A 58-year-old man hospitalized for confusion is evaluated for elevated serum creatinine. He has a history of cirrhosis due to chronic hepatitis C infection, and evaluation at the time of admission revealed hepatic encephalopathy and spontaneous bacterial peritonitis. Since admission, the patient's mental status has gradually improved with lactulose and cefotaxime therapy, but his renal functioning has worsened. At home, he takes furosemide, spironolactone, and nadolol, all of which were stopped at the time of admission. Temperature is 37 C (98.6 F), blood pressure is 98/62 mm Hg, and pulse is 102/min. Physical examination shows jaundice, spider angiomas, ascites, and leg edema. He has no skin rash. Serum creatinine and urine output since admission are shown below. Urinalysis reveals 1-2 erythrocytes/hpf with no significant casts or protein. Renal ultrasound shows normal-size kidneys with no hydronephrosis. There has been no improvement in renal function with intravenous saline and albumin infusion. Which of the following is the most likely mechanism of this patient's renal dysfunction?

Question

A 58-year-old man hospitalized for confusion is evaluated for elevated serum creatinine.  He has a history of cirrhosis due to chronic hepatitis C infection, and evaluation at the time of admission revealed hepatic encephalopathy and spontaneous bacterial peritonitis.  Since admission, the patient's mental status has gradually improved with lactulose and cefotaxime therapy, but his renal functioning has worsened.  At home, he takes furosemide, spironolactone, and nadolol, all of which were stopped at the time of admission.  Temperature is 37 C (98.6 F), blood pressure is 98/62 mm Hg, and pulse is 102/min.  Physical examination shows jaundice, spider angiomas, ascites, and leg edema.  He has no skin rash.  Serum creatinine and urine output since admission are shown below.  Urinalysis reveals 1-2 erythrocytes/hpf with no significant casts or protein.  Renal ultrasound shows normal-size kidneys with no hydronephrosis.  There has been no improvement in renal function with intravenous saline and albumin infusion.  Which of the following is the most likely mechanism of this patient's renal dysfunction?

Quizplus · Accepted Answer

11ec25c8_d4de_f11e_bc81_0738cd22ead8_MD0003_00 Hepatorenal syndrome (HRS) is an important complication of end-stage liver disease. It is characterized by a significant decrease in glomerular filtration in the absence of another clear cause of renal dysfunction, minimal hematuria (<50 erythrocytes/hpf), and lack of improvement with volume resuscitation. HRS occurs as cirrhosis progresses and patients develop splanchnic arterial dilation and an overall decrease in vascular resistance. This, in turn, activates the renin-angiotensin system and results in local renal vasoconstriction with decreased perfusion and glomerular filtration. The most common inciting factors of HRS include spontaneous bacterial peritonitis and gastrointestinal bleeding. Definitive therapy involves return of liver function through either hepatic recovery (eg, abstinence from alcohol) or transplantation. For patients who are unlikely to have a quick recovery and are not candidates for liver transplantation, other temporizing options to increase renal perfusion include splanchnic vasoconstrictors (eg, midodrine, octreotide, norepinephrine) and albumin. Dialysis is of limited benefit but may be attempted to help bridge to liver transplantation. (Choice A) Acute tubular necrosis is one of the main differential diagnoses of HRS, and patients with cirrhosis are especially susceptible. Aminoglycosides, iodinated contrast dye, and hypotension are the most common causes; however, urinalysis shows muddy brown, granular casts. (Choice B) Patients with hepatitis C are at risk for a number of immune-mediated complications, including membranoproliferative glomerulonephritis, which commonly occurs in association with mixed cryoglobulinemia syndrome (an immune complex deposition disorder). Urinalysis usually reveals dysmorphic red cells, red cell casts, and protein. (Choice C) Patients with intravascular volume depletion may demonstrate acute kidney injury, but in the absence of another insult such as acute tubular necrosis, renal function should improve with volume resuscitation and discontinuation of diuretics. (Choice D) Acute interstitial nephritis (AIN) is frequently caused by antibiotics (such as those administered for spontaneous bacterial peritonitis) or infection (although AIN is not typically associated with hepatitis C infection). However, urinalysis demonstrates an active sediment with white cells and white cell casts. Educational objective: Hepatorenal syndrome is characterized by a decrease in glomerular filtration in the absence of other causes of renal dysfunction, minimal hematuria, and lack of improvement with volume resuscitation. It occurs due to splanchnic arterial dilation, decreased vascular resistance, and local renal vasoconstriction with decreased perfusion. References: Hepatorenal syndrome: aetiology, diagnosis, and treatment. (http://www.ncbi.nlm.nih.gov/pubmed/25649410) Hepatorenal syndrome: update on diagnosis and treatment. (http://www.ncbi.nlm.nih.gov/pubmed/26558188)

A 58-Year-Old Man Hospitalized for Confusion Is Evaluated for Elevated