22 research outputs found

    Glycosuria in glomerular diseases: histopathology and clinical correlations

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    There are doubts about the presence of glycosuria and the progress of glomerular disease. Some reports suggest that glycosuria could be an index of a more severe tubulointerstitial lesion. We investigated the presence of glycosuria in 60 patients with primary glomerular diseases: 17 patients (28%) had glycosuria and 43 patients (72%) were glycosuria free. The two groups were similar in age, arterial pressure and sex. Serum creatinine was higher in patients with glycosuria (2.0 ± 1.7 vs 1.3 ± 0.9 mg/dl, P<0.05). The protein excretion rate was 7.5 ± 3.7 vs 5.3 ± 4.2 g/day (P>0.05) in patients with and without glycosuria, respectively, while serum albumin was lower in patients with glycosuria (1.7 ± 0.6 vs 2.7 ± 1.0 g/dl, P<0.05). Several histological forms were present in the group with glycosuria, with membranous glomerulonephritis being the most frequent. Histological evidence of tubular atrophy and interstitial fibrosis prevailed in patients with glycosuria, suggesting a poor prognosis for these patients. We may conclude that the presence of glycosuria in patients with glomerular disease is associated with more pronounced tubular atrophy and interstitial fibrosis and therefore imply a poorer prognosis

    Comparative study of IgA nephropathy with and without crescents

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    Glomerular crescents were analyzed as a prognostic factor in retrospectively reviewed data from 144 patients with biopsy-proven IgA nephropathy. Crescents were found in 26 (18%) patients, and detected in 2 to 100% of glomeruli in each specimen. In 5% of the patients more than 50% of the glomeruli were affected. Thirty patients with IgA nephropathy without crescents were studied as a control group. Mean age was 30.3 ± 9.4 and 30.2 ± 12.0 years for the patients with and without crescents, respectively, and males prevailed in both groups. The length of follow-up was 23.2 ± 41.6 months for patients with crescents and 29.3 ± 35.3 months for patients without crescents. Eighty percent of the patients with crescents were hypertensive, compared to 27% of the non-crescent control group (P < 0.05). Mean serum creatinine at the time of diagnosis was 3.9 ± 2.9 and 1.9 ± 2.1 mg/dl for the patients with and without crescents, respectively. Initial urinary protein excretion was higher in patients with crescents (4.6 ± 3.5 vs 1.2 ± 0.9 g/day; P < 0.05). At the end of follow-up 17 patients (77.3%) from the crescent group and 3 (11.1%) from the non-crescent group had end-stage renal disease (P < 0.0001). The presence of crescents was associated with higher levels of initial serum creatinine and urinary protein excretion, and a higher frequency of hypertension and progression to end-stage renal disease

    Síndrome nefrótica associada à esquistossomose hepatointestinal

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    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 (pA nefropatia esquistossomótica está classicamente vinculada à fornia hepatoesplênica da esquistossomose. Ao longo dos últimos anos 24 casos de pacientes esquistossomóticos hepato-intestinais e portadores de síndrome nefrótica foram estudados. Com o objetivo de verificar a possível participação etiológica da esquistossomose na gênese da nefropatia, analisamos este grupo comparativamente ao grupo de 37 doentes portadores de síndrome nefrótica idiopática. Ambos os grupos apresentaram distribuição distinta dos tipos histológicos de glomerulopatia. No grupo de esquistossomóticos houve predomínio estatisticamente significante de glomerulonefrite proliferativa mesangial (33.3%), enquanto no grupo controle houve predomínio da glomerulonefrite membranosa (32.4%). A positividade para IgM à imunofluorescência foi de 94.4% nos doentes esquistossomóticos versus 55.0% no grupo controle (

    Comparação entre diagnósticos clínicos e histológicos no pós-transplante renal Clinical and histological diagnosis agreement in kidney transplantation

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    OBJETIVO: Para determinar o acerto obtido pelos diagnósticos efetuados em uma unidade de transplante renal, foram analisados 40 episódios de disfunção renal aguda que ocorreram no período pós-transplante. MÉTODOS: Os pacientes foram submetidos a biópsia renal por ocasião do episódio de insuficiência renal ao mesmo tempo em que o diagnóstico clínico era realizado pelos membros da equipe. RESULTADOS: Foram realizados 19 diagnósticos de necrose tubular aguda (NTA), 18 de rejeição celular aguda (RCA), dois de rejeição humoral (RH) e um de nefrotoxicidade (NTX) pela ciclosporina A (CyA). O diagnóstico de NTA foi confirmado pela histologia em 84,21%, o de RCA, em 83,33%, o de RH em 100% e o único diagnóstico de NTX realizado se apresentou como NTA à biópsia. No total, a clínica foi concordante com a histologia em 82,5% das vezes. CONCLUSÃO: Os autores concluíram que existe uma boa acurácia nos diagnósticos clínicos de RCA, NTA e RH realizados em um centro experiente em transplante renal.<br>PURPOSE: To assess the agreement between clinical and histopathological diagnosis in a renal transplantation center, 40 episodes of acute renal failure were studied. METHODS: Kidney biopsies were performed at the moment that a clinical diagnosis was made by the staff. RESULTS: Nineteen episodes of acute tubular necrosis (ATN), eighteen episodes of acute cellular rejection (ACR), 2 humoral rejections and 1 acute cyclosporin nephrotoxicity episodes were diagnosed. ATN episodes were confirmed by renal biopsy in 84.21%, ACR episodes in 83.33%, humoral rejections in 100%. Renal biopsy showed ATN in the occurrence of clinical cyclosporin nephrotoxicity. Total agreement was 82.5%. CONCLUSION: There is a good relationship between clinical and histopathological diagnosis in the post-transplantation period. Diagnostic mistakes occurred mainly when oliguria was present

    Effects Of Extracorporeal Shockwave Lithotripsy On Renal Growth And Function: An Animal Model

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    The long-term effects of extracorporeal shockwave lithotripsy (SWL) on children are unclear. At 40 days of age, with an average weight of 166 g, 34 Wistar white rats were divided into three groups: 9 rats (control group) received no shockwaves, 10 rats (Group 1 received 1000 shockwaves at 16.0 kV, and 15 animals (Group 2) received 1000 shockwaves at 17.2 kV. Six months later, at maturity, body weight; lithium and creatinine; fractional sodium, potassium, and lithium excretion; and the clearances of lithium and creatinine were measured, and the kidneys were studied grossly and histologically. We found no significant changes in overall animal or renal growth between the post-SWL groups and the control group. However, there were significant changes in renal function, mainly in Group 2; the animals of this group presented a significant increase in blood lithium and potassium, besides a significant decrease in the fractional potassium excretion compared with the control group. Furthermore, the animals in Group 2 showed permanent histologic renal changes, including red cells in Bowman's capsule and glomerular congestion. The disorders caused by SWL are compatible with hyporeninemic hypoaldosteronism, an inappropriate low plasma renin activity and aldosterone deficiency. We conclude that SWL does not affect either overall animal or renal growth but may cause permanent histologic damage and significant changes in renal function.8319119
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