Saudi Journal of Kidney Diseases and Transplantation

: 2020  |  Volume : 31  |  Issue : 3  |  Page : 687--692

Chylous nephrogenic ascites in a hemodialysis patient

Muhammad Abdul Mabood Khalil1, Mohamad Khairulsadek Haji Jukmin2, Vui Heng Chong1, Jackson Tan1,  
1 Department of Renal Medicine, RIPAS Hospital, Bandar Seri Begawan BA1710, Brunei Darussalam
2 Faculty of Medicine, University of New South Wales, Sydney, Australia

Correspondence Address:
Muhammad Abdul Mabood Khalil
Department of Renal Medicine, RIPAS Hospital, Bandar Seri Begawan BA1710
Brunei Darussalam


Chylous nephrogenic ascites is rare in hemodialysis (HD) patients. We would like to share a rare case of chylous nephrogenic ascites in a HD patient. The patient has a history of straw-colored nephrogenic ascites which was drained through pigtail five times in the past. Later on, the ascites became turbid and milky. The chloroform test of the ascitic fluid showed fat globules with Oil Red-O stain, and the triglyceride concentration of ascitic fluid was 168.14 mg/dL (1.93 mmol/L) satisfying the criteria of chylous ascites. We believe that this may be caused by microtrauma from repeated pigtail insertions for ascites which was compounded by inadequate HD and noncompliance with fluids. Routine investigations including screening for malignancy, tuberculosis, cirrhosis, and heart failure did not reveal any other possible causes. Although there are few case reports of chylous ascites in peritoneal dialysis patients, it has never been reported in patients on HD.

How to cite this article:
Mabood Khalil MA, Haji Jukmin MK, Chong VH, Tan J. Chylous nephrogenic ascites in a hemodialysis patient.Saudi J Kidney Dis Transpl 2020;31:687-692

How to cite this URL:
Mabood Khalil MA, Haji Jukmin MK, Chong VH, Tan J. Chylous nephrogenic ascites in a hemodialysis patient. Saudi J Kidney Dis Transpl [serial online] 2020 [cited 2020 Sep 23 ];31:687-692
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Full Text


End-stage renal disease (ESRD) patients on maintenance hemodialysis (HD) may develop ascites. HD-associated ascites is also known as nephrogenic ascites. It was first reported around the 1970s in ESRD patients.[1] It is often seen in HD patients but also may be seen in the early stages of renal disease. There are various proposed pathogenic mechanisms for for nephrogenic ascites. These include changes in the permeability of the peritoneal membrane, inadequate dialysis, poor nutrition, hypoalbuminemia, hyperparathyroidism, and congestive heart failure.[2],[3],[4] It is a diagnosis of exclusion. Infection, malignancy, cirrhosis liver, and heart failure should be ruled out before the diagnosis of nephrogenic ascites can be made.[5] Nephrogenic ascites commonly produces straw-colored ascitic fluid, but here, we present a rare case of chylous ascitic fluid which was turbid and milky in color.

 Case Report

A 52-year-old man who is known diabetic, hypertensive, dyslipidemic, ESRD on three times per week HD, and having nephrogenic ascites presented with one-week history of progressively worsening abdominal distension and discomfort on March 25, 2018. It was accompanied by bilateral leg and genital swelling. The patient admitted to having poor compliance with fluid intake. His dialysis was initiated on March 7, 2017, initially through right permanent catheter and then through right brachiocephalic arteriovenous fistula. His course was complicated by nephrogenic straw color ascites since August 2017. He had repeated admissions for straw-colored nephrogenic ascites in the past one year. Previously, his ascites were always straw colored and exudative. Extensive workup in the past did not reveal any malignancy, tuberculosis, cirrhosis, or heart failure. Ascites was drained five times through pigtail over the last one year. It was inserted three times on the right lower quadrant lateral to rectus sheath at different points. Twice insertion was done on lower left quadrant lateral to the rectus sheath at different points. Besides diabetes (14 years), hypertension (10 years), and dyslipidemia (10 years), he has a history of pulmonary tuberculosis (TB), which was treated 15 years ago. However, there was no history of cough, hemoptysis, weight loss, or night sweat during this admission. There was also no history of altered bowel habits, bleeding from the gastrointestinal tract, weight loss, liver problems, or cardiac issues. Examination during his initial presentation revealed fluid overload and most notably tense abdominal distension from ascites. In addition, he also has high blood pressure (169/96 mm Hg) and marked scrotal and pedal edema. There were no stigmata of liver disease or abdominal organomegaly. Respiratory examination revealed fine crackles at the lung bases. The cardiovascular examination was unremarkable. He was dialyzing through right brachiocephalic arteriovenous fistula three times per week. Review of his dialysis adequacy showed that it was never optimal. Urea reduction ratios for the last 12 months were 54%/56%/51%. His dry weight was 108 kilograms, but unfortunately, he could never achieve it most of the time because of noncompliance with the fluid. His average weight gain was 3–3.5 kg between sessions. His ultrafiltration rate ranged between 6.94 and 8.10 mL/kg/h. His dialysate flow was 500 mL/h. His blood flow was 250–280 mL/min.

Ascitic fluid tap was done. In contrast to the past, this time, the fluid was turbid and milky on gross examination. As a result, repeat extensive workup was done. His blood and ascitic fluid investigations are summarized in [Table 1] and [Table 2]. Serum ascites albumin gradient was 0 g/L. The ascitic fluid was turbid, and on centrifuging, it was grossly milky in contrast to previous straw color [Figure 1].{Table 1}{Table 2}{Figure 1}

It was exudative with protein of 45.57 g/L. Ascitic fluid white cell count was 130 cells/ mm3, with 77% of cells being neutrophils. The ascitic fluid analysis showed scattered lymphocytes and macrophages, but no malignant cells were seen. Because of turbidity and milkiness ascitic fluid, triglyceride (TG) estimation was done which was reported as 168.14 mg/dL (1.93 mmol/L). The chloroform test of the ascitic fluid showed fat globules with Oil Red-O stain. In view of history of TB, extensive screening was done to rule out TB. Interferon-gamma test for screening of TB was negative. Smear for acid-fast bacillus (AFB) in sputum and ascitic fluid was negative. Sputum and ascitic fluid cultures for AFB were also negative. The AFB culture for early morning sputum was also negative. Ascitic fluid culture and Gram staining did not reveal any organism.

The echocardiogram revealed a good left ventricular function with an ejection fraction of 63%. There was no evidence of any abnormality of heart valves, diastolic dysfunction, right heart failure, pulmonary artery hypertension, constrictive pericarditis, or restrictive cardiomyopathy. The ultrasound of the abdomen revealed moderately large volume of ascites. The liver showed a normal homogeneous echogenicity and normal portal vein diameter. No malignant cells were seen in ascitic fluid by a cytopathologist. Review of ascitic for malignant cells was also done multiple times in the past admissions, and none reported malignant cells. CT abdomen was also done, and it showed tense ascites without any documented peritoneal or abdominal pathology. After extensive workup and in the absence of any specific etiology, the patient was labeled as having nephrogenic chylous ascites. A pigtail ascitic drain was inserted on the left lower quadrant lateral to rectus sheath, and about 12 L of turbid milky fluid was drained over a period of 4 days with albumin infusion at the end of every therapeutic drainage. He had daily HD to offload fluid for consecutive five days, before resuming his usual three times a week schedule. Dietary advice was given to increase protein intake and reduce fluid intake. His blood flow was increased to 350 mL/min. A bigger dialyzer of 1.6 m2 was used. Unfortunately, he remained noncompliant with fluids, and despite corrective measures, nephrogenic chylous ascites persisted during subsequent future follow-up. Unfortunately, the patient died on February 20, 2019, due to septicemia.


Chylous nephrogenic ascites is rare in patients with chronic kidney disease. Chylous ascites is usually milky in appearance. Biochemically, TG content of greater than 110 mg/dL is required for diagnosis.[6],[7] Our patient ascitic fluid has a TG concentration of 168.14 mg/dL (1.93 mmol/L). The chloroform test of the ascitic fluid showed fat globules with Oil Red-O stain indirectly supporting chylous ascites.

Chylous ascites is an uncommon finding in the general population, with an incidence of 1 per 20,000 admissions.[8] Common abdominal therapeutic interventions and trauma are well-known causes for chylous ascites[9]. The most common causes of a traumatic chylous ascites in developed countries are malignancy and lymphatic abnormalities. Infection like TB is common in developing countries.[10] The mechanisms underlying the chylous ascites were thought to be due to obstruction of the lymphatic system resulting in leakage of lymph fluids into the peritoneal cavity from the dilated lymphatic vessels. It can also be due to surgery or trauma to the thoracic duct, causing leakage through the lymphoperitoneal fistula.[11] Cirrhotic liver and right heart failure can also cause chylous ascites.[11] Increased formation of hepatic lymph in cirrhosis and increased lymphatic pressure in right heart failure are the proposed mechanism for chylous ascites. Nephrotic syndrome has been reported to cause chylous ascites, though the underlying mechanism is not well understood.[12],[13],[14]

Chylous nephrogenic ascites is very rare in a HD patient. Our literature search came across a few reports in peritoneal dialysis (PD). Chung et al. and Ramos et al. in their case reports reported chylous ascites due to PD catheter insertion.[8],[15] In a case series on complication of PD catheter insertion, chylous ascites was reported in 0.5% of all patients.[16] Chyloperitoneum was reported by Lewy et al. which resolved over a period of time in a PD patient.[17] Lee et al. reported successful treatment of chylous ascites with subcutaneous octreotide in a PD patient.[18] We believe that this is the first reported case of chylous ascites in a HD patient. We have ruled out other possible causes such as TB, malignancy, liver, and heart failure through extensive workup investigations. Our patient has never been on PD in the past. His history included straw-colored nephrogenic ascites, for which pigtail was inserted five times for drainage of ascites. Most of the cases reported in PD occurred post PD catheter insertion speculating trauma to abdominal lymphatics. Our patients had pigtail insertion three times on the right side and two times on the left side. We assume that repeated trauma to small lymphatic vessels due to multiple pigtail insertions could have led to conversion of straw-colored nephrogenic ascites to chylous ascites. Other contributing factors may include noncompliance with fluid and inadequate HD as evidenced by low urea reduction ratio over the last few months. Unfortunately, despite dietary manipulation and optimization of HD prescription, his chylous ascites persisted. Later on, the patient died of septicemia.


Chylous ascites can rarely occur in a HD patient. The exact cause is not known. Microtrauma, noncompliance with fluid, and inadequate dialysis may be contributing factors. It may become recalcitrant to treatment, despite dietary manipulation and provision of adequate HD.

Conflict of interest: None declared.


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