A Curious Case of a Rapid Resolution of Acute Tubular Necrosis After Portal Vein Decompression in a Cirrhotic Patient With Underlying Hepatorenal Syndrome: A Case Report and Literature Review

Abstract

Introduction: Acute kidney injury is a common complication in cirrhosis and is associated with a poor prognosis. Splanchnic vasodilatation triggered by portal hypertension with subsequent renal vasoconstriction appears to play a central role in the hemodynamic changes and the decline in renal function in cirrhotic patients. We report a case of a 54-year-old female with decompensated alcoholic cirrhosis and underlying type 2 hepatorenal syndrome (HRS) based on a low urine sodium and bland urinalysis, who presented with confusion and abdominal pain. Abdominal duplex ultrasound revealed acute non-occlusive portal and superior mesenteric vein thrombosis with increased portal pressure. The patient subsequently developed acute tubular necrosis (ATN) with a serum creatinine of 4.0 mg/dL from a baseline of 0.9 mg/dL. The diagnosis was made based on high urine sodium and the presence of urinary granular cast. Due to worsening renal function, hemodialysis was initiated. Mechanical thrombectomy of the superior mesenteric and portal vein thrombus was performed with a substantial decrease of portal pressure. Her renal function recovered significantly and returned to baseline 4 days after the procedures. In conclusion, a rise in portal pressure from extensive portal vein thrombosis in this case led to the profound renal hypoperfusion and worsening of HRS which led to ATN. Thus, decompression of portal hypertension and reversal of hemodynamics using TIPS and mechanical thrombectomy might have beneficial effects in other cirrhotic patients with similar presentation. Further studies are warranted to prove this theory.Figure 1Figure 2