Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve kidney, five biopsy and seven necropsy specimens, all from schistosomiasis mansoni patients were studied by light and immunoflurescent microscopy in an attempt to detect antigen in the glomerular walls. Deposits of IgM, IgG,I gA, IgE, complement C3 and fibrinogen were observered in most cases. Antigen was successfully detected in two cases(one biopsy and one necropsy specimen), both exhibiting proliferative glomerulonephritis. The only clinical manifestation was a slight proteinuria. IgG antibodies eluted from the sutopsy kidney homogenates showed specific binding mostly to Schistosoma mansoni gut, thus spggesting that the fixed antibodies (eluates) are, at least partially, consituted by antibodies similar to the anti-circulating antigen. These data reinfroce the hypothesis that renal injury in schistosomiasis is mediated through an immune complex disease.
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PMID:Human schistosomiasis: Schistosoma mansoni antigen detection in renal glomeruli. 6 11

Percutaneous needle biopsy of the kidney on eight nephrotic patients with Schistosoma mansoni and chronic Salmonella paratyphi A infection showed diffuse proliferative glomerular change in all biopsies. Capillary basement membrane was normal. Diffuse granular deposits were detected in the glomerular mesangial cells by direct staining with fluorescein labelled anti-IgG anti-IgM. No fluorescence was obtained with rabbit anti-Salmonella paratyphi A. After treatment with ampicillin and niridazole, a reduction of cellular proliferation and mesangial matrix expansion was observed. Simultaneously following treatment there occurred a dramatic clinical improvement with cessation of proteinuria and a return of plasma protein levels and serum complement (C3) to normal values.
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PMID:Renal biopsy in Schistosoma-Salmonella associated nephrotic syndrome. 82 21

In this work, 180 golden hamsters were infected with Schistosoma mansoni and 30 hamsters matched for age and sex served as controls. According to the number of injected cercariae, infected hamsters were divided into six main groups (20, 50, 100, 150, 200 and 250 cercariae). Each group was divided into five subgroups, according to the duration of infection after which animals were sacrificed (4, 6, 8, 12 and 24 weeks). Control and infected hamsters were subjected to laboratory evaluations (serum creatinine, blood urea nitrogen, cholesterol, albumin, total protein and urine protein concentration) and histopathologic examinations of kidney and liver tissues. A significant proteinuria, hypoalbuminemia and hypercholesterolemia was observed in schistosome infected (50 cercariae or more) but not in the controls and the group infected with 20 cercariae. There was significant correlation between these changes and duration of infection and the number of adult worm recovered from the mesenteric circulation at the end of the experiments. Histopathologic evaluation showed appearance of the circulating schistosome antigens, circulating anodic antigen (CAA) and circulating cathodic antigen (CCA), and of IgG glomerular deposits by the 6th week following infection; mesangial hypercellularity appeared early after infection (6-8 weeks), renal amyloid deposition appeared later (8-12 weeks). Egg antigens were not detected in the renal glomeruli. There was a significant correlation between the pathologic changes and duration of infection and the number of recovered adult worms from the mesenteric circulation. No histopathologic lesions were detected in controls and the group injected with 20 cercariae. A significant correlation was found between hepatic periportal fibrosis, amyloidosis and immune complex, deposition in the renal glomeruli. Hamsters did not tolerate infection with 150 cercariae or more for more than 12 weeks, and 20 cercariae caused no detectable glomerular disease. From this study, we concluded that S. mansoni infection causes nephropathy in the Syrian golden hamster. The disease became biochemically and histopathologically manifest by the 6th week following infection. Both immune complex deposition and renal amyloidosis stand as major pathogenic mechanisms. CAA and CCA are the major responsible antigens. Hepatic disease has an impact on the kidney lesion. 50 cercariae are the best dose to produce disease without early death of the animal. There is a significant correlation between the kidney disease and the duration and the load of S. mansoni infection.
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PMID:Schistosoma mansoni nephropathy in Syrian golden hamsters: effect of dose and duration of infection. 194 25

Schistosomiasis is a parasitic disease of the tropics which is estimated to affect up to 300 million people worldwide. In endemic areas the childhood age group has the highest prevalence and intensity of infection. There are several distinct species of schistosomes. The principal organ system involved in Schistosoma haematobium infection is the urinary tract since parasite eggs penetrate the bladder and are excreted in the urine. Hematuria, proteinuria, leukocyturia and symptoms like dysuria or nocturia are the most common clinical presentations. Heavily infected patients show obstructive uropathy of different severity which may lead to renal failure. Intestinal schistosomiasis is caused by Schistosoma mansoni infection. Initial symptoms can be diarrhea and blood-tinged stool. Chronic infection is characterized by fibrotic involvement of the liver and consecutive portal hypertension. The diagnosis of schistosomiasis depends on the demonstration of schistosome eggs in human excreta or biopsy material. Imported cases of schistosomiasis to Europe show an increasing tendency due to expanding international travel. Furthermore imported cases are usually not diagnosed until years after the patients have left an endemic area. The treatment of choice is a single dose of praziquantel 40 m/kg bodyweight resulting in cure rates of around 90% and considerable reversibility of pathological abnormalities due to schistosome infections.
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PMID:Schistosomiasis in childhood. 327 25

Ninety-eight Zimbabweans with glomerulonephritis characterised by nephrotic proteinuria were studied. There was no evidence to implicate Schistosoma mansoni or S. haemotobium in the aetiology, although schistosomiasis was diagnosed in 54 patients in the series. Similarly, Plasmodium malariae proved unimportant as a cause of the nephrotic syndrome, only one patient showing focal segmental glomerulosclerosis which was associated with subclinical quartan malarial infection. Nevertheless, infections were shown to play a major role in the genesis of glomerulonephritis which was associated with beta-haemolytic streptococcal, hepatitis B and syphilitic infection in 45 patients in the series. The major patterns of disease in childhood proved to be membranous glomerulopathy associated with hepatitis B antigenaemia. In young adults post-streptococcal proliferative glomerulonephritis constituted the commonest disease pattern. In older adult patients a miscellany of primary and secondary glomerulonephritides was encountered but proliferative glomerulonephritis, which was both idiopathic and streptococcus-related, predominated.
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PMID:Patterns of glomerulonephritis in Zimbabwe: survey of disease characterised by nephrotic proteinuria. 636 74

Thirty Syrian golden hamsters were infected with Schistosoma mansoni and 10 were used as negative controls. Hamsters were infected by 50 cercaria; 15 were treated by praziquantil in doses of 100 mg/kg at 12, 13, 14 and 15 weeks postinfection, and 15 hamsters were left as positive control. Five from each subgroup were sacrificed at 24, 28 and 32 weeks postinfection. Animals were subjected to weekly analysis for total plasma protein, serum creatinine, albumin, cholesterol, 24-hour urine volume, and urinary total protein excretion. At the end point, animals were sacrificed and the mesenteric venous plexus was explored for adult worms. Kidney and liver specimens were examined by light microscopy, immunofluorescence microscopy, and electron microscopy. Complete parasite eradication was achieved in treated animals. Although there were significantly higher plasma total protein, albumin, and lower cholesterol in the treated group, there were no significant differences in proteinuria or renal histopathologic changes between treated and untreated animals. We conclude that in golden hamsters, with complete and early parasite eradication no regression occurs in S. mansoni-related nephropathy. Moreover, we suggest that in this glomerulopathy, short exposure to an antigen may be sufficient to set in motion a cascade of events which is irreversible and which leads to permanent glomerular damage.
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PMID:Infectious glomerulopathy induced by a defined agent (Schistosoma mansoni): progression despite early elimination of the causal agent. 808 76

A case of nephrotic syndrome in which Schistosoma mansoni infection associated with membranoproliferative glomerulonephritis type 1 is reported. In endemic areas glomerulopathy secondary to Schistosoma mansoni has been described. Although not commonly seen in mainland United States, Schistosoma mansoni infection should be considered in the differential diagnosis of proteinuria in persons who have visited or are from endemic regions.
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PMID:Nephrotic syndrome associated with Schistosoma mansoni infection. 835 16

Thirty Syrian golden hamsters were infected with Schistosoma mansoni and 10 were used as negative controls. Hamsters were infected by 100 cercariae; 15 were treated by praziquantel in doses of 100 mg/kg at 12, 13, 14 and 15 weeks postinfection, and 15 hamsters were left as positive control. Five from each subgroup were sacrificed at 24, 28 and 32 weeks after infection. Animals were subjected to weekly analysis for total plasma protein, serum albumin and urinary total protein excretion. At the end point, animals were sacrificed and the mesenteric venous plexus was explored for adult worms. Liver and splenic specimens were examined by light microscopy, and immunofluorescence microscopy. Complete parasite eradication was achieved in the treated animals. Although, there were significantly higher plasma total protein and albumin in the treated group, there was no significant differences in proteinuria. Histopathological examination of liver specimens showed highly significant reduction of granulomas, CAA and CCA, while amyeloid deposition showed minimal reduction in treated animals. Histopathological examination of splenic specimens showed highly significant reduction of fibrosis, granulomas, CAA and CCA, while follicular hyperplasia and amyeloid deposition showed non significant reduction.
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PMID:Effect of anti-schistosomal treatment on schistosomal hepatic pathology: an experimental study in Syrian golden hamsters. 875 59

One hundred and twenty Syrian golden hamsters were infected with Schistosoma mansoni cercariae and 20 served as negative controls (group I). Of the S. mansoni-infected hamsters, 20 served as positive controls (group II) and 100 hamsters were treated for 12 weeks post-infection by loading with S. mansoni adult worm antigen. Animals were divided into groups according to the dose of adult worm antigen injected: group III (5-fold increase in circulating antigen concentration), group IV (10-fold increase), group V (20-fold increase), group VI (40-fold increase), and group VII (80-fold increase). Each of the groups was subdivided into four groups (sacrificed at 1, 2, 4 or 7 days after initiation of antigen loading or the corresponding time points in the case of the control groups). At sacrifice, blood and urine were obtained for laboratory assessment (serum creatinine, protein, albumin, cholesterol and urinary proteins). Kidney, liver and spleen tissue specimens were obtained for light, immunofluorescent and electron microscopic examinations. At sacrifice, significant proteinuria, hypoalbuminaemia and hypercholesterolaemia were observed in S. mansoni-infected hamsters when compared with negative control animals. Histopathologic assessment showed changes compatible with those previously reported, mainly immune complex glomerular deposits, mesangial proliferation and renal amyloid deposits. Significant laboratory improvement was observed in animals treated with antigen loading, especially those treated with 80-fold antigen excess and sacrificed at 7 days postinitiation of treatment. Histopathologic evaluation showed significantly less immune complex glomerular deposits, less mesangial hyperplasia, and less amyloid deposits in hamsters treated with antigen loading. It is concluded that induction of antigen excess by antigen loading induces biochemical and histopathologic regression of schistosomal-specific nephropathy in S. mansoni-infected Syrian golden hamsters.
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PMID:Schistosomal-specific nephropathy in Syrian golden hamsters: treatment by induction of antigen excess. 894 76

Health questionnaires and parasitologic examinations of urine and stool were performed upon a stratified random sample of 7,710 individuals from 1,109 households in 21 rural communities in Fayoum Governorate, Egypt in 1992 to investigate the prevalence of, risk factors for, and changing pattern of, infection with Schistosoma sp. in the governorate. A subset, every fifth household, or 1,038 subjects, had physical and ultrasound examinations to investigate prevalence of, and risk factors for, morbidity. The prevalence of S. haematobium ranged from 0% to 27.1% and averaged 13.7%. The geometric mean egg count (GMEC) was 10.0 eggs/10 ml of urine. Age-stratified prevalence and intensity of infection were 18-25% and 10-15 eggs/10 ml of urine in those 5-25 years of age. Schistosoma mansoni were detected in inhabitants of 13 communities, but 78.5% of the infections were focally present in a group of 4 satellite hamlets around a single village. The overall prevalence of S. mansoni in the governorate was 4.3% and the GMEC was 44.0 ova/g of stool. Risk factors for infection with either species were male gender, an age <20 years, living in smaller communities, and exposures to canal water by males. Histories of burning micturation, blood in the urine, or prior schistosomiasis and reagent strip-detected hematuria and proteinuria were risks for S. haematobium, but not for S. mansoni. Both urinary tract and higher grades of hepatic morbidity were rare. Obstructive uropathy was present in 6.3% of the subjects and was more common in males and older people. Ultrasonography-detected bladder lesions were present in 5.2% and correlated with S. haematobium only in younger subjects and in those with hematuria and proteinuria. The prevalences of hepatomegaly, splenomegaly, and periportal fibrosis (PPF) were associated with each other and increased with age and in males. Ultrasonography-detected hepatomegaly and splenomegaly were weakly associated with S. mansoni infections only in children. The prevalence of PPF was greater in the 4 communities with >25% S. mansoni infection rates in comparison with the 17 other villages and ezbas. Transmission of S. mansoni is focally well established in Fayoum, which also has the highest prevalence of S. haematobium in the governorates surveyed by the Epidemiology 1, 2, 3 Project. However, both urinary tract and hepatic morbidity are relatively rare in the governorate. This probably results from the long-standing schistosomiasis control program in Fayoum, which suppressed intensity more than prevalence of infection, leading to less community morbidity.
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PMID:The epidemiology of schistosomiasis in Egypt: Fayoum Governorate. 1081 1


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