A 34-year-old female with systemic lupus erythematosus was admitted due to progressive lower leg edema, massive ascites, and nausea after treatment of bed rest, salt and water restriction, diuretics, intravenous administration of albumin and methylprednisolone, and repeated paracentesis for 2 months. On physical examination, her blood pressure was 127/82 mm Hg, pulse rate 84 beats/min, respiratory rate 20 breaths/min, and body temperature 37 C. Her abdomen was markedly distended and her lower extremities were severely edematous. The results obtained in laboratory investigations were as follows: white blood cells (WBCs) 5.8 x 109/L (normal range 4.5-11 x 109/L), hemoglobin 89 g/L (normal range 120-160 g/L), platelets 220 x 109/L (normal range 150-350 x 109/L), serum blood urea nitrogen (BUN) 13.5 mmol/L (normal range 2.5-7 mmol/L), creatinine 170 mumol/L (normal range 50-110 mumol/L), albumin 19 g/L (normal range 37-53 g/L), alanine aminotransferase 0.24 mukat/L (normal range 0-0.66 mukat/L), aspartate aminotransferase 0.60 mukat/L (normal range 0.08-0.76 mukat/L), C-reactive protein 0.286 mg/dL (normal range 0-0.5 mg/dL), complement 3 (C3) 0.4 g/L (normal range 0.8-1.5 g/L), complement 4 (C4) 0.1 g/L (normal range 0.2-0.4 g/L), and double-strand DNA (dsDNA) 263 IU/mL (normal range <30 IU/mL). Urine protein excretion was 4.86 g/day. Chest X-ray showed massive bilateral pleural effusion. The WBC count of ascitic fluid was 10/mm3. The serum-ascites albumin gradient was 1.4 mg/dL. The results of bacteria culture, acid-fast stain, malignant cell, and tuberculosis- polymerase chain reaction of ascites were negative. The Doppler of the main portal vein, inferior vena cava, major portal branches, and hepatic vein were patent without obstruction. The abdominal computed tomography scan revealed massive ascites (Figure 2A). The echocardiogram showed no pericardial effusion and preserved left ventricle systolic function. Unfortunately, progressive massive ascite accumulation gave rise to breathing difficulty and decreased urine output, despite an increase in serum albumin from 19 g/L to 28 g/L after the aforementioned treatments for 1 month at the hospital. The serum BUN and creatinine levels were increased to 30.5 mmol/L and 720 mumol/L from 13.5 mmol/L and 170 mumol/L, respectively. Disseminated intravascular coagulation (DIC) was within a normal range. Her lupus activity did not respond to plasma exchange, methylprednisolone 1000 mg pulse therapy, oral prednisolone 60 mg daily, or cyclosporine 100 mg twice daily. Her renal failure, leg edema, and refractory ascites could not be controlled by HD due to frequent intradialytic hypotension, which could not be corrected by prophylactic fresh frozen plasma infusion, sequential ultrafiltration, and reduction in dialysate temperature during HD. Therefore, continuous flow control reinfusion of ascites into a dialyzer during HD was designed to alleviate the ascites. A paracentesis pigtail catheter was inserted into the abdominal cavity and connected to a sterile three-way stopcock. When ascite reinfusion was planned, a set of dialysis tubing was connected with the sterile three-way stopcock to draw out the ascites at the speed of 12-15 mL/min (720-900 mL/h) into the dialyzer to mix with the blood by the roller pump during HD. The mixed blood and ascites were then channeled into the systemic circulation during a 4-hour HD session (Figure 1A). The ultrafiltration rate of the dialyzer was maintained at around 1 L/h to allow fluid removal from the blood and infused ascites in each 4-hour HD session. After seven sessions of continuous reinfusion of ascites into the dialyzer during HD, ~20 L of ascites were drawn out. The body weight and abdominal girth decreased from 50.2 kg to 37 kg and from 92 cm to 72 cm, respectively (Figure 3). The serum albumin level increased from 30 to 35 g/L (Figure 3). There was no intradialytic hypotension, fever, gastrointestinal bleeding, or DIC. Her respiratory distress and general condition also improved after the procedures. The levels of complements C3 and C4 also increased from 0.4 g/dL to 0.7 g/dL and from 0.1 g/dL to 0.13 g/dL, respectively. After the ascites subsided, the paracentesis pigtail catheter was removed. A piece of omentum was obtained by peritoneoscopy for the evaluation of the cause of refractory ascites. The pathologic finding of the omentum was chronic inflammation with cell infiltration, congestion, and fibrosis (Figure 4).
In the following 60 months, the serum creatinine level was around 120 mumol/L on immunosuppressive agents. There were no further episodes of refractory ascites. The patient also had an increase in muscle mass.