Diagnosis and Course of Nephrogenic Ascites

Mauk, P M; Schwartz, Jerome; Lowe, James E.; Smith, JD; Graham, D.Y.

doi:10.1001/archinte.1988.00380070075018

Cited by 19 publications

(11 citation statements)

References 8 publications

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“…The syndrome of nephrogenic ascites is largely a diagnosis of exclusion, but it has been seen in association with PCD without liver involvement. 7 Although several tumor markers were all within normal ranges in our patient, and no malignant cells were seen in ascites after several cytological examinations, malignant neoplasm could not be completely excluded, because a laparoscopic peritoneal biopsy was not performed.…”

Section: Discussionmentioning

confidence: 64%

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POEMS syndrome caused refractory ascites in a polycystic disease patient undergoing hemodialysis

Higuchi

Kamijo

Koyama

et al. 2003

Clinical and Experimental Nephrology

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A 60-year-old man with polycystic disease (PCD) undergoing hemodialysis was admitted to our hospital because of refractory ascites in September 2000. He had been diagnosed with probable chronic inflammatory demyelinating polyradiculopathy 6 months before admission. Though the ascites was bloody and exudative, the cytology was normal and cultures of bacteria and acid-fast bacillus were both negative. Hepatic venous outflow obstruction was excluded by several radiological examinations. Because of the presence of polyneuropathy, organomegaly, endocrine abnormality, M-protein, plasma cell dyscrasia, and skin lesions, POEMS, syndrome was diagnosed; this had caused the refractory ascites. Initial prednisolone therapy was effective for the refractory ascites, but it was not effective in preventing recurrence. He died due to cachexia in December 2000. This is a very rare case of the presence of both PCD and POEMS syndrome in a patient.

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Section: Discussionmentioning

confidence: 64%

“…7 The patient was given 55 mg of prednisolone orally every day from September 28, 2000. After the administration of prednisolone, his body weight remained at around 55 kg, the amount of ascites did not increase, and the generalized lymphadenopathy was attenuated (size of lymph nodes decreased from 1 to 3 cm to around 0.5 cm).…”

Section: Case Reportmentioning

confidence: 99%

POEMS syndrome caused refractory ascites in a polycystic disease patient undergoing hemodialysis

Higuchi

Kamijo

Koyama

et al. 2003

Clinical and Experimental Nephrology

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“…On biopsy, the peritoneum grossly appears normal but histological examination usually shows chronic inflammatory and mesothelial cells with a variable degree of fibrosis [10,11].…”

Section: Discussionmentioning

confidence: 99%

A Real Neglected Problem With a Grave Prognosis: Nephrogenic Ascites

et al. 2020

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Nephrogenic ascites is described as a clinical condition of refractory ascites in patients with end-stage renal disease (ESRD) on renal replacement therapy. This entity was first described in 1970. Many nephrologists do not believe in nephrogenic ascites. The underlying etiologies can be multifactorial including a combination of poor nutrition, inadequate dialysis and ultrafiltration, increased peritoneal membrane permeability, and overall uremia. The nephrogenic ascites is a rare syndrome and is often associated with a grave prognosis especially if it is not diagnosed early and treated. In the present study, we report a 27-year-old woman with past medical history of diabetes type 1 (diagnosed at age 11), ESRD secondary to diabetic nephropathy on hemodialysis (diagnosis in December 2017), bilateral diabetic retinopathy, ovarian cyst, hypertension, and anxiety who presented to the emergency department for evaluation of intractable abdominal pain, nausea and vomiting for 2-day duration. She was found to have large ascites. Diagnostic paracentesis was done and found to be exudative with serum ascites albumin gradient (SAAG) of 0.7. After detailed workup, hepatic, cardiac, infectious and malignant causes for ascites were ruled out. The diagnosis of ascites of nephrogenic origin was made. Given the patient's situation and her inability of self-care, she is not a good candidate for intra-abdominal dialysis. The patient has been treated conservatively with salt/fluid restriction and intensive hemodialysis with ultrafiltration.

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“…In a review [17] of nephro genic ascites, a serum-ascites albumin difference of less than 0.9 g/dl may be derived from high vascular perme ability resulting from peritoneal inflammation in at least some cases. Mauk et al [19] noted that microscopic ex amination of biopsied peritoneum from these patients often disclosed chronic inflammatory changes and mesothelial cell reaction along with varying degrees of fibro sis, although the peritoneum usually appeared normal. Therefore, the iron deposition, although unproven histo logically, might have played a role in changing the perme ability of the peritoneum, or in impairing subdiaphragmatic lymphatic outflow from the peritoneal cavity, both of which are presumed to be pathogenetic factors in nephrogenic ascites.…”

Section: Discussionmentioning

confidence: 99%

Treatment of a Patient with End-Stage Renal Disease, Severe Iron Overload and Ascites by Weekly Phlebotomy Combined with Recombinant Human Erythropoietin

Nomura¹,

Osawa²,

Karai³

1990

Nephron

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A 41-year-old hemodialyzed woman developed ascites and was found to have secondary iron overload. The dose ofadministered iron was approximately 11–12 g, and her serum ferritin level was 15,000 ng/ml (15,000 μg/l). There were no signs of congestive heart failure, fluid overload, or liver cirrhosis. A program of weekly phlebotomy combined with recombinant human erythropoietin (rhEPO) therapy was tried to eliminate the iron congestion. After 9 months of this therapy, about 5 g of iron had been removed. The ascites completely disappeared, and her serum ferritin level fell to 5,800 ng/ml (5,800 μg/l). This suggests that such combined therapy would be useful when iron overload must be corrected rapidly. Before therapy, the sterile ascitic fluid showed exudative characteristics with 3.7 g/dl (37 g/l) of total protein. The serum-ascites albumin difference was 0.6 g/dl (6 g/l), and the fluid contained 1,400 inflammatory cells/mm³ (1.4 × 10⁹/l). Notably, the serum-ascites albumin difference increased in parallel with iron elimination. These findings suggested that iron deposition may have played a role in changing the permeability of the peritoneum, or in impairing lymphatic drainage, both of which are presumed to be pathogenetic factors of nephrogenic ascites.

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Diagnosis and Course of Nephrogenic Ascites

Cited by 19 publications

References 8 publications

POEMS syndrome caused refractory ascites in a polycystic disease patient undergoing hemodialysis

POEMS syndrome caused refractory ascites in a polycystic disease patient undergoing hemodialysis

A Real Neglected Problem With a Grave Prognosis: Nephrogenic Ascites

Treatment of a Patient with End-Stage Renal Disease, Severe Iron Overload and Ascites by Weekly Phlebotomy Combined with Recombinant Human Erythropoietin

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