A 68-year-old Sinhalese woman with a palliative self-expanding metal stent (SEMS) placed for an inoperable hilar cholangiocarcinoma a year ago presented with worsening obstructive jaundice of 2 weeks and mild cholangitis. She had poorly controlled type 2 diabetes and hypertension. She was on gliclazide 40 mg twice daily, amlodipine 5 mg twice daily, and prazosin 1 mg twice daily. She was unemployed and her social, environmental, and family history were unremarkable. She had no history of tobacco smoking or alcohol consumption. Her abdominal, respiratory, and neurological examinations were unremarkable. Her vital signs (pulse rate, 92 beats per minute; blood pressure, 130/80 mmHg; temperature, 36.8 °C), and urine output were within normal limits, but inflammatory markers were elevated (white blood cells, 11.2 × 109/L; C-reactive protein, 30 mg/L). She had elevated bilirubin levels (total bilirubin, 60 μmol/L; direct bilirubin, 31 μmol/L) and low albumin levels (27.5 g/L). Her renal functions were within normal limits. Ultrasonography showed intrahepatic duct dilatation with the SEMS in situ. Since this was indicative of a blocked stent, PTC-guided internal biliary stenting through the SEMS was attempted and failed. Therefore, an 8G - 25 cm EBD was left in the dilated left biliary system. Post procedure, she developed a high biliary output of 3–4 liters per day and went into oliguric AKI with metabolic acidosis, most probably due to inadequate fluid replacement and hypovolemia. A cholangiogram confirmed that the EBD was in place with contrast entering the duodenum. Abdominal ultrasonography did not reveal any intra-abdominal fluid collection. The EBD was closed to control the persistently high drainage, and she underwent hemodialysis for the AKI. Although there was temporary improvement of renal function over the next 2 weeks, she proceeded to develop gross ascites with worsening renal functions again. Decompensated cirrhosis with hepatorenal syndrome (HRS) was suspected. Her ascitic fluid was positive for coliforms suggesting superadded bacterial peritonitis. After a combination of therapy with intravenously administered antibiotics, terlipressin, and albumin she recovered and her bilirubin and creatinine levels returning to baseline. She was discharged on diuretics and antibiotic prophylaxis for spontaneous bacterial peritonitis. On her 6-month follow-up, she was asymptomatic with marked reduction of the ascites and her renal functions were normal. Her comorbidities were well controlled.