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Kidney Week

Abstract: SA-PO0380

When the Liver, Kidneys, and Cancer Collide: Understanding AKI in Malignancy with Ascites

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Imber, Jared G., The University of Texas Health Science Center at Houston John P and Katherine G McGovern Medical School, Houston, Texas, United States
  • Khan, Mubeen M., The University of Texas Health Science Center at Houston John P and Katherine G McGovern Medical School, Houston, Texas, United States
Introduction

Hepatorenal syndrome (HRS) is a functional cause of acute kidney injury (AKI) traditionally associated with cirrhosis and portal hypertension. It is classified into rapidly progressive HRS - AKI and more chronic HRS - CKD. Patients with ascites are at increased risk of AKI due to reduced effective arterial volume and neurohormonal activation, and HRS - AKI is typically unresponsive to volume expansion.

Case Description

A 62 year old man with metastatic prostate cancer involving the liver and bone presented with dyspnea and worsening abdominal distension prior to a scheduled paracentesis. He was hemodynamically stable but had new hyponatremia and AKI, with urine sodium <10 mEq/L. After a large volume paracentesis and albumin infusion, his serum sodium and estimated glomerular filtration rate (eGFR) improved. Ascites fluid studies were not initially obtained because the ascites was presumed malignant.

Later in the hospital stay, the patient's kidney function worsened. Repeat paracentesis with ascites fluid analysis revealed a high serum ascites albumin gradient (SAAG). Despite albumin infusions, the eGFR continued to decline. Plasma renin and aldosterone levels were elevated. Given progressive AKI in the setting of liver metastases and portal hypertension physiology, midodrine and octreotide were initiated for suspected hepatorenal - like syndrome. Unfortunately, his clinical status deteriorated, and he was transitioned to hospice care.

Discussion

This case demonstrates that hepatorenal physiology can occur in malignancy related portal hypertension, even without cirrhosis. Liver metastases likely produced elevated SAAG ascites and neurohormonal activation despite adequate volume resuscitation. Albumin may transiently improve effective arterial volume, but patients with HRS - AKI typically do not respond. Paracentesis may temporarily improve renal perfusion by reducing intraabdominal pressure, but clinicians should consider hepatorenal physiology when evaluating AKI in patients with liver metastases and ascites.