Karalyan Naira Yu., Tatoyan Marina R., Semerjyan Anna B., Nersisyan Narek H., Semerjyan Zara B., Hakobyan Lina H., Karalyan Zaven A.
Department of Pathological Anatomy and Clinical Morphology, Armenia Yerevan State Medical University, 2 Koryun St., Yerevan 0025, Armenia
Department of Cytology, Histology and Embryology, Armenia Yerevan State Medical University, 2 Koryun St., Yerevan 0025, Armenia
Ann Parasitol. 2018;64(4):343-350. doi: 10.17420/ap6404.170.
Glomerulonephritis due to African swine fever (ASF) is well documented. However, there is absence of good understanding of mechanisms involved in the development of pathology development. This study examines glomerulonephritis in association with acute infection induced by II genotype (Georgia 2007) of ASF virus. Taken together, the results of urinary analysis and the renal histological analysis led to the diagnosis of diffuse endocapillary proliferative glomerulonephritis with severe tubular injury associated with acute ASF (Georgia 2007). According to the pathogenesis, we have found that the diffuse endocapillary proliferative glomerulonephritis associated with the acute ASF develops with a delay of one to two days compared to development of hemophagocytic lymphohistiocytosis. The diagnosis of endocapillary proliferative glomerulonephritis confirms the characteristic of pathological changes in the composition of urine and urine sediment. The development of acute proliferative glomerulonephritis begins at 3 dpi, and finished at 4–6 dpi with the development of tubular necrosis. Our study demonstrates local macrophage proliferation. Local proliferation may be an important mechanism for amplifying macrophage-mediated renal injury. We have shown that the development of diffuse acute proliferative glomerulonephritis during ASF does not coincide with the presence of the virus in the blood or kidney tissues, but coincides with the developmental of ASFV derived hemophagocytic lymphohistiocytosis. The development of hemophagocytic lymphonocytosis also begins at least at 2–3 dpi and continues up to the terminal stage of the disease.
非洲猪瘟（ASF）引起的肾小球肾炎已有充分记录。然而，对于其病理发展所涉及的机制仍缺乏深入了解。本研究探讨了与II型（格鲁吉亚2007株）ASF病毒诱导的急性感染相关的肾小球肾炎。综合尿液分析和肾脏组织学分析结果，诊断为弥漫性毛细血管内增生性肾小球肾炎伴严重肾小管损伤，与急性ASF（格鲁吉亚2007株）相关。根据发病机制，我们发现与急性ASF相关的弥漫性毛细血管内增生性肾小球肾炎的发展比噬血细胞性淋巴组织细胞增生症的发展延迟1至2天。毛细血管内增生性肾小球肾炎的诊断证实了尿液和尿沉渣成分中病理变化的特征。急性增生性肾小球肾炎在感染后3天开始发展，并在4至6天随着肾小管坏死的发展而结束。我们的研究显示了局部巨噬细胞增殖。局部增殖可能是放大巨噬细胞介导的肾损伤的重要机制。我们已经表明，ASF期间弥漫性急性增生性肾小球肾炎的发展与血液或肾脏组织中病毒的存在不一致，但与ASFV衍生的噬血细胞性淋巴组织细胞增生症的发展一致。噬血细胞性淋巴细胞增生症的发展也至少在感染后2至3天开始，并持续到疾病的终末期。
