Chronic glomerulonephritis associated with hepatosplenic schistosomiasis mansoni

Ramos, Eduardo Antônio Gonçalves; Andrade, Zilton A.

doi:10.1590/s0036-46651987000300008

Cited by 5 publications

(4 citation statements)

References 15 publications

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“…Arterial hypertension was observed in 37% of the cases in the SRS group, in 29.6% of the EGDS group, and 28% of the DSRS group, without a statistically significant difference. Even though some authors have described structural alterations of the kidney in schistosomiasis patients [70,71], the etiology of the hypertension is unknown. There are no data available to its incidence among patients who have not undergone surgery.…”

Section: Esophagogastric Devascularization With Splenectomymentioning

confidence: 99%

Portal hypertension in mansonic schistosomiasis

1991

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Mansonic schistosomiasis is an endemic disease in Brazil, with an estimated 10-12 million people infested. Among its clinical manifestations, the hepatosplenic form causes portal hypertension which, in turn, brings about severe digestive hemorrhage, the most serious complication of the disease. Normally, the patients are young, and have hepatosplenomegaly, hypersplenism without clinical manifestations, and slightly reduced hepatic function. The angiographic findings are characteristic, differing from those of hepatic cirrhosis. In Brazil, the definitive treatment for gastrointestinal hemorrhage is surgery, which should be done under elective conditions whenever possible. During a short period of time, known as the "risk period" (the time between the hemorrhagic episode and the surgery), propranolol has been used to prevent further bleeding. Surgical treatment is indicated only after the first episode, and never on a prophylactic basis. In 1977, a prospective, randomized trial was begun in order to assess the delayed results of the 3 surgical operations most widely used in this country. The study was interrupted after 94 patients had been operated on due to the high incidence of encephalopathy in the group who underwent classical splenorenal shunt. After a follow-up of at least 60 months and, at most, 130 months, the results showed that classical splenorenal shunt caused encephalopathy in 39.3% of the cases and distal splenorenal shunt in 14.8%. None of those submitted to esophagogastric devascularization with splenectomy developed encephalopathy. The 3 procedures showed similar rates of hemorrhagic recurrence.

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Section: Esophagogastric Devascularization With Splenectomymentioning

confidence: 99%

Portal hypertension in mansonic schistosomiasis

1991

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“…Nowadays other patterns, such as focal segmental glomeru- losclerosis, have also been described [3]. Ramos and Andrade [21] showed that the types of glomerulonephritis which predominantly involved the renal mesangium, such as the mesangioproliferative and membranoproliferative types, when taken together, are more frequent in hepatosplenic patients than in a control group. Immunofluorescence studies demonstrated deposits of IgG, IgM, and C3 chiefly in the mesangium in this pattern of glomerular changes.…”

Section: Discussionmentioning

confidence: 99%

Glomerular Detection of Schistosomal Antigen by Immunoelectron Microscopy in Human Mansonian Schistosomiasis

DeBrito

Nussenzveig²,

Carneiro³

et al. 1999

Int J Surg Pathol

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Schistosomal antigens (S. mansoni) were detected in glomeruli of nine patients with nephropathy and nephrotic syndrome by immunoelectron microscopy. The criteria for patients' selection were presence of intestinal schistosomiasis and absence of any surgical or other medical diseases, particularly lupus erythematosus, syphilis, and hepatitis B and C, which could explain the renal disease. When examined by light microscopy, kidney biopsies showed type I membranoproliferative glomerulonephritis in four patients, focal segmental glomerulosclerosis in two, and mesangioproliferative glomerulonephritis, membranous glomerulonephritis, and minimal change disease in one each of the remaining three patients. Immunofluorescence showed mainly immunoglobulin G (IgG), IgM, and different complement components (C3, Clq) deposits, particularly in the mesangial area, in eight patients. All patients had gold-labeled schistosomal antigen deposits in their glomeruli, chiefly in mesangial cells and matrix, along the glomerular membrane, and occasionally in the cytoplasm of epithelial cells. Although membranous glomerulonephritis has been rarely described in association with schistosomiasis and minimal change disease may be occasionally caused by an infectious disease like syphilis, the absence of definite experimental models and epidemiologic data suggests that coincidental pathologies without causal relationship with schistosomiasis cannot be ruled out to explain these findings.

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“…A variety of anatomopathological patterns of glomerular lesions have been associated with schistosomal glomerulopathy, due mainly to the intensity of infection, the emergence of portal hypertension and the association with infections by other pathogens (van Marck et al 1977, Ramos & Andrade 1987, Zeid et al 1994, Chisty et al 2002, Barsoum 2004). The diversity observed among the lesions associated with schistosomiasis motivated a clinicopathologic classification of schistosomal glomerulopathies, endorsed in 1992 by the African Association of Nephrology (AFRAN) (Barsoum 2004), that recognized the five categories of glomerular diseases shown in Table I.…”

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confidence: 99%