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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2015  |  Volume : 26  |  Issue : 4  |  Page : 773-777
Nephrogenic ascites - Still an intractable problem?

Department of Nephrology, St. Martha's Hospital, Bengaluru, Karnataka, India

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Date of Web Publication8-Jul-2015


Nephrogenic ascites or ascites associated with renal failure is seen in end-stage renal disease in-patients on hemodialysis but has been described occasionally in earlier stages of renal failure. The cause can be multifactorial and a combination of inadequate dialysis and ultrafiltration, poor nutrition and increased peritoneal membrane permeability in uremia. Generally, the onset of nephrogenic ascites is insidious and portends a grim long-term prognosis. We describe herein three patients who presented with refractory ascites of nephrogenic origin and review this entity.

How to cite this article:
Nayak-Rao S. Nephrogenic ascites - Still an intractable problem?. Saudi J Kidney Dis Transpl 2015;26:773-7

How to cite this URL:
Nayak-Rao S. Nephrogenic ascites - Still an intractable problem?. Saudi J Kidney Dis Transpl [serial online] 2015 [cited 2023 Jan 30];26:773-7. Available from: https://www.sjkdt.org/text.asp?2015/26/4/773/160214

   Introduction Top

Nephrogenic ascites or ascites associated with renal failure was first reported in the early 1970s in patients with end-stage renal disease (ESRD). [1] It is most often seen in patients on hemodialysis, but has been described earlier in the course of renal failure occasionally. The putative causes for the occurrence of nephrogenic acites include inadequate dialysis and ultrafiltration, poor nutrition and increased peritoneal membrane permeability in combination with impaired peritoneal lymphatic reabsorption. [2],[3],[4],[5],[6],[7],[8] We describe herein three patients who presented with refractory ascites of nephrogenic origin and review this entity.

   Case Reports Top

Case 1

A 47-year-old lady, ESRD secondary to chronic interstitial nephritis on twice-weekly maintenance hemodialysis (HD) since three years, presented with progressively worsening abdominal distension of six months duration. On examination, she was a thin-built lady weighing 50 kg with pallor; no icterus or lymphadenopathy was noted. Abdominal examination revealed massive ascites, peripheral edema 3+ till mid calf with small reducible umbilical hernia and no palpable organomegaly. Her cardiac and respiratory systems were normal. Her laboratory investigations revealed hemoglobin (Hb) of 9.2 g/dL, blood urea of 97 mg/ dL, serum creatinine of 9.7 mg/dL with normal serum electrolytes, serum calcium of 9.7 mg/ dL and serum phosphorus of 4.9 mg/dL. Ascitic fluid analysis revealed protein of 4.2 mg/dL, albumin of 2.1 g/dL, sugar of 94 mg/ dL and lactate dehydrogenase (LDH) of 77 U/L and serum-ascites albumin gradient or gap (SAAG) was 1.4, with serum albumin being g/dL. The ascitic fluid white cell count was 150 cells/mm 3 , with 60% cells being lymphocytes. Cultures of fluid were negative for bacterial and fungal elements and the acid fast bacilli (AFB) smear as well as smear for malignant cells were negative. Work-up for liver disease by ultrasound Doppler of the hepatic and portal veins was normal and cardiac function by 2D-ECHO revealed ejection fraction of 55%. Markers for hepatitis B and C virus were negative. Her urea reduction rate (URR) on dialysis was low at 52%. She was diagnosed to have nephrogenic ascites and underwent aggressive 5 h sessions of thriceweekly dialysis with gradual reduction in target dry weight from 50 kg to 47 kg over four weeks. This was accompanied by dietary salt restriction and oral nutritional protein supplementation. Therapeutic large volume paracentesis was also performed twice in a month with intravenous albumin infusions to relieve her of abdominal discomfort. A gradual reduction in ascites was noted in three months and her abdominal girth had reduced by about 50% with management.

Case 2

A 50-year-old lady, ESRD secondary to diabetic nephropathy on maintenance HD twiceweekly since one year, presented with progressively increasing ascites of four months duration. She had recently attained menopause and the patient attributed her abdominal distension to this. Examination revealed a cachexic lady with severe ascites. Her dry weight was between 45 and 49 kg. Her investigations revealed Hb of 8.9 g/dL, blood urea of 102 mg/dL, serum creatinine of 7.9 mg/dL, normal serum electrolytes, serum calcium of 8.9 mg/ dL and serum phosphorus of 5.2 mg/dL. Serum albumin was low at 2.9 and ascitic fluid albumin was 2.1 with a SAAG of 0.8 g/dL. Ascitic fluid analysis revealed an exudate with lymphocytic predominance. A complete workup for hepatic, cardiac and malignant causes was negative. Her URR on dialysis was 54%. Hepatitis B and C markers were negative.

Abdominal tuberculosis was initially suspected; however, ascitic fluid adenosine deaminase was low and mycobacterial polymerase chain reaction of the fluid was also negative. She received thrice-weekly 5 h dialysis sessions with fluid removal of 3-4 L per session; however, this was poorly tolerated by the patient due to frequent hypotensive episodes occurring during dialysis. She also underwent therapeutic large volume paracentensis to relieve her abdominal discomfort. Nutritional supplementation was given with a high-protein diet. Despite adequacy of HD improving to URR of 71% and target dry weight reducing to 44 kg from her previous weight of 49 kg, there had been only minimal improvement in her general condition in the last five months.

Case 3

A 53-year-old male, ESRD secondary to type2 Diabetes mellitus on maintenance HD for two years, presented with ascites of six months duration. He was on twice-weekly HD with target weight of 68-70 kg, which had been progressively reduced since the last two months. On examination, his blood pressure was 130/80 mm Hg, he had moderate to massive ascites and no palpable abdominal organomegaly was noted. His investigations revealed Hb of 8.6 g/dL, blood urea of 84 mg/ dL, serum creatinine of 7.4 mg/dL, serum calcium of 8.7 mg/dL and serum phosphorus of 3.9 mg/dL. His URR on dialysis was 56%. Ascitic fluid analysis revealed an exudate with protein of 5.4 g/dL, albumin of 2.3 g/dL, LDH of 145 U/L and cell count of 250, 95% of which were lymphocytes. Serum albumin was low at 2.7 g/dL, with SAAG of <1.0. Culture of fluid was negative and AFB and malignant cells were negative. A complete evaluation to look for cardiac and hepatic causes was negative. He was diagnosed to have dialysisrelated ascites. His dialysis treatments were intensified and his dry weight was gradually reduced by 1.0 kg/week till 66 kg. At the last follow-up of four months, there has been a minimal reduction in ascites.

   Discussion Top

These three cases bring to light the condition termed as dialysis-related ascites, a problem that has been most often described in ESRD patients on HD. The entity of nephrogenic ascites or ascites associated with renal failure was initially reported by Mahoney et al in 1970. [1] Since then, this issue has been addressed in few reviews and some case reports. [2],[3],[4],[5],[6],[7],[8] Nephrogenic ascites has been known by several names such as nephrogenous ascites, dialysis ascites, HD-associated ascites and idiopathic ascites. The term nephrogenic ascites is preferred as the onset of ascites may occur earlier in the course of renal failure and well before the initiation of dialysis. The exact incidence of nephrogenic ascites is not known; however, the incidence may be slightly higher in developing countries like India. To the best of our knowledge, no data exist on the prevalence of this diagnosis at presentation or at patient follow-up.

Nephrogenic ascites could be possibly due to a combination of factors such as poor nutrition, late presentation leading to delay in initiation of appropriate renal replacement therapy and inadequate dialysis. Dialysis not being covered by the state or insurance policies necessitates patients to fund their own treatments, and this leads to poor compliance with the dialysis schedule. Marked center to center variability in incidence of nephrogenic ascites of 0.7-20%, wide age of onset of 11-71 years (mean 42 years) and male preponderance (male:female = 2:1) has been reported. [9] The largest case series of nephrogenic ascites in 138 patients was reported by Gluck et al. [5] The diagnosis of nephrogenic ascites is one of exclusion and needs a thorough work-up to rule out hepatic, cardiac, infective and malignant causes of ascites. In about 15% of cases, an extensive evaluation may reveal secondary causes for ascites [Table 1].
Table 1: Recommended evaluation for nephrogenic ascites.

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The pathogenesis of ascites remains inconclusive. Several pathogenetic factors including hepatic vein hydrostatic pressure, fluid retention, increased peritoneal membrane permeability and impaired peritoneal lymphatic drainage have been considered [Table 2]. Fluid retention has been observed in ⅔ of the reported patients in some reviews. [2],[5] However, the role of fluid retention and ascites formation is not clearly defined because dialysis patients display signs of fluid overload frequently without demonstrable ascites. Changes in peritoneal membrane permeability due to uremic toxins, [2],[5] exposure to dialysis solutions, [5] renin-angiotensin activation, circulating immune complexes [10] and iron deposition [11] have all been implicated in ascites formation. Histologically, the peritoneum is grossly normal; microscopy can been normal, [12] but more often shows chronic inflammation and mesothelial cell proliferation with variable degree of submesothelial fibrosis. [13] The rate of ascites removal in nephrogenic ascites has been seen to be much slower than in patients with ascites and normal renal function. [2] This was demonstrated by Morgan et al, [6] wherein radiolabeled albumin was used to estimate the rate of reasorption and transfer across the peritoneal membrane. Impaired peritoneal fluid drainage was demonstrated in patients with nephrogenic ascites. Rate of clearance of albumin was lower at a median value of 14 mL/h (range 10-21 mL/ h) compared with a median value of 45 (range 10-75 mL/h) in those with ascites of other etiology. This is however normalized after successful kidney transplant, suggesting an effect of uremia. Secondary hyperparathyroidism as a possible cause and subsequent cure of ascites after parathyroidectomy has been described in one patient. [7]
Table 2: Possible pathogenetic mechanisms for nephrogenic ascites.

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In nephrogenic ascites, ascitic fluid analysis reveals exudate (high protein), low ascitic albumin gradient (SAAG <1.0) and low neutrophil count. Patients frequently present with moderate to massive ascites, hypertension, minimal lower extremity edema, cachexia and a history of dialysis-associated hypotension. [5] Nephrogenic ascites is usually associated with a grave prognosis. The average survival ranges from seven to 10.7 months, with 44% of patients dying within 15 months of diagnosis. [5] Management of nephrogenic ascites is complex [Table 3] and includes a combination of intensive dialysis with good ultrafiltration, intradialytic albumin infusions along with a highprotein diet. Strict volume control has been emphasized in the treatment of nephrogenic acites by Gunal et al. [14] Intensive dialysis is effective in ⅓ to ¼ of patients as early as within three weeks. Continuous ambulatory peritoneal dialysis (CAPD) and peritoneovenous shunts (PVS) are the other treatment options. The efficacy of PVS to treat massive refractory ascites has been reported by Holm et al. [15] In their study of 14 patients on chronic maintenance hemodialysis (average of 20.4 ± 2.9 months) with refractory ascites of nephrogenic origin, 12 patients obtained significant relief after placement of a PVS. Of these patient, nine patients (75%) survived for one year and six patients (50%) had survived for three or more years, thereby improving the previous dismal prognosis of patients with nephrogenic ascites. [16] Hemodynamic improvement has been noted after PVS in patients who did not tolerate excessive ultrafiltration before. [16] Objective improvements were also noted in nutritional status, with weight gain and subjective improvement in appetite and physical activities. Complications of shunt placement are seen in about half of the cases, and include catheter tip migration, infection and occlusion. These complications necessitate either minor/ major revisions or removal of the shunt.
Table 3: Therapeutic options for nephrogenic ascites.

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CAPD is also effective in the treatment of ascites by controlling ascites formation. [17] This is by reducing the intraperitoneal fluid protein concentration thus limiting osmotic fluid shift into the peritoneal space. Within six months of continued treatment, the amount of total protein excretion in the dialysis effluent decreases over time from 26.5 to 50 g/day to 7 to 9.5 g/day, with a subsequent rise in serum protein and albumin levels and resolution of ascites. Therapies with less-predictable outcomes include instillation of intraperitoneal corticosteroids and binephrectomy. The definitive therapy is renal transplantation and nearly all reported patients with nephrogenic ascites have had a complete resolution within two to six weeks after successful transplantation. Recurrence of ascites may occur after loss of graft function.

Our patients were all on twice-weekly dialysis with resultant low URR, reflecting that they were underdialyzed and intensification of the dialysis regimen resulted in some objective improvement.

In conclusion, nephrogenic ascites is a rare condition with grave prognosis and a multifactorial cause. Although no prospective studies have been performed comparing the various treatment modalities, on the basis of the current data, intensive dialysis, kidney transplantation, CAPD and PVS placement offer the best hope for an improvement in quality of life and recovery.

   References Top

Mahoney JF, Gutch CF, Holmes JH. Intractable ascites in chronic dialysis patients. Am Soc Nephrol 1970;4:51.  Back to cited text no. 1
Gotloib L, Servadio C. Ascites in patients undergoing maintenance hemodialysis. Report of six cases and physiopathologic approach. Am J Med 1976;61:465-70.  Back to cited text no. 2
Cintin C, Joffe P. Nephrogenic ascites. Case report and review of the literature. Scand J Urol Nephrol 1994;28:311-4.  Back to cited text no. 3
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. 4
Glück Z, Nolph KD. Ascites associated with end-stage renal disease. Am J Kidney Dis 1987;10:9-18.  Back to cited text no. 5
Morgan AG, Terry SI. Impaired peritoneal fluid drainage in nephrogenic ascites. Clin Nephrol 1981;15:61-5.  Back to cited text no. 6
Nasr EM, Joubran NI. Is nephrogenic ascites related to secondary hyperparathyroidism? Am J Kidney Dis 2001;37:E16.  Back to cited text no. 7
Hammond TC, Takiyyuddin MA. Nephrogenic ascites: A poorly understood syndrome. J Am Soc Nephrol 1994;5:1173-7.  Back to cited text no. 8
Mauk PM, Schwartz JT, Lowe JE, Smith JL, Graham DY. Diagnosis and course of nephrogenic ascites. Arch Intern Med 1988;148:1577-9.  Back to cited text no. 9
Twardowski ZJ, Alpert MA, Gupta RC, Nolph KD, Madsen BT. Circulating immune complexes: Possible toxins responsible for serositis (pericarditis, pleuritis, and peritonitis) in renal failure. Nephron 1983;35:190-5.  Back to cited text no. 10
Besbas N, Söylemezoglu O, Saatçi U, et al. Peritoneal hemosiderosis in pediatric patients with nephrogenic ascites. Nephron 1992;62: 292-5.  Back to cited text no. 11
Wang F, Pillay VK, Ing TS, Armbruster KF, Rosenberg JC. Ascites in patients treated with maintenance hemodialysis. Nephron 1974;12: 105-13.  Back to cited text no. 12
Singh S, Mitra S, Berman LB. Ascites in patients on maintenance hemodialysis. Nephron 1974;12:114-20.  Back to cited text no. 13
Gunal AI, Karaca I, Celiker H, Ilkay E, Duman S. Strict volume control in the treatment of nephrogenic ascites. Nephrol Dial Transplant 2002;17:1248-51.  Back to cited text no. 14
Holm A, Rutsky EA, Aldrete JS. Shortand long-term effectiveness, morbidity, and mortality of peritoneovenous shunt inserted to treat massive refractory ascites of nephrogenic origin analysis of 14 cases. Am Surg 1989;55: 645-52.  Back to cited text no. 15
Morgan AG, Sivapragasam S, Fletcher P, Terry SI. Hemodynamic improvement after peritoneovenous shunting in nephrogenic ascites. South Med J 1982;75:373-4.  Back to cited text no. 16
Ing TS, Daugirdas JT, Popli S, et al. Treatment of refractory hemodialysis ascites with maintenance peritoneal dialysis. Clin Nephrol 1981;15:198-202.  Back to cited text no. 17

Correspondence Address:
Shobhana Nayak-Rao
Department of Nephrology, St. Martha's Hospital, Bengaluru 560 001, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.160214

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