
Glucose: 70 mg/dL
The patient's presentation includes generalized edema (anasarca) along with laboratory abnormalities. What is the most likely underlying diagnosis that explains her overall clinical presentation?
- A. Liver failure
- B. Nephrotic syndrome (Correct Answer)
- C. Antithrombin III deficiency
- D. Prothrombin gene mutation
- E. Factor V Leiden
Hepatorenal syndrome Explanation: ***Nephrotic syndrome***
- The patient presents with **anasarca** (generalized edema), **asymmetric lower extremity swelling**, and laboratory findings consistent with **nephrotic syndrome**.
- Classic features present: **anasarca** (from hypoalbuminemia and fluid retention), **hypercoagulable state** leading to DVT (loss of antithrombin III in urine), and **renal dysfunction** (elevated creatinine 1.7 mg/dL).
- The **hypocalcemia (5.7 mg/dL)** is explained by low albumin—total calcium appears low because ~40% of serum calcium is albumin-bound; ionized calcium is likely normal.
- Nephrotic syndrome is characterized by: heavy proteinuria (>3.5 g/day), hypoalbuminemia, hyperlipidemia, and edema—this patient's presentation fits this diagnosis.
- Risk factors include diabetes (diabetic nephropathy is a common cause of nephrotic syndrome in adults).
*Liver failure*
- Although **anasarca** and **edema** can occur in liver failure due to decreased albumin synthesis and portal hypertension, the laboratory values do not show typical signs of severe hepatic dysfunction (e.g., elevated transaminases, bilirubin, or prolonged INR).
- The **elevated creatinine** and **hypercoagulable state with DVT** point more towards a primary renal issue rather than liver failure.
- Liver failure typically causes **hypocoagulability**, not the hypercoagulability seen here.
*Antithrombin III deficiency*
- This is a **hereditary thrombophilia** that increases the risk of **venous thromboembolism**, which could explain the DVT.
- However, it does **not explain** the patient's **anasarca**, **hypocalcemia**, **elevated creatinine**, or generalized fluid retention.
- This would be a complication of nephrotic syndrome (acquired AT-III deficiency from urinary loss), not the primary diagnosis.
*Prothrombin gene mutation*
- This is another **genetic thrombophilia** (G20210A mutation) that increases the risk of **blood clots**.
- Similar to Antithrombin III deficiency, it accounts for DVT risk but **fails to explain** the widespread edema, electrolyte abnormalities, and renal dysfunction.
*Factor V Leiden*
- The **Factor V Leiden mutation** is the most common inherited cause of **thrombophilia**, predisposing individuals to venous thromboembolism.
- While relevant to explaining DVT in isolation, it does **not explain** the patient's severe generalized edema, hypocalcemia, or renal impairment—all of which are key to this clinical presentation.
Hepatorenal syndrome US Medical PG Question 7: A 58-year-old man presents to the Emergency Department after 3 hours of intense suprapubic pain associated with inability to urinate for the past day or two. His medical history is relevant for benign prostatic hyperplasia (BPH) that has been under treatment with prazosin and tadalafil. Upon admission, he is found to have a blood pressure of 180/100 mm Hg, a pulse of 80/min, a respiratory rate of 23/min, and a temperature of 36.5°C (97.7°F). He weighs 84 kg (185.1 lb) and is 175 cm (5 ft 7 in) tall. Physical exam, he has suprapubic tenderness. A bladder scan reveals 700 ml of urine. A Foley catheter is inserted and the urine is drained. Initial laboratory tests and their follow up 8 hours after admission are shown below.
Admission 8 hours after admission
Serum potassium 4.2 mmol/L Serum potassium 4.0 mmol/L
Serum sodium 140 mmol/L Serum sodium 142 mmol/L
Serum chloride 102 mmol/L Serum chloride 110 mmol/L
Serum creatinine 1.4 mg/dL Serum creatinine 1.6 mg/dL
Serum blood urea nitrogen 64 mg/dL Serum blood urea nitrogen 62 mg/dL
Urine output 250 mL Urine output 260 mL
A senior attending suggests a consultation with Nephrology. Which of the following best justifies this suggestion?
- A. Estimated glomerular filtration rate (eGFR)
- B. Urine output (Correct Answer)
- C. Serum creatinine (SCr)
- D. Serum blood urea nitrogen (BUN)
- E. Serum potassium
Hepatorenal syndrome Explanation: ***Urine output***
- The patient's **urine output is severely reduced** at 260 mL over 8 hours (approximately **32.5 mL/hour**), which constitutes **oliguria** (defined as <0.5 mL/kg/hr; this patient at 84 kg should produce ≥42 mL/hr).
- Despite **relief of the post-renal obstruction** via Foley catheterization, the persistent oliguria indicates **intrinsic kidney injury** rather than simple mechanical obstruction.
- The combination of **oliguria persisting after decompression** + **rising serum creatinine** (1.4→1.6 mg/dL) meets **KDIGO criteria for Stage 2 AKI** (urine output <0.5 mL/kg/hr for ≥12 hours).
- This requires **urgent nephrology consultation** to assess for acute tubular necrosis (ATN), guide fluid management during potential post-obstructive diuresis, and consider renal replacement therapy if oliguria worsens.
*Serum creatinine (SCr)*
- The serum creatinine **rose from 1.4 to 1.6 mg/dL** despite bladder decompression, which is concerning and suggests intrinsic renal injury.
- However, creatinine is a **lagging indicator** of kidney function - it takes 24-48 hours to reflect acute changes in GFR, whereas **urine output is a real-time indicator** of kidney function.
- While the rising creatinine supports the need for nephrology involvement, **urine output is the more immediate and actionable parameter** that prompted the attending's suggestion at this early time point.
*Estimated glomerular filtration rate (eGFR)*
- eGFR is **calculated from serum creatinine** using equations that assume steady-state conditions, which **do not apply in acute kidney injury**.
- In the **acute setting with rapidly changing kidney function**, eGFR calculations are unreliable and can significantly overestimate or underestimate true GFR.
- Clinicians rely more on **urine output and serial creatinine measurements** rather than eGFR when managing AKI.
*Serum blood urea nitrogen (BUN)*
- The BUN decreased slightly from 64 to 62 mg/dL, remaining elevated but showing minimal change after catheterization.
- Elevated BUN can reflect **pre-renal azotemia, dehydration, or upper GI bleeding** and is less specific for intrinsic kidney injury than oliguria.
- The **BUN:Cr ratio** is approximately 40:1 (64/1.6), suggesting a **pre-renal component**, but this alone doesn't justify urgent nephrology consultation as strongly as the persistent oliguria does.
*Serum potassium*
- Serum potassium levels remain **normal** (4.2→4.0 mmol/L) and do not indicate a metabolic emergency.
- While **hyperkalemia** is a common complication of AKI that would warrant nephrology involvement, this patient's potassium is well-controlled and not the driving concern at this time.
Hepatorenal syndrome US Medical PG Question 8: A 49-year-old man presents to the emergency department with abdominal discomfort, fever, and decreased urination. He has a history of liver cirrhosis due to chronic hepatitis C infection. His blood pressure is 90/70 mm Hg, pulse is 75/min, and temperature 38°C (100.4°F). On physical examination he is jaundiced, and he has tense ascites with generalized abdominal tenderness. There is pitting edema to the level of his upper thighs. Which of the following excludes the diagnosis of hepatorenal syndrome in this patient?
- A. Low albumin levels
- B. Normal renal ultrasound
- C. Presence of 30 red cells/high powered field in the urine (Correct Answer)
- D. Low urea levels
- E. Prolonged prothrombin time
Hepatorenal syndrome Explanation: ***Presence of 30 red cells/high powered field in the urine***
- **Hepatorenal syndrome (HRS)** is a diagnosis of exclusion characterized by **functional renal failure** in the setting of severe liver disease without intrinsic renal pathology. The presence of significant red blood cells in the urine (e.g., >50 RBCs/HPF is a more definitive cutoff often used, but 30 RBCs/HPF is highly suspicious) indicates an **intrinsic renal problem**, such as glomerulonephritis or acute tubular necrosis, which would exclude HRS.
- HRS typically presents with **benign urinary sediment**, meaning few or no red blood cells, white blood cells, or casts, as the kidneys themselves are structurally intact.
*Low albumin levels*
- **Hypoalbuminemia** is a common finding in patients with **cirrhosis** due to impaired hepatic synthesis and is often associated with ascites and edema.
- It is a predisposing factor for HRS development, but its presence does not exclude or confirm the diagnosis.
*Normal renal ultrasound*
- A **normal renal ultrasound** indicates the absence of **structural kidney disease** (e.g., obstruction, polycystic kidneys, or severe chronic kidney disease) that could otherwise explain the renal failure.
- This finding is **consistent with HRS**, as HRS is a functional renal failure without gross renal structural abnormalities, thus it does not exclude the diagnosis.
*Low urea levels*
- **Urea synthesis occurs in the liver**, and in patients with severe **cirrhosis**, the liver's ability to produce urea from ammonia may be impaired.
- Therefore, **low urea levels (or disproportionately low BUN relative to creatinine)** can be seen in advanced liver disease, even with renal impairment, and do not exclude HRS.
*Prolonged prothrombin time*
- A **prolonged prothrombin time (PT)** is a hallmark of severe **liver dysfunction** due to reduced synthesis of coagulation factors.
- It indicates the severity of the underlying liver disease and is a common finding in patients who develop HRS, therefore, it does not exclude the diagnosis.
Hepatorenal syndrome US Medical PG Question 9: A 67-year-old man is brought to the emergency department when he was found obtunded at the homeless shelter. The patient is currently not responsive and smells of alcohol. The patient has a past medical history of alcohol use, IV drug use, and hepatitis C. His temperature is 99°F (37.2°C), blood pressure is 95/65 mmHg, pulse is 95/min, respirations are 13/min, and oxygen saturation is 95% on room air. The patient is started on IV fluids, and his pulse decreases to 70/min. On physical exam, the patient has an abdominal exam notable for distension and a positive fluid wave. The patient displays mild yellow discoloration of his skin. The patient has notable poor dentition and poor hygiene overall. A systolic murmur is heard along the left sternal border on cardiac exam. Pulmonary exam is notable for mild bibasilar crackles. Laboratory values are ordered, and return as below:
Hemoglobin: 10 g/dL
Hematocrit: 32%
Leukocyte count: 7,500 cells/mm^3 with normal differential
Platelet count: 227,000/mm^3
Serum:
Na+: 125 mEq/L
Cl-: 100 mEq/L
K+: 5.0 mEq/L
HCO3-: 24 mEq/L
BUN: 51 mg/dL
Glucose: 89 mg/dL
Creatinine: 2.2 mg/dL
Ca2+: 10.0 mg/dL
AST: 22 U/L
ALT: 19 U/L
Urine:
Color: Amber
Nitrites: Negative
Sodium: 12 mmol/24 hours
Red blood cells: 0/hpf
Over the next 24 hours, the patient produces very little urine. Which of the following best explains this patient’s renal findings?
- A. Liver failure (Correct Answer)
- B. Nephrotoxic agent
- C. Dehydration
- D. Postrenal azotemia
- E. Congestive heart failure
Hepatorenal syndrome Explanation: ***Liver failure***
- The patient's history of **alcohol use**, **hepatitis C**, **ascites** (abdominal distension with fluid wave), and **jaundice** (yellow skin discoloration) are all signs of severe liver disease/cirrhosis.
- In the context of advanced liver failure, this patient has developed **hepatorenal syndrome (HRS)**, a critical complication characterized by **functional renal failure** due to severe renal vasoconstriction without intrinsic kidney damage.
- Key diagnostic features of HRS include: elevated **BUN** and **creatinine**, markedly **low urine sodium (<20 mEq/L)**, **oliguria** that does not improve with volume expansion, and absence of other causes of renal failure.
- The urine sodium of **12 mmol/24 hours** is pathognomonic for HRS, indicating maximal sodium retention by the kidneys in response to decreased effective arterial blood volume.
*Nephrotoxic agent*
- While IV drug use can be associated with certain nephrotoxic exposures, there is no direct evidence in the clinical presentation (e.g., specific drug use leading to toxicity, muddy brown casts on urinalysis) to support this.
- **Acute tubular necrosis (ATN)** from nephrotoxins typically presents with urine sodium **>40 mEq/L** and granular casts, which are absent here.
- The patient's underlying liver disease with characteristic low urine sodium provides a more comprehensive explanation for the renal dysfunction.
*Dehydration*
- The patient's **blood pressure** is low, but he responded to IV fluids with a decreased pulse, suggesting some improvement in volume status, yet his renal function worsened with persistent oliguria.
- While dehydration can cause **prerenal azotemia**, the lack of improvement after IV fluid resuscitation, extreme oliguria, very low urine sodium in the context of advanced cirrhosis with ascites point strongly towards hepatorenal syndrome rather than simple hypovolemia.
- True prerenal azotemia from dehydration typically improves with fluid administration, which did not occur here.
*Postrenal azotemia*
- This condition is caused by an **obstruction** to urine outflow, such as a kidney stone, enlarged prostate, or tumor.
- There are no clinical signs or symptoms (e.g., flank pain, difficulty urinating, hydronephrosis on imaging) in the patient's presentation to suggest an obstructive cause.
- Postrenal obstruction typically requires **bilateral** obstruction or obstruction in a single functioning kidney to cause significant azotemia.
*Congestive heart failure*
- While the patient has **bibasilar crackles** and a cardiac murmur, these are non-specific findings that might be related to volume overload from liver disease or endocarditis from IV drug use.
- **Cardiorenal syndrome** can cause renal dysfunction, but typically presents with more prominent signs of heart failure and urine sodium is often higher (>40 mEq/L) when diuretics are used.
- The patient's profound liver failure with ascites, jaundice, and the characteristic very low urine sodium provide a much stronger and more direct explanation for the progressive renal dysfunction as hepatorenal syndrome.
Hepatorenal syndrome US Medical PG Question 10: A 54-year-old man with known end-stage liver disease from alcoholic cirrhosis presents to the emergency department with decreased urinary output and swelling in his lower extremities. His disease has been complicated by ascites and hepatic encephalopathy in the past. Initial laboratory studies show a creatinine of 1.73 mg/dL up from a previous value of 1.12 one month prior. There have been no new medication changes, and no recent procedures performed. A diagnostic paracentesis is performed that is negative for infection, and he is admitted to the hospital for further management and initiated on albumin. Two days later, his creatinine has risen to 2.34 and he is oliguric. Which of the following is the most definitive treatment for this patient's condition?
- A. Liver transplantation (Correct Answer)
- B. Transjugular intrahepatic portosystemic shunt (TIPS)
- C. Peritoneovenous shunt
- D. Hemodialysis
- E. Cessation of alcohol use
Hepatorenal syndrome Explanation: ***Liver transplantation***
- This patient is presenting with **hepatorenal syndrome (HRS)** as indicated by the worsening renal function, presence of cirrhosis, ascites, and lack of response to albumin. **Liver transplantation** is the only definitive treatment as it addresses the underlying liver dysfunction causing HRS.
- While other treatments like vasoconstrictors and albumin can temporarily stabilize the patient, they do not cure the underlying pathophysiology.
*Transjugular intrahepatic portosystemic shunt (TIPS)*
- TIPS can be used to reduce **portal hypertension** and treat complications like refractory ascites or variceal bleeding.
- However, TIPS is generally **contraindicated in HRS** with severe renal impairment due to the risk of worsening liver function and encephalopathy.
*Peritoneovenous shunt*
- A peritoneovenous shunt is a rarely used procedure to drain **ascites** from the peritoneal cavity into the venous system.
- It does not address the underlying **renal dysfunction** or liver failure and carries a high risk of complications like infection and coagulation abnormalities.
*Hemodialysis*
- Hemodialysis can be used as a **bridge therapy** to manage acute renal failure in HRS, but it is not a definitive treatment.
- It provides renal support but does not correct the **hemodynamic derangements** or underlying liver disease.
*Cessation of alcohol use*
- While essential for slowing the progression of liver disease, **cessation of alcohol** can improve liver function in some cases.
- In a patient with end-stage cirrhosis and acute-on-chronic renal failure (HRS), it is **not an immediate or definitive treatment** for the acute crisis.
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