Membranoproliferative glomerulonephritis in a carcinoma with unknown primary: an autopsy study.

Kidney disease frequently complicates malignancy and its treatment. Although many solid and hematologic cancers may involve the renal parenchyma, clinical sequelae are usually not prominent. Published reports cite membranous nephropathy as the most common malignancy-associated glomerulopathy, occurring with many carcinomas and occasionally with leukemia and lymphoma followed by minimal change disease. Rarely membranoproliferative glomerulonephritis (MPGN) has been reported in patients with malignancy. The mechanism by which malignancy induces disease remains unproved, but may involve deposition of tumor antigen in the subepithelial space with in situ immune complex formation and subsequent complement activation. Treatment of the underlying malignancy may lead to resolution of nephrotic syndrome, lending indirect support to this theory. We report a rare autopsy case of a patient with metastatic carcinoma (with unknown primary) associated with MPGN. The association between MPGN and metastatic carcinoma with unknown primary is uncommon and has not been previously reported in the literature.

Frequency and role of hepatitis-C virus and type II cryoglobulinemia in membranoproliferative glomerulonephritis.

BACKGROUND: Many studies have claimed a major role of chronic hepatitis-C virus (HCV) infection in immune-mediated diseases such as membranoproliferative glomerulonephritis (MPGN). Chronic HCV infection is also known to produce essential mixed cryoglobulinemia (EMC), which in turn may manifest as vasculitis and cryoglobulinemic MPGN. OBJECTIVE: The aim of the study therefore, was to determine frequency of association and pathogenetic role of HCV infection as well as that of EMC in MPGN patients. METHODS: Fifty-three adult patients of MPGN were studied for HCV, HBsAg, EMC, C3, anti-nuclear antibody (ANA), rheumatoid factor serologically. Histopathology, immunofluorescence (IF) were conducted in all patients and electron microscopy (EM) in those who were found HCV positive. Simultaneously 37 follow-up patients of HCV associated chronic hepatitis were investigated for EMC, renal functions and urinalysis done for evidence of glomerulonephritis (GN). RESULTS: Thirteen percent MPGN patients were HCV positive, however, no viral particle could be seen in electron microscopy in glomeruli of these patients. There was no serologic evidence of HCV induced immune complex GN. None of the MPGN patients showed cryoglobulinaemia. Similarly none from HCV associated chronic hepatitis group had EMC nor showed evidences of glumerulonephritis. CONCLUSION: Thirteen percent of adult MPGN patients in north India were seropositive for HCV, indicating significant association. However, clear evidence in favour of its pathogenetic role was lacking in our study. Secondly, this study reveals that MPGN is non-cryoglobulinemic and HCV is not a major cause in our population compared to what is reported from other countries. These observations need confirmation by a larger study.

A case of membranoproliferative glomerulonephritis associated with a hydatidiform mole

We treated a 54-year-old woman who was suffering from membranoproliferative glomerulonephritis associated with a complete type of hydatidiform mole. The renal manifestations were proteinuria and hematuria. A renal biopsy, performed before gynecologic management, disclosed focal and segmental subendothelial deposits with a proliferation of the mesangial cell and showed irregularly thickened capillary loops by light and electronmicroscoy. Genralized edema, proteinuria and hematuria were completely recovered by suction and curettage of the hydatidiform mole with prophylactic chemotherapy. The clinical manifestation of earlier presented 3 cases have been the nephrotic syndrome. The common feature of them was a complete remission of the nephropathy after the removal of the hydatidiform mole. The relationship between the hydatidiform mole and glomerulonephritis remains unresolved at present. But we concluded that the hydatidiform mole might be a cause of glomerulonephritis in this case.

Ultrastructural alterations in glomerulophathy associated with hydatidosis in sheep

En el presente trabajo se investigaron las alteraciones ultraestructurales en el glomérulo renal de ovejas con hidatidosis. Utilizando microscopía electrónica de transmisión, fueron examinadas muestras renales de 39 ovejas, 34 de ellas con hidatidosis y 5 sin la parasitosis. Adicionalmente, fue realizado un estudio bioquímico a través de dosaje sérico de creatinina, úrea, proteínas totales y albumina. Las alteraciones ultraestructurales identificadas fueron la presencia de depósitos densos mesangiales, subendoteliales e intramembranosos; proliferación de células mesangiales con áreas de esclerosis segmentaria e interposición de células mesangiales con formación de neo-membrana. Durante el estudio bioquímico se observó un aumento significativo de proteínas totales séricas en el grupo experimental en relación con el de control. El estudio demostró que la glomerulonefritis asociada a hidatidosis en ovinos puede ser clasificada en 4 categorías: lesiones mínimas, glomerulonefritis mesangial, glomerulonefritis segmentaria y focal, y glomerulonefritis membranoproliferativa, siendo predominantemente proliferativa y mesangial

Mesangial proliferative glomerulonephritis in chronic obstructive pulmonary disease.

Ten patients of chronic obstructive pulmonary disease were studied for changes in ultrastructure of the glomeruli, serum immunoglobulin and complement levels. The glomeruli showed proliferation in the mesangium in 90% patients and electron dense deposits in the mesangium in 30% patients. IgA and IgG were usually elevated whereas complements were usually depressed in most of these patients. It is suggested that repeated respiratory infections in these subjects may be responsible for mesangioproliferative type of glomerulonephritis, high IgA and IgG levels. The complements are activated and they take part in immune complex formation getting deposited in mesangium.

Glomerulonefritis membranoproliferativa y recidiva en trasplante renal: reporte de un caso y revisión de la literatura / Membranoproliferative glomerulonephritis and recidivation in renal transplantation: Report of one case and literature review

La glomerulonefritis membranoproliferativa es causa del 5 a 7 de insuficiencia renal crónica terminal y tiene una alta incidencia de recidiva en el trasplante renal; los hallazgos de de Hipertensión Arterial Sistémica, proteinuria, edema y deterioro progresivo de la función renal sugieren el diagnóstico. Existe una alta correlación con niveles de complemento y factor C 3 nefrítico. El diagnóstico definitivo se basa en los hallazgos histológicos característicos como: engrosamiento de la membrana basal glomerular, proliferación mesangial y formación de dobles contornos, en la microscopía de luz, así como acúmulo de depósitos densos subendoteliales (tipo I) o endoteliales (Tipo II) en microscopía electrónica. La recidiva de la glomerulonefritis membranoproliferativa tipo I es del 20 y 1/3 de estos pacientes pierden el injerto. En el caso de la tipo II la recidiva es del 80 y únicamente 10 pierden el riñón trasplantado. No existe ninguna correlación con niveles de complemento o factor C 3 nefrítico. No existe ningún tratamiento específico para detener la enfermedad. Algunos reportes sugieren que lo más importante es controlar los mecanismos no inmunológicos de progresión del daño renal, tales como hipertensión arterial sistémica, proteinuria e hipercolesterolemia

Estudo, ao microscópio óptico e eletrônico, do rim de cäes natural e experimentalmente infectados com Leishmania (Leishmania) chagasi / Optical and electron microscopic study of the kidney of dogs naturally and experimentally infected with Leishmania (Leishmania) chagasi

Os autores estudaram os rins de 4 cäes infectados con Leishmania (Leishmania) chagasi. Dois animais (um macho e uma fêmea) naturalmente infectados foram sacrificados 18 meses após sua permanencia no laboratório. Dois machos foram inoculados por via endovenosa, com 1x10***6 promastigotas da cepa MHO/BR/70/BH46 e sacrificados após 18 meses e 2 anos, respectivamente. Em todos os animais os rins estavam lesados. As alteraçöes encontradas foram: (1) glomerulonefrite mesangioproliferativa focal ou difusa, com pronunciada hipertrofia e hiperplasia das células mesangiais e com alargamneto da matriz; (2) espessamento da membrana basal com depósitos eletrodensos; (3) nefrite intersticial intertubular crônica com exsudaçäo plasmocitária intensa. (4) degeneraçäo albuminosa dos túbulos renais. Baseados nos achados os autores discutem os prováveis mecanismos patogenéticos