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Hantavirus infection with severe proteinuria and podocyte foot-process effacement

机译:汉坦病毒感染伴重度蛋白尿和足细胞足突

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Nephropathia epidemica, a zoonosis caused by Hantavirus infection (most commonly subtype Puumala) is associated with flu-like symptoms and acute kidney failure. Kidney manifestations are characterized predominantly by tubulointerstitial nephritis, hemorrhage into medullary tissues, interstitial edema, and tubular cell necrosis. Kidney failure is accompanied by proteinuria, and in some cases, nephrotic-range proteinuria may occur. However, the cellular mechanisms of proteinuria remain to be elucidated. We describe a Hantavirus (Puumala) infection in a 27-year-old man with acute kidney failure and severe and rapidly reversible proteinuria. Light microscopy of a kidney biopsy specimen showed only minor changes of glomeruli. However, transmission electron microscopy revealed podocyte foot-process effacement. Immunofluorescence staining of the slit diaphragm protein podocin and the tight junction protein ZO-1 revealed a partial mislocalization of these proteins. Together, these findings highlight that Hantavirus infection may perturb podocyte integrity, resulting in glomerular proteinuria. These alterations of podocytes and consequently the glomerular filtration barrier may be transient and resolve within weeks.
机译:肾炎,一种由汉坦病毒感染(最常见的是Puumala亚型)引起的人畜共患病,与流感样症状和急性肾衰竭有关。肾脏表现的主要特征是肾小管间质性肾炎,髓组织出血,间质性水肿和肾小管坏死。肾衰竭伴有蛋白尿,在某些情况下,可能发生肾病范围蛋白尿。然而,蛋白尿的细胞机制仍有待阐明。我们描述了一个27岁的男子,患有急性肾功能衰竭和严重的和快速可逆的蛋白尿的汉坦病毒(普纳马拉)感染。肾脏活检标本的光学显微镜仅显示肾小球的微小变化。然而,透射电子显微镜显示足细胞足突消失。缝隙隔膜蛋白podocin和紧密连接蛋白ZO-1的免疫荧光染色显示这些蛋白的部分错位。总之,这些发现表明汉坦病毒感染可能会扰动足细胞的完整性,从而导致肾小球蛋白尿。足细胞的这些改变以及因此的肾小球滤过屏障可能是短暂的,并在数周内消失。

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