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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2015  |  Volume : 26  |  Issue : 5  |  Page : 1013-1014
Recurrent ascites secondary to endometriosis in a dialysis patient

1 Department of Medicine, RIPAS Hospital, Bandar Seri Begawan, Brunei
2 Department of Surgery, RIPAS Hospital, Bandar Seri Begawan, Brunei, Brunei
3 Department of Renal Medicine, RIPAS Hospital, Bandar Seri Begawan, Brunei

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Date of Web Publication7-Sep-2015

How to cite this article:
Saad AS, Chong CL, Ping LY, Tan J, Chong VH. Recurrent ascites secondary to endometriosis in a dialysis patient. Saudi J Kidney Dis Transpl 2015;26:1013-4

How to cite this URL:
Saad AS, Chong CL, Ping LY, Tan J, Chong VH. Recurrent ascites secondary to endometriosis in a dialysis patient. Saudi J Kidney Dis Transpl [serial online] 2015 [cited 2020 May 31];26:1013-4. Available from: http://www.sjkdt.org/text.asp?2015/26/5/1013/164594
To the Editor,

Ascites is not uncommon in patients with endstage renal disease (ESRD) undergoing hemodialysis. [1],[2] Factors contributing to ascites in renal failure patients may include peritoneal membrane changes, fluid overload, reduced lymphatic drainage, cardiac failure and hypoproteinemia. [1],[2] Nephrogenic ascites is now an increasingly recognized entity. We report a case of a 40-year-old lady with ESRD with recurrent ascites secondary to endometriosis diagnosed by laparoscopy.

A 40-year-old lady with ESRD undergoing regular hemodialysis was referred for evaluation of recurrent ascites. Her past medical history was relevant for diabetes mellitus, hypertension and resolved previous menstruation problem of more than 10 years. However, she was not aware of the diagnosis of her problem. Her current problem started six months earlier, when she was admitted with abdominal distension due to ascites. This was tapped for symptomatic relief. Ascitic fluid was straw colored and analysis revealed high protein and normal cell count, consistent with exudative ascites. It was negative for malignancy and any organisms including acid fast bacilli. Thyroid function and tumor markers (carcinoembryonic antigen, carbohydrate antigen [CA] 125, CA153, CA 19-9 and alfa-feto protein) were all normal apart from mildly elevated CA125 marker at 130.5 U/mL (normal <35 U/mL). Evaluation for liver disease (viral hepatitis B and C) and cardiac failure were negative. Echocardiogram showed left ventricular hypertrophy and mildly dilated chambers but good ejection fraction. The dilated chambers were attributed to fluid overload. Ultrasound scan followed by a computed tomography (CT) scan of the abdomen showed congested liver and small ascites. There was no pancreatic, biliary, ovarian, pelvis, peritoneal or mesenteric abnormalities such as nodules or contrast enhancement. Upper gastro-intestinal endoscopy revealed no varices or portal hypertension changes. After the negative investigations, the ascites was thought to be related to her ESRD state and she was managed with adjustment of her dialysis regime. The ascites recurred several times and required repeated admissions for paracentesis. In view of the persistent cholestatic liver profile, a liver biopsy was performed. Unfortunately, the procedure was complicated by hemoperitoneum that was successfully managed with bed rest, heparinfree dialysis and blood transfusion. The liver biopsy showed normal architecture with features of hepatolysis, but with no significant fibrosis, which ruled out liver disease as the cause of recurrent ascites. After several further admissions for therapeutic paracentesis for symptomatic relief, the patient agreed and we proceeded with a diagnostic laparoscopy. During laparoscopy, 1 L of serous fluid was drained. There were no peritoneal or mesenteric abnormalities noted in the abdomen or no features of sclerosing encapsulating peritonitis was seen. However, in the pelvis, a chocolate-colored membrane was seen over the pelvic peritoneum involving part of the sigmoid colon. Ascitic fluid cytology showed numerous foamy and scattered siderophages along with hyperplastic mesothelial cell groups and moderate amount of chronic inflammatory cell infiltrates, with no evidence of malignant cells. Biopsies of the peritoneum that consisted of irregular brown tissue revealed features consistent with endometriosis tissue. A diagnosis of endometriosis resulting in recurrent ascites was made. Interestingly, after the surgery, the patient became amenorrhic, and also had improvement of her ascites.

Endometriosis presenting with ascites is rare and only 63 cases have been reported in the literature since it was first described in 1954. [3] To the best of our knowledge, endometriosis leading to recurrent ascites in a patient with renal failure has not been previously reported. The pathogenesis is not exactly known but several mechanisms have been postulated. [3],[4],[5],[6],[7] Rupture of endometrioma result in blood-stained exudative ascites or even frank hemoperitoneum, mimicking acute abdomen. Another postulated mechanism is endometriosis obstruction of the lymphatic drainage in the diaphragmatic area, resulting in fluid accumulation. The third mechanism involved shedding of blood and endometrial cells, resulting in peritoneal irritation and ascites formation. This can also lead to dense adhesion and abdominal cocoon. The latter two mechanisms are associated with chronic presentation. In most reported cases, the endometriosis had been extensive. In our case, the endometriosis was limited but the presence of renal failure probably acted synergistically.

Most reported patients presented with abdominal distension, anorexia/weight loss, abdominal pain and menometrorrhagia, which were the most frequently encountered clinical symptoms, whereas pelvic mass was the most common physical finding. [3],[4],[7] The investigation of choice is laparoscopy and affected areas typically appear as black, dark brown or bluish puckered lesions, nodules or small cysts containing old hemorrhage surrounded by variable extent of fibrosis on the ovaries, serosal surface and peritoneum. Ultrasound or CT imaging may show cystic mass in the pelvis, common location of endometrioma. In the earlier cases, surgeries were mainly carried out for suspected acute abdomen and diagnosis made after surgery. With laparoscopy, diagnosis can be made earlier and hormonal therapy have been reported to be effective. The cessation of menstruation cycle after surgery led to improvement of her condition and confirmed the role of endometriosis, even though not extensive, can lead to recurrent ascites, especially in patients with risk factor such as renal failure.

Conflict of interest: None declared.

   References Top

Cintin C, Joffe P. Nephrogenic ascites. Case re-port and review of the literature. Scand J Urol Nephrol 1994;28:311-4.  Back to cited text no. 1
Glück Z, Nolph KD. Ascites associated with endstage renal disease. Am J Kidney Dis 1987; 10:9-18.  Back to cited text no. 2
Gungor T, Kanat-Pektas M, Ozat M, Zayifoglu Karaca M. A systematic review: Endometriosis presenting with ascites. Arch Gynecol Obstet 2011;283:513-8.  Back to cited text no. 3
Spitzer M, Benjamin F. Ascites due to endome-triosis. Obstet Gynecol Surv 1995;50:628-31.  Back to cited text no. 4
Han SH, Reynolds TB, Fong TL. Nephrogenic ascites. Analysis of 16 cases and review of the literature. Medicine (Baltimore) 1998;77:233-45.  Back to cited text no. 5
del Rey-Moreno A. Abdominopelvic complications of endometriosis. In: Chaudhury K, edr. Endometriosis- Basic Concepts and Current Research Trends. InTech; 2012. Available from: http://www.intechopen.com/books/...abdominal-complications. [Last accessed on 2013 Dec 06].  Back to cited text no. 6
Ussia A, Betsas G, Corona R, De Cicco C, Koninckx PR. Pathophysiology of cyclic hemorrhagic ascites and endometriosis. J Minim Invasive Gynecol 2008;15:677-81.  Back to cited text no. 7

Correspondence Address:
Dr. Vui Heng Chong
Department of Medicine, RIPAS Hospital, Bandar Seri Begawan
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DOI: 10.4103/1319-2442.164594

PMID: 26354581

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