Renal amyloidosis and schistosomiasis

Barsoum, Rashad S.; Bassily, S.; Soliman, Mahmoud A.; Ramzy, Maher Fouad; Milad, M; Hassaballa, Abdel-Monem

doi:10.1016/0035-9203(79)90156-1

Cited by 27 publications

(17 citation statements)

References 22 publications

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“…Amyloidosis caused by schisto somal infection may stand as another pathogenic mecha nism in causing this glomerulopathy. Amyloidosis secon dary to schistosomal infection was reported in mice [14], rabbits [15] and humans [16]. Formation of amyloidosis on top of schistosomal infection may be explained by persis tent stimulation of the immunologically competent cells by schistosomal infection which will result in more primi tive or alternate pathways of protein synthesis leading to formation of amyloid [17].…”

Section: Discussionmentioning

confidence: 99%

<i>Schistosoma mansoni </i>Nephropathy in Syrian Golden Hamsters: Effect of Dose and Duration of Infection

Sobh

Moustafa

Ramzy

et al. 1991

Nephron

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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 a 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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Section: Discussionmentioning

confidence: 99%

<i>Schistosoma mansoni </i>Nephropathy in Syrian Golden Hamsters: Effect of Dose and Duration of Infection

Sobh

Moustafa

Ramzy

et al. 1991

Nephron

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“…Microalbuminuria may indicate the early phase of such a manifestation [17]. Proteinuria and nephrotic syndrome development is rare.…”

Section: Glomerulopathymentioning

confidence: 99%

Schistosomiasis

El-Garem¹

1998

Digestion

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Schistosomiasis is a man-made disease related to water contact in the agricultural fields and affecting millions of people in developing countries in the tropical and subtropical parts of Africa, Asia and South America. It is a bisexual trematode living in the portal blood and perivesical venous plexus. Its life cycle necessitates the presence of an intermediate host – a fresh water mollusc – that differs according to place. The pathogenetic stage is the ova that initiate an immunologically delayed hypersensitivity cell-mediated reaction in the organs where they are deposited. The liver, colon, urinary bladder and ureter are the main organs affected; however, any organ can be affected, even the skin and the brain. The review discusses the pathogenesis, pathology, diagnosis: parasitological and immunological, the clinical picture, treatment and control. The present status of the research work on vaccination is also presented.

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“…It has also been reported in rodent filariasis (Growel and Votava 1975). human schistosomiasis (Andrade and Rocha 1979, Barsoum et al 1979) anJ rodent and human alveolar hydatidosis (Ozeretskovskaya et al 1978. Ali-Khan et al 1983a& 1983b, Ali-Khan and Rausch 1987.…”

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confidence: 99%