Laboratório de Biologia Celular, Instituto Oswaldo Cruz/FIOCRUZ, Manguinhos, Rio de Janeiro, Rio de Janeiro, Brazil.
Parasitol Res. 2009 Dec;106(1):111-20. doi: 10.1007/s00436-009-1637-0. Epub 2009 Sep 26.
Experimental acute infection with Trypanosoma cruzi in mice promotes an intense myocarditis and other systemic changes. However, the network of pathophysiological disorders and renal injury caused by the infection has not been elucidated. Our previous results with a murine model observed a discrete acute myocarditis and high mortality with significant inflammatory kidney injury with T. cruzi infection. The aim of this study was to investigate the mechanisms of kidney injury caused by the parasite in mice during the experimental acute phase. Results employing BALB/c mice infected with T. cruzi of Y strain showed renal injury on the 6th day postinfection (dpi) caused by a transitory decrease of renal blood flow. Acute kidney injury (AKI) was also observed similar to the model of ischemia/reperfusion lesion in these infected mice. The injury was not related to the presence (or multiplication) of parasites. Only rare nests were microscopically detected, and the presence of scattered parasites in renal parenchyma was seen on the 15th dpi. Thus, it was observed that during the acute phase of the disease, AKI in infected mice is linked to early cardiovascular effects, including heart failure, caused by striking inflammatory lesions in the myocardium, which lead to the high mortality rate of animals.
实验性急性克氏锥虫感染小鼠可引发强烈的心肌炎和其他全身变化。然而，感染引起的病理生理紊乱和肾脏损伤的网络尚未阐明。我们以前的研究结果表明，在感染克氏锥虫的小鼠模型中，观察到离散的急性心肌炎和高死亡率，并伴有严重的炎症性肾损伤。本研究旨在探讨寄生虫在实验性急性阶段引起小鼠肾脏损伤的机制。结果表明，用 Y 株克氏锥虫感染 BALB/c 小鼠，在感染后第 6 天（dpi）观察到肾脏损伤，这是由短暂的肾血流量减少引起的。在这些感染的小鼠中也观察到类似于缺血/再灌注损伤模型的急性肾损伤（AKI）。这种损伤与寄生虫的存在（或繁殖）无关。只有少数巢在显微镜下被检测到，在感染后的第 15 天可以看到散在的寄生虫存在于肾实质中。因此，在疾病的急性阶段，感染小鼠的 AKI 与早期心血管效应有关，包括心力衰竭，这是由心肌炎症病变引起的，导致动物的高死亡率。
