A 51-year-old female was diagnosed to have essential hypertension since 12 years and CKD since last 4 years. She progressed to end-stage renal disease 2 years back and was initiated on maintenance hemodialysis. For initial 1-year, she was on twice-weekly hemodialysis, which was subsequently increased to thrice weekly. She presented to us with complaints of progressive painless abdominal distension of 8-month duration along with anorexia and weight loss. There was no history of abdominal pain, altered bowel habits, pedal edema, fever, jaundice and no history to suggest hypothyroidism or connective tissue disease. There was no history of diabetes mellitus, jaundice, abdominal surgery and anti-tubercular treatment in past. Her medication included prazosin 10 mg/day, amlodipine 10 mg/day, calcium carbonate 1500 mg/day, twice weekly subcutaneous erythropoietin, oral iron and multivitamin. On examination, she had normal sensorium with blood pressure of 180/120 mm of Hg, pulse rate - 110/min, respiratory rate - 20/min, was afebrile and pale. Her abdomen was symmetrically distended with fluid thrill. There were no visible veins; hernial sites were normal with no cutaneous stigmata of chronic liver disease. Patient had hemoglobin of 7.7 g/dl, total leukocyte count (TLC) of 10400/mm3, with normal differential, platelet count 2.50 lakh/mm3, mean corpuscular volume 90.8 fl, mean corpuscular hemoglobin 30.1 pg/cell, mean corpuscular hemoglobin concentration 33.2 g/dl, normal coagulogram, urea 197 mg/dl, creatinine 9.4 mg/dl, sodium 144 mEq/L, potassium 6.1 mEq/L, chloride 110 mEq/L, aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase were 27, 15 and 254 IU/L respectively, bilirubin 0.8 mg/dl, total protein and albumin 6.5 and 2.7 g/dl, calcium 9.7 mg/dl, phosphorous 9.3 mg/dl, and intact parathyroid hormone 346.8 pg/mL. The serology was negative for hepatitis B, hepatitis C and human immunodeficiency virus. On tapping, the ascitic fluid was hemorrhagic and showed TLC of 70/mm3 with 70% polymorphonuclear cells, protein was 3.8 g/dl, sugar 83 mg/dl, with adenosine deaminase of 32 IU/L, and serum ascites albumin gradient of 0.8. The Ziehl-Neelsen stain and Gram-stain were negative, as was the culture for Mycobacterium tuberculosis, and pyogenic organisms. The TB polymerase chain reaction and ascitic fluid for malignant cytology were also negative. Other cancer markers such as cancer antigen (CA) 125, CA 19-9, and carcinoembryonic antigen were also normal. Her electrocardiogram revealed left ventricular hypertrophy with strain pattern, while echocardiography revealed mild mitral regurgitation, left ventricular ejection fraction of 45-50% with no evidence of systolic or diastolic dysfunction. An ultrasound abdomen performed showed gross ascites, bilateral contracted kidneys and cholelithiasis while other abdominal organs were normal. Subsequently, a contrast-enhanced computed tomography (CECT) abdomen was performed which revealed gross ascites with peritoneal enhancement and hyper-densities within fluid, in addition to the finding of contracted kidneys and cholelithiasis [Figure 1]. Suspecting inadequate dialysis, the patient was subjected to daily dialysis. However, there was no improvement in her ascites, and it required repeated therapeutic aspiration. To ascertain the cause of refractory ascites, the patient was subjected to exploratory laparotomy, which showed hemorrhagic ascitic fluid, thickened peritoneum and dense adhesions in-between the bowel loops and bowel loops with the abdominal wall. Keeping the possibility of cocoon abdomen, an intra-operative peritoneal biopsy was taken, which showed hyalinized fibrocollagenous tissue devoid of any lining epithelium with fibrin deposition and inflammatory cell infiltrate. There was no evidence of granulomatous inflammation or malignancy in biopsy specimen [Figure 2]. A diagnosis of cocoon abdomen secondary to uremia was made, and the patient was managed with daily intensive hemodialysis. Over next 1-month, there was gradual improvement in her symptoms along with decrease in ascites.