Dengue virus (DENV) infections may result in asymptomatic cases or evolve into a severe disease, which involves multiple organ failure. Renal involvement in dengue can be potentially related to an increased mortality. Aiming to better understand the role of DENV in renal injury observed in human fatal cases, post-mortem investigations were performed in four DENV-4 renal autopsies during dengue epidemics in Brazil. Tissues were submitted to histopathology, immunohistochemistry, viral quantification, and characterization of cytokines and inflammatory mediators. Probably due the high viral load, several lesions were observed in the renal tissue, such as diffuse mononuclear infiltration around the glomerulus in the cortical region and in the medullary vessels, hyalinosis arteriolar, lymphocytic infiltrate, increased capsular fibrosis, proximal convoluted tubule (PCT) damage, edema, PCT debris formation, and thickening of the basal vessel membrane. These changes were associated with DENV-4 infection, as confirmed by the presence of DENV-specific NS3 protein, indicative of viral replication. The exacerbated presence of mononuclear cells at several renal tissue sites culminated in the secretion of proinflammatory cytokines and chemokines. Moreover, it can be suggested that the renal tissue injury observed here may have been due to the combination of both high viral load and exacerbated host immune response.
Background: The renal length and cortical echogenicity have shown correlation to the renal function and histological changes in CKD patients. The aim of this study was to assess the accuracy of crude and composite ultrasound parameters based on kidney measurements and cortical echogenicity to detect renal dysfunction and histological changes. Methods: Kidney sonography and biopsy were performed in 112 patients. Histological changes were graded in 0, < 25%, ≥25%, ≤50 and > 50% of the sample. Cortical echogenicity was graded relative to liver or spleen parenchyma: less than, equal to and higher than the liver/spleen. Kidney length, the kidney length/body height ratio (KL/H) and cortical thickness were obtained. Each parameter was multiplied by a cortical echogenicityweighting arbitrary factor: 1.17, 1 or 0.69 for cortex less than, equal to or higher than the liver, respectively. The GFR was estimated using the CKD-EPI formula. The accuracy of crude and composite parameters to identify patients with a high creatinine, a low GFR and histological changes were evaluated. Results: The discriminative power of kidney length and cortical thickness for renal dysfunction and histological changes was improved after weighting for cortical echogenicity. However, the best discriminative was the kidney length to height ratio weighted towards renal echogenicity (w-KL/H). Conclusion: w-KL/H exceeded the other parameters as a marker of renal impairment and histological changes in CKD. Calculation of the w-KL/H index may be of help as a non-invasive tool to identify patients with significant renal disease and might be useful to guide therapeutic decisions.
25% <50%), e grave (>50%). RESULTADOS: a) II, FI, ES, EI e creatinina elevada ocorreram menos no grau 0 de ecogenicidade cortical; b) PM, hipertensão arterial e espessura normal do parênquima foram preditores do grau 1 de ecogenicidade cortical; c) FI, EI, creatinina elevada e parênquima fino foram preditores do grau 2 de ecogenicidade cortical; d) Excluindos os obesos, em jovens com hematócrito baixo, a pirâmide proeminente foi mais comum; e) Creatinina elevada e OG foram preditores de rins pequenos. CONCLUSÃO: A ecogenicidade cortical foi um sensível marcador de doença parenquimatosa renal. Lesões distintas mais do que o grau de severidade da lesão contribuiram para o aumento da ecogenicidade cortical. O EI aumenta exponencialmente o efeito da FI na ecogenicidade cortical.]]>
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