Renal transplant patients with preformed anti-HLA antibodies: early biopsy findings and clinical outcomes / Pacientes transplantados renais com anticorpos anti-HLA pré-formados: achados precoces de biópsia e desfechos clínicos

Abstract Introduction: Renal fibrosis is the end point of a process that begins at transplant, with ischemia reperfusion and early inflammation, and progresses over time with immunological and non-immunological phenomena. Early identification of morphological markers and intervention could improve graft function and survival. Objective: to evaluate the correlation between intensity and specificity of pre-transplant anti-HLA antibodies and kidney allograft pathology in order to identify early risk factors or markers of allograft dysfunction. Methods: A retrospective cohort of kidney transplant recipients with pre-transplant anti-HLA antibodies who underwent graft biopsy within the first two years post-transplant was divided into two groups according to the specificity of anti-HLA antibodies: nonspecific (non-DSA, n = 29) and specific (DSA+, n = 16). Kidney graft pathology, renal function, and proteinuria were analyzed. Results: general characteristics were similar in both groups, except for the higher dose of thymoglobulin in DSA+ group (p < 0.05). The non-DSA group had higher scores for glomerulosclerosis, interstitial inflammation (i) and interstitial fibrosis (ci) (p < 0.05) and higher incidence of cell-mediated acute rejection. No statistical difference in incidence of antibody-mediated rejection, renal function, and proteinuria was observed during follow up. Discussion and conclusions: the difference in inflammation scores and interstitial fibrosis may be associated to the higher incidence of acute cell-mediated rejection and polyomavirus nephropathy in the Non-DSA group. We also should take into account the protective effect of higher doses of thymoglobulin, reducing ischemia reperfusion injury in the DSA+ group. The short follow-up might have been insufficient to detect long-term changes in allograft tissue, renal function, and proteinuria.

Resumo Introdução: A fibrose renal é o desfecho de um processo iniciado no transplante, com reperfusão, isquemia e inflamação precoce, que progride ao longo do tempo com fenômenos imunológicos e não imunológicos. A identificação de marcadores morfológicos e a intervenção precoce poderiam melhorar a função e a sobrevida do enxerto. Objetivo: Avaliar a correlação entre intensidade e especificidade de anticorpos anti-HLA pré-transplante alterações histológicas do enxerto renal, de forma a identificar fatores de risco ou marcadores de disfunção precoces do aloenxerto. Métodos: O presente estudo incluiu uma coorte retrospectiva de receptores de transplante renal sensibilizados com anticorpos anti-HLA no pré-transplante submetidos a biópsia de enxerto nos primeiros dois anos após o transplante. Os grupos foram divididos em função da especificidade dos anticorpos anti-HLA: sem anticorpos doador-específicos (não-DSA, n = 29) e com anticorpos doador-específicos (DSA+, n = 16). Alterações histológicas do enxerto renal, função renal e proteinúria foram analisados. Resultados: Os dois grupos tinham características gerais semelhantes, exceto pela dose mais elevada de timoglobulina administrada nos indivíduos do grupo DSA+ (p < 0,05). O grupo não-DSA teve escores mais elevados de glomeruloesclerose, inflamação intersticial (i) e fibrose intersticial (ci) (p < 0,05), além de maior incidência de rejeição celular aguda (RCA). Não foi observada diferença estatística na incidência de rejeição mediada por anticorpos, função renal ou proteinúria durante o seguimento. Discussão e Conclusões: A diferença nos escores de inflamação e fibrose intersticial pode estar associada à maior incidência de RCA e nefropatia por poliomavírus no grupo não-DSA. Devemos considerar ainda o efeito protetor das doses mais elevadas de timoglobulina na redução da lesão por isquemia-reperfusão no grupo DSA+. O curto período de seguimento pode ter sido insuficiente para detectar alterações de longo prazo no tecido do aloenxerto, função renal e proteinúria.

Evaluation of frequency of autoimmune hepatitis autoantibodies in children with type 1 diabetes / Frecuencia de anticuerpos de hepatitis autoinmune en niños con diabetes tipo I

Background: Diabetes mellitus type 1 (T1DM) is one of the childhood diseases with growing prevalence. Various accompanying autoimmune diseases were seen with type 1 diabetes. The most common autoimmune diseases with T1DM are autoimmune thyroiditis and celiac disease. In some reports, autoimmune hepatitis has been reported in association with DM-1. Objectives: The aim of this study was to evaluate autoimmune hepatitis autoantibodies in children with T1DM. Materials and methods: In this crosssectional study, 202 children with T1DM were evaluated (47.5% were males and 52.5% were girls). Liver enzymes, autoimmune hepatitis related autoantibodies such as anti-nuclear antibodies (ANA), anti-smooth muscle (ASMA) and anti liver and kidney microsomal antibodies (LKM-1) were measured. Liver ultrasound was done for participants and biopsy of liver was taken for children with increased echogenicity of the liver, hepatomegaly or elevated liver enzymes. Results analyzed by statistical software spss-16, Descriptive statistics and chi-square test, paired T-TEST. Level of less than 5% was considered statistically significant. Results: In 6 patients ANA and in 4 patients (2%) ASMA was positive,1 patient was ASMA positive but ANA negative. None of the patients were Anti LKM-1 positive. 3 patients had positive ANA and ASMA, and increased liver echogenicity on ultrasound simultaneously. Histological evaluation was showed that 2 patients had findings in favor of autoimmune hepatitis. Conclusion: Auto antibodies were positive in 10 cases. ANA was positive in 6 (2.97%) of all cases. ASMA was positive in 4 (1.98%) cases. Increased echogenicity was found in 3 cases. Histological evaluation showed 2 patients had biopsy confirmed autoimmune hepatitis. AIH-2 was not seen among our cases.

Antecedentes: La diabetes mellitus tipo 1 (DM1) es una de las enfermedades infantiles con mayor prevalencia. Se observaron varias enfermedades autoinmunes acompañantes con diabetes tipo 1. Las enfermedades autoinmunes más comunes con DM1 son la tiroiditis autoinmune y la enfermedad celíaca. En algunos reportes, se ha encontrado hepatitis autoinmune en asociación con DM-1. Objetivos: El objetivo de este estudio fue evaluar los autoanticuerpos de hepatitis autoinmunes en niños con DM1. Materiales y métodos: En este estudio transversal, se evaluaron 202 niños con DM1 (47,5% eran hombres y 52,5% eran niñas). Se midieron las enzimas hepáticas, los autoanticuerpos autoinmunes relacionados con la hepatitis, como los anticuerpos antinucleares (ANA), el músculo liso (ASMA) y los anticuerpos microsomales hepáticos y renales (LKM-1). Se realizó una ecografía hepática para los participantes y se tomó una biopsia del hígado para niños con mayor ecogenicidad del hígado, hepatomegalia o enzimas hepáticas elevadas. Los resultados fueron analizados por el software estadístico spss-16 usando estadística descriptiva y prueba de chi-cuadrado, T-TEST pareado. Se consideró estadísticamente significativo un nivel menor del 5%. Resultados: En 6 pacientes con ANA y en 4 pacientes (2%) ASMA fue positiva, 1 paciente fue ASMA positiva pero ANA negativa. Ninguno de los pacientes fue anti LKM-1 positivo. 3 pacientes tuvieron ANA y ASMA positivas, y aumentaron la ecogenicidad hepática en la ecografía simultáneamente. La evaluación histológica mostró que 2 pacientes tenían hallazgos a favor de la hepatitis autoinmune. Conclusión: Los autoanticuerpos fueron positivos en 10 casos. ANA fue positivo en 6 (2,97%) de todos los casos. La ASMA fue positiva en 4 (1,98%) casos. Se encontró mayor ecogenicidad en 3 casos. La evaluación histológica mostró que 2 pacientes tenían biopsia confirmada de hepatitis autoinmune. AIH-2 no fue visto entre nuestros casos.

Presença de aglutininas anti-Leptospirasppem bovinos abatidos em frigorífico no extremo sul do estado da Bahia e fatores de risco associados / Presence of agglutinins anti-Leptospira in slaughtered bovine in the extreme south of Bahia and risk factors

INTRODUÇÃO: A bovinocultura no Brasil é uma das principais atividades que compõem o agronegócio do país, sendo o segundo maior rebanho do mundo. O estado da Bahia tem papel importante neste setor, sendo o 10º estado em número de animais abatidos no Brasil em 2015 (4,4% dos animais abatidos no Brasil). Mesmo com índices animadores, a produtividade da pecuária baiana ainda é baixa, tendo as doenças infecciosas e parasitárias como principais entraves à sua melhora. Dentre essas doenças a leptospirose apresenta uma prevalência de 45,42% nos bovinos no estado da Bahia em prévio inquérito. OBJETIVOS: Assim, o presente projeto teve como objetivo: i) analisar a sororeatividade contra Leptospira de bovinos abatidos em estabelecimento com serviço de inspeção federal, no estado da Bahia, utilizando o teste microaglutinação (MAT), ii) avaliar qual o sorovar predominante na população animal pesquisada, iii) avaliar os rins dos animais abatidos em estabelecimento com serviço de inspeção federal, no estado da Bahia quanto a presença de lesões macroscópicas e a sua associação com as reações positivas ao MAT, vi) avaliar possíveis fatores de risco que poderão propiciar o desencadeamento da infecção por Leptospira. Foram analisados soros de 400 bovinos abatidos...

INTRODUCTION: cattle raising in Brazil is one of the activities that comprise the agribusiness of the country, the second largest herd in the world. The state of Bahia has an important role in this sector, being the 10th state in the number of animals slaughtered in Brazil in 2015 (4.4% of the animals slaughtered in Brazil). Despite encouraging rates, productivity of the Bahian livestock is still low, and infectious and parasitic diseases as major barriers to improvement. Among these diseases leptospirosis has a prevalence of 45.42% in cattle in the state of Bahia in a previous survey. OBJECTIVES: The present project aimed to: i) analyze the seroreactivity against Leptospira from bovine animals slaughtered in establishments with federal inspection service in the state of Bahia, using the microscopic agglutination test (MAT), ii) assess what the predominant serovar in animal population studied, iii) evaluate the kidneys of animals slaughtered in an establishment with federal inspection service in the state of Bahia and the presence of gross lesions and their association with the positive reactions to the MAT, vi) evaluate possible risk factors that may promote the onset of Leptospira infection. 400 slaughtered cattle sera were analyzed...

Detección de antígenos del virus del dengue en tejidos post mórtem / Detection of dengue virus antigen in post-mortem tissues

El panorama epidemiológico del dengue ha empeorado durante la última década. Las dificultades para prevenir su transmisión, así como la ausencia de una vacuna o tratamiento específico, lo convierten en un riesgo que desafía las medidas de salud pública y desborda la capacidad de los centros de salud y los sistemas de investigación a muchos niveles. Actualmente, la mayoría de los estudios sobre la patogenia de la infección centran su atención en la respuesta inmunitaria de las células T casi exclusivamente en infecciones secundarias y están dirigidos a identificar los mecanismos implicados en el desarrollo de la permeabilidad vascular y de los eventos hemorrágicos que lo acompañan. En este reporte se describe el caso de una menor de 45 días de edad con signos clínicos de dengue grave, cuyo diagnóstico se confirmó por reacción en cadena de la polimerasa de transcripción inversa en muestras de tejido post mórtem y por herramientas de apoyo diagnóstico de inmunohistoquímica, las cuales detectaron antígenos virales en todos los órganos obtenidos en la necropsia. Este caso subraya la importancia del estudio de las infecciones primarias asociadas a dengue grave, particularmente en niños, en quienes es más probable el desarrollo de la forma grave de la enfermedad sin una infección previa, y, además, pone de relieve la importancia de un diagnóstico que no se limite a las muestras de tejido hepático en el estudio de la patogenia de la infección viral.

The epidemiological situation of dengue has worsened over the last decade. The difficulties in preventing its transmission and the absence of a vaccine or specific treatment have made dengue a serious risk to public health, health centers and research systems at different levels. Currently, most studies on the pathogenesis of dengue infection focus on the T-cell immune response almost exclusively in secondary infections and are aimed at identifying the mechanisms involved in the development of vascular permeability and bleeding events that accompany the infection. This report describes the case of a baby girl less than 45 days of age with clinical signs of severe dengue, whose diagnosis was confirmed by reverse transcription polymerase chain reaction in post-mortem tissue samples and by the ancillary diagnostic use of immunohistochemistry, which detected viral antigens in all organs obtained at autopsy. This case highlights the importance of studying primary infections associated with severe dengue, particularly in children, who are more likely to develop the severe form of the disease without previous infection, and it further stresses the importance of a diagnosis that should not be based solely on the examination of liver tissue samples when studying the pathogenesis of the viral infection.

Evaluation of renal function and immune system cells in elderly individuals from São Paulo City

OBJECTIVES: Both renal function and immune system function decline with age. Although controversial, a significant number of studies have shown that the decline in kidney function is associated with the worsening of the immune system. These findings are reinforced by the increased susceptibility to infections and deficient immunization coverage after vaccination both in patients with chronic renal disease and in elderly individuals. Our objective was to evaluate a non-institutionalized elderly population from São Paulo City and correlate the estimated glomerular filtration rate with the percentage of lymphocytes in circulation. METHODS: A random population of 237 individuals (107 men and 130 women), ranging in age from 60 to 101 years, who were enrolled in the Health, Well-Being and Aging Study was evaluated for renal function (Modification on Diet in Renal Disease formula) and lymphocyte percentage (flow cytometry). RESULTS: Aging was associated with a decrease in the estimated glomerular filtration rate in both male and female individuals. We did not identify a significant correlation between the estimated glomerular filtration rate and either the percentage of CD4, CD8, and B cells or CD4/CD8 ratio. The median percentage of CD8+ T cells was significantly lower in individuals with an estimated glomerular filtration rate >60 mL/min/1.73 m². CONCLUSIONS: In this study, no statistical correlation was found between the estimated glomerular filtration rate and either the lymphocyte phenotype (CD4+,CD8+, and CD19+ cells) or the CD4/CD8 ratio in blood.

IgA nephropathy: an update on pathogenesis and classification

IgA nephropathy is a primary glomerulopathy characterized by deposition of IgA containing immune deposits in the kidney. Its diagnosis is based on histopathologic and immunoflourescence studies on renal biopsy. The disorder is poorly understood. This review is focused on updates regarding its pathogenesis and discussion on a new proposed histopathological classification of IgA nephropathy

Role of IL-1alpha in Cisplatin-Induced Acute Renal Failure in Mice

BACKGROUND/AIMS: For unknown reasons, caspase-1 -/- mice, protected against cisplatin-induced acute renal failure (ARF), are deficient in interleukin (IL)-1alpha. We thus asked whether IL-1alpha deficiency underlies the mechanism of protection against cisplatin-induced ARF in these mice. METHODS: Cisplatin (30 mg/kg) was injected intraperitoneally into wild-type C57BL/6 mice to produce a cisplatin-induced model of ARF. IL-1alpha was measured in control vehicle- and cisplatin-treated wild-type animals. We also examined whether IL-1alpha -/- mice were similarly protected against cisplatin-induced ARF. Additionally, infiltration of CD11b- and CD49b-positive cells, as markers of macrophages, natural killer, and natural killer T cells (pan-NK cells), was investigated in wild-type and IL-1alpha -/- mice. RESULTS: Compared with vehicle-treated mice, renal IL-1alpha increased in cisplatin-treated wild-type mice beginning on day 1. IL-1alpha -/- mice were shown to be protected against cisplatin-induced ARF. No significant difference in the infiltration of neutrophils or CD11b- and CD49b-positive cells were observed between wild-type and IL-1alpha -/- mice. CONCLUSIONS: Mice deficient in IL-1alpha are protected against cisplatin-induced ARF. The lack of IL-1alpha may explain, at least in part, the protection against cisplatin-induced ARF observed in caspase-1 -/- mice. Investigation of the protective mechanism (s) in IL-1alpha -/- mice in cisplatin-induced ARF merits further study.

Immunohistochemical study for the diagnosis of Alport's syndrome.

BACKGROUND: Alport's syndrome (AS) is the most common cause of inherited glomerular disease in Thailand. The majority of cases show X-linked inheritance, which is caused by mutations in the gene coding for the alpha5 chain of type IV collagen in the glomerular basement membrane (GBM) and epidermal basement membrane (EBM). Such mutation usually leads to a reduction in protein amount, thus, immunohistochemical studies have been considered in diagnostic evaluation. OBJECTIVE: To study the expression of alpha[IV] collagen chains in the skin as an alternative approach to diagnose AS. MATERIAL AND METHOD: Eleven unrelated probands with proven AS, 7 relatives with abnormal urinalysis, 4 suspected individuals, and 8 normal controls were enrolled. A punch skin biopsy and immunofluorescence staining of the tissue specimens for alpha1, alpha3 and alpha5[IV] collagen chains was performed. RESULTS: The alpha5[IV] chain was absent in the EBM in all male AS patients while a discontinuing pattern was observed in all females except one. The findings are specific for AS with a sensitivity of 91%. Studies in relatives and suspected individuals also confirmed the advantage of this approach as demonstrated by the absence and discontinuation of alpha5[IV] staining in all males and females, respectively. We also analyzed their expressions in the kidney tissue and demonstrated abnormal alpha3 and alpha5[IV] staining in five of six samples. CONCLUSION: Immunohistochemical study of the skin should be used as a screening method in patients suspected of AS, as it is much less invasive. Moreover, it is a useful adjunct to conventional examination of biopsied renal tissue.

Interleukin 2 receptor expression in renal biopsies and the diagnosis of acute allograft rejection.

The aim of the study is to test the diagnostic usefulness of assessing interleukin 2 receptor (IL2R) expression in infiltrating lymphocytes in renal biopsies from patients with suspected acute renal allograft rejection and to compare the NIH-CCTT and the Banff 97 systems of classifying the histopathologic changes in acute renal allograft rejection. The expression of interleukin 2 (IL2) and IL2R, as shown immuno-histochemically, is the final step in T cell mediated acute renal allograft rejection. Renal biopsies obtained from 40 patients clinically suspected to have early acute allograft rejection were examined histologically to diagnose acute allograft rejection and classified by the two systems. Frozen sections of the biopsies were stained with specific antibody for the presence of IL2R. 31 of the 40 patients were histologically and clinically confirmed to have acute allograft rejection. There was significant correlation with this diagnosis and the demonstration of IL2R on infiltrating lymphocytes. The CCTT system of grading correlated better with the presence of IL2R and the confirmed diagnosis of acute allograft rejection. The immunohistochemical demonstration of IL2R is a useful adjunct in the evaluation of biopsies suspected to show changes of acute cellular rejection. Since IL2 expression reflects the relative proportion of activated lymphocytes in the cellular infiltrate, it is proposed that the degree of IL2 expression may reflect the response of the use of monoclonal antibodies (Humanised/Chimaerised) as anti rejection therapy.

Correlation between the renal C1q deposition and serum anti-C1q antibody: a potential role of anti-C1q antibody in lupus nephritis.

The anti-C1q antibody has been shown to be associated with lupus patients with renal involvement. We conducted a study to determine the relationship between the serum anti-C1q titer and the renal deposition of C1q. The serum anti-C1q was measured in 26 healthy controls and 47 systemic lupus erythematosus (SLE) patients who were divided into 2 groups as non-nephritis and nephritis SLE. We analyzed the relationship between the anti-C1q titers and SLE, renal C1q staining and the WHO classification for lupus nephritis. The result revealed that the serum anti-C1q was present in 50.8% of the SLE patients, that its levels in those with renal involvement were significantly higher than in the normal control group (61.540 +/- 87.720 U/ml vs 15.750 +/- 2.530 U/ml, p = 0.005). Besides, the serum anti-C1q levels were higher in the patients with lupus nephritis with C1q deposition in the kidney tissue (66.038 +/- 91.141 U/ml vs 16.652 +/- 3.097 U/ml, p < 0.01). There seems to be evidence supporting that the autoantibody anti-C1q might play a pathogenic role in lupus nephritis.

Detection of immunoglobulin G in the lung and liver of hamsters with visceral leishmaniasis

Several organs are affected in visceral leishmaniasis, not only those rich in mononuclear phagocytes. Hypergammaglobulinemia occurs during visceral leishmaniasis; anti-Leishmania antibodies are not primarily important for protection but might be involved in the pathogenesis of tissue lesions. The glomerulonephritis occurring in visceral leishmaniasis has been attributed to immune complex deposition but in other organs the mechanism has not been studied. In the current study we demonstrated the presence of IgG in the lung and liver of hamsters with visceral leishmaniasis. Hamsters were injected intraperitoneally with 2 x 10(7) amastigotes of Leishmania (Leishmania) chagasi and the presence of IgG in the liver and lung was evaluated at 7, 15, 30, 45, 80 and 102 days postinfection (PI) by immunohistochemistry. The parasite burden in the spleen and liver increased progressively during infection. We observed a deposit of IgG from day 7 PI that increased progressively until it reached highest intensity around 30 and 45 days PI, declining at later times. The IgG deposits outlined the sinusoids. In the lung a deposit of IgG was observed in the capillary walls that was moderate at day 7 PI, but the intensity increased remarkably at day 30 PI and declined at later times of infection. No significant C3 deposits were observed in the lung or in the liver. We conclude that IgG may participate in the pathogenesis of the inflammatory process of the lung and liver occurring in experimental visceral leishmaniasis and we discuss an alternative mechanism other than immune complex deposition

CD4+ T cells participate in the nephropathy of canine visceral leishmaniasis

Renal involvement in visceral leishmaniasis (VL) is very frequent. The renal lesions of humans and dogs are similar but their pathogenesis has not been clearly elucidated. There is growing evidence that the cellular immune response is involved in the pathogenesis of immunologically mediated glomerulonephritis. Since T cells could participate in the pathogenesis of nephropathy, in the present study we investigated the possible involvement of CD4+ and CD8+ T cells in the nephropathy of canine VL. Six dogs naturally infected with Leishmania (Leishmania) chagasi from the endemic area in the Northeast of Brazil, the town of Teresina in the State of Piauí, were studied. An expressive inflammatory infiltrate of CD4+ T cells both in glomeruli and in interstitium was present in 4 animals and absent in 2. CD8+ T cells were detected only in one animal. CD4+ T cells alone were observed in 3 animals; when CD8+ T cells were present CD4+ T cells were also present. CD4+ T cells were observed in cases of focal segmental glomerulosclerosis, diffuse membranoproliferative glomerulonephritis, diffuse mesangial proliferative glomerulonephritis and crescentic glomerulonephritis. CD8+ T cells were present only in a case of crescentic glomerulonephritis. Leishmania antigen was detected in glomeruli and in interstitial inflammatory infiltrate in 4 animals and immunoglobulins were observed in 4 dogs. In this study we observed that T cells, in addition to immunoglobulins, are present in the renal lesion of canine VL. Further studies are in progress addressing the immunopathogenic mechanisms involving the participation of immunoglobulins and T cells in canine VL nephropathy

Immune complex mediated lesions in experimental Kala azar: an ultrastructural study.

Immune complexes play an important role in causation of renal lesions in various diseases. Circulating immune comlexes (CIC) are described in Kala azar. Role of CIC in pathogenesis of Kalaazar is discussed in present study. BALB/C mice were experimentally infected with L. donovani promastigotes. After visceralisation of infection, sera and kidneys of infected mice were preserved. Leishmanial antigen specific CIC could be demonstrated in 100% of infected mice by PEG ELISA, while they were absent in control mice. Ultrastructural pattern of renal lesions in infected mice showed presence of focal small electron dense deposits in glomerular basement membrane and subepithelial space, resembling immune complexes (humps). Rarely subendothelial and mesangial hypercellularity was present. These findings point towards a definite role of CIC in pathogenesis of renal lesions in Kalaazar.

Glycosphingolipid antigens from Leishmania (L.) amazonensis amastigotes. Binding of antiglycosphingolipid monoclonal antibodies in vitro and in vivo

Specific glycosphingolipid antigens of Leishmania (L.) amazonensis amastigotes reactive with the monoclonal antibodies (MoAbs) ST-3, ST-4 and ST-5 were isolated, and their structure was partially elucidated by negative ion fast atom bombardment mass spectrometry. The glycan moieties of five antigens presented linear sequences of hexoses and N-acetylhexosamines ranging from four to six sugar residues, and the ceramide moieties were found to be composed by a sphingosine d18:1 and fatty acids 24:1 or 16:0. Affinities of the three monoclonal antibodies to amastigote glycosphingolipid antigens were also analyzed by ELISA. MoAb ST-3 reacted equally well with all glycosphingolipid antigens tested, whereas ST-4 and ST-5 presented higher affinities to glycosphingolipids with longer carbohydrate chains, with five or more sugar units (slow migrating bands on HPTLC). Macrophages isolated from footpad lesions of BALB/c mice infected with Leishmania (L.) amazonensis were incubated with MoAb ST-3 and, by indirect immunofluorescence, labeling was only detected on the parasite, whereas no fluorescence was observed on the surface of the infected macrophages, indicating that these glycosphingolipid antigens are not acquired from the host cell but synthesized by the amastigote. Intravenous administration of 125I-labeled ST-3 antibody to infected BALB/c mice showed that MoAb ST-3 accumulated significantly in the footpad lesions in comparison to blood and other tissues.

An allograft kidney showing both features of IgA nephropathy and membranous glomerulonephritis: a case report

We report a case of glomerular disease with both mesangial IgA and subepithelial IgG deposits in the allograft kidney. The patient was a 36 year-old man who had received a renal allograft 1 year previously. Fifteen days before admission, he discovered a microscopic hematuria without clinical evidences of allograft rejection. Light microscopy showed diffuse increase of mesangial matrix without mesangial cell proliferation. Capillary walls were diffusely and mildly thickened. Immunofluorescence microscopy demonstrated both granular deposits of IgA in the mesangium and IgG along the capillary walls. On electron microscopy, electron-dense deposits were identified not only in the mesangium but also on the epithelial side of the glomerular basement membrane.

Complemento, daño renal y lepra murina / Complement, renal damage and murine leprosy

A pesar de que la lepra de los ratones es una enfermedad sistémica, el tejido renal de los animales infectados rara vez es invadido por el Mycobacterium lepraemurium. Nuestros resultados indicaron que los animales afectados con el Mycobacterium lepraemurium desarrollaron un defecto en sus niveles de complemento hemolítico que es proporcional al grado de infección. El defecto afecta principalmente la vía clásica de activación del complemento y menor marcadamente la vía alterna. La inactivación de la actividad de complemento, mientras transcurre la infección, disminuye la posibilidad del daño medido por completo y prolonga la vida del huésped murino; ésta es, sin duda, una eficiente estrategia del microorganismo para prolongar también su supervivencia

Efeito da rifampicina sobre a reserva adrenocortical de cortisol em pacientes com tuberculose / Effect of rifampicin upon the adrenocortical reserve of cortisol in patients with tuberculosis

A tuberculose é causa conhecida de insuficiência adrenocortical primária. A administraçäo de rifampicina, parte do esquema tríplice empregado no tratamento da tuberculose, induz a síntese de enzimas hepáticas que aceleram o metabolismo do cortical, Uma vez que a rifampicina pode preciptar crise adrenal em tuberculose com funçäo adrenocortical comprometida, avaliamos possíveis alteraçöes na reserva de corticol em 33 pacientes com tuberculose, subdivididos em dois grupos: Grupo I - 17 pacientes (13M/4F, 21-45 anos) foram estados antes e, novamente, 30 dias após instituiçäo do esquema tríplice; Grupo 2 - 16 pacientes (13M/3F, 18-64 anos) foram estudados ao fim de seis meses de tratamento e, novamente 30 dias após sua interrupçäo. Como controles utilizamos 32 indivíduos normais, pareados para sexo e idade. Em cada estudo determinamos os níveis séricos de cortisol antes e 50 minutos após estímulo com ACTH (250µg i.v.). Nenhum paciente apresentou clínica de insuficência adrenal ou calcificaçöes nas radiográfias de abdome. Os valores do cortisol basal e pós ACTH (em µg/dl, X ñ DP) no Grupo 1 foram: 20,3 ñ 8,5 e 32,9 ñ 8,5 (antes) e 16,3 ñ 5,1 e 30,3 ñ 6,4 (após 30 dias de tratamento); no Grupo 2 foram: 19,1 ñ 7,3 e 35,4 ñ 12,1 (após seis meses de tratamento) e 18,4 ñ 4,6 e 31,7 ñ 8,2 (30 dias após a internaçäo). Nos controles normais obtivemos: 11,3 ñ 3,4 e 26,3 ñ 4,8, definindo limites críticos inferiores (LCL) de 5,7 e 18,4 para cortisol basal e pós-ACTH, respectivamente. Nenhum paciente apresentou níveis basais ou pós-ACTH de cortisol abaixo do LCI. A instituiçäo (Grupo 1) ou interrupçäo (Grupo 2 do tratamento com rifampicina näo modificou a resposta do cortisol ao estímulo com ACTH. Os dois grupos näo diferenciaram quanto aos níveis e repostas do cortisol. Assim, reduçäo da reserva de cortisol näo foi detectada em nenhum de 33 pacientes com tuberculose estudados prospectivamente, nos quais o tratamento breve ou prolongado com rifampicina näo resultou em alteraçöes significantes da resposta ao estímulo com ACTH

Nephrotic syndrome associated with hepatointestinal schistosomiasis

Schistosomal nephropathy has long been related to the hepatosplenic form of schistosomiasis. In the last few years, 24 patients with hepatointestinal schistosomiasis and the nephrotic syndrome were studied. Aiming at evaluating a possible etiologic participation of schistosomiasis in the development of the nephropathy, this group was comparatively studied with a group of 37 patients with idiopathic nephrotic syndrome. Both groups had a different distribution of the histologic lesions. In the group with schistosomiasis there was a statistically significant prevalence of proliferative mesangial glomerulonephritis (33.3%), whereas in the control group there was prevalence of membranous glomerulonephritis (32.4%). On immunofluorescence, IgM was positive in 94.4% of the patients with schistosomiasis versus 55.0% in the control group (P < 0.01). In the group with schistosomiasis, 8 patients evidenced mesangial proliferative glomerulonephritis and 5, membranoproliferative glomerulonephritis. In both histological types immunofluorescence showed IgM and C3 granular deposits in the glomeruli. The data in this study suggests that mesangial proliferative and membranoproliferative glomerulonephritis, with glomerular granular IgM and C3 deposits, represent the renal lesions of the schistosomiasis associated nephropathy

La oncocercosis y su relación con el aparato urinario / Onchocercosis and its relationship with urinary tract

La oncocercosis es una enfermedad parasitaria que tradicionalmente se ha considerado como un padecimiento que afecta exclusivamente a los tejifos oculares y cutáneos. Sin embargo, ya se ha demostrado que existen también otras alteraciones sistématicas, renales y neurológicas especialmente inducidas durante el tratamiento con microfilaricidas. En este artículo se hace una revisión de los aspectos renales de la oncocercosis que incluyen la presencia de microfilarias de onchocerca volvulus en orina (microfilaruria), así como de hematuria y proteinuria en pacientes infectados con esta filaria. Estas manifestaciones renales pueden observarse en oncocercosos que no se encuentran bajo tratamiento, pero su aparición es especialmente notable durante la quimioterapia tanto con microfilaricidas como con macrofilaricidas. No obstante que estas alteraciones pueden desaparecer o no después de finalizado el tratamiento, aparentemente tienen muy poca influencia en el cuadro clínico general de la oncocercosis. Se hace hincapié en los posibles mecanismos por los cuales las microfilarias de 0. volvulus pasan de los tejidos cutáneos hacia el torrente sanguíneo y, desde allí, hacia la orina. Asimismo, se comentan los mecanismos propuestos para explicar el lesión renal, mecanismos que al parecer tienen un origen inmunológico basado en el depósito de complejos inmunitarios en la membrana basal de glomérulo.