ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: PO0238

Hepatorenal Syndrome Type 1 as a Consequence of Transarterial Chemoembolization

Session Information

  • AKI Mechanisms - 3
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Report

  • 103 AKI: Mechanisms

Authors

  • Morales-Alvarez, M. Catalina, Mount Sinai Beth Israel Hospital, New York, New York, United States
  • Giniyani, Larab L., Mount Sinai Beth Israel Hospital, New York, New York, United States
  • Davidovich, Alexander, Mount Sinai Beth Israel Hospital, New York, New York, United States
Introduction

Hepatorenal syndrome (HRS) is characterized by marked kidney dysfunction in the setting of advanced liver disease. HRS can manifest in two different patterns, type 1, representing an acute onset of kidney injury and type 2, corresponding to the chronic manifestation of kidney injury secondary to liver dysfunction. Here we present a case of HRS type 1 following transarterial chemoembolization (TACE) in a patient with advanced cirrhosis and hepatocellular carcinoma (HCC).

Case Description

A 69-year-old male presented to the hospital with worsening weakness, lethargy and decreased urinary output. His family stated the symptoms began shortly after his last session of TACE the week prior. There were no fevers, sick contacts or recent travel. He had underlying CKD stage IIIa (baseline SCr 1.7 mg/dL) and alcoholic cirrhosis with HCC treated with partial resection and multiple sessions of TACE. On admission, the SCr was 9 mg/dL associated with symptomatic hyperkalemia, anion gap metabolic acidemia, severe hyponatremia, junctional bradycardia and hypotension. Additionally, urinary sodium was < 20 mmol/L with a bland sediment. Once admitted to the ICU, he required vasopressors and emergent hemodialysis. He was given HRS treatment with albumin 1gm/Kg/day plus vasopressin for 2 days. His urine output and kidney function improved back to baseline in the following days with no further requirement of hemodialysis.

Discussion

HRS represents an entity of kidney dysfunction secondary to severe renal vasoconstriction in response to splanchnic vasodilation. HRS occurs in states of advance liver disease. Our patient had alcoholic cirrhosis and HCC. TACE had been implemented as a palliative treatment to the unresected lesions. Iodinated contrast and chemotherapeutic agents are used in low dose with this therapeutic option, however, several cases of acute kidney injury have been reported likely due to contrast induce nephropathy. The need for renal replacement therapy has been not extensively reported but overall long-term outcomes were satisfactory. HRS as a consequence of TACE has never been described but given the laboratory findings and significant improvement following treatment we suspected this case was HRS type 1