Máthé A, Dobos-Kovács M, Vörös K
Department and Clinic of Internal Medicine, Faculty of Veterinary Science, Szent Istvdn University, H-1078 Budapest, Istvin u. 2, Hungary.
Acta Vet Hung. 2007 Dec;55(4):511-23. doi: 10.1556/AVet.55.2007.4.10.
Histological and electron microscopic examinations of the kidneys of 8 dogs suffering from fatal, naturally acquired Babesia canis infection and nephropathy are presented. Seven animals were treated with imidocarb dipropionate on average 4.5 days prior to death. Severe anaemia was present only in 2 cases. Degenerative histological changes observed mostly in the proximal convoluted tubules included vacuolar-hydropic degeneration, necrosis and detachment of renal tubular epithelial (RTE) cells from the basement membrane. Necrotic debris occasionally formed acidophilic casts within the tubules. In some cases, necrosis of the whole tubule was observed. Haemoglobin casts in the tubules and haemoglobin droplets in RTE cells seldom appeared. No significant histological changes were seen in the glomeruli. Ultrastructural lesions in RTE cells included nuclear membrane hyperchromatosis, karyopyknosis, karyolysis, swelling or collapse of mitochondria with fragmentation of cristae and vacuolar-hydropic degeneration in the endoplasmic reticulum and microvilli. Nuclear oedema was also observed. Many RTE cells exhibiting necrosis collapsed. Vacuolar-hydropic degeneration and necrosis were also observed in the glomerular and interstitial capillary endothelium. The severe acute tubular necrosis described in this study is probably the result of hypoxic renal injury. Systemic hypotension leading to vasoconstriction in the kidneys might be the most important cause of renal hypoxia in B. canis infections, but anaemia may also contribute to inadequate oxygenation. Imidocarb should be applied with caution in patients with possible renal involvement until further data become available on its potential nephrotoxicity in dogs.
本文呈现了对8只患有致命性自然感染犬巴贝斯虫及肾病的犬的肾脏进行组织学和电子显微镜检查的结果。7只动物在死亡前平均4.5天接受了双丙酸咪唑苯脲治疗。仅2例出现严重贫血。组织学上观察到的主要发生在近端曲管的退行性变化包括空泡 - 水样变性、肾小管上皮（RTE）细胞坏死及与基底膜分离。坏死碎片偶尔在管腔内形成嗜酸性管型。在某些情况下，观察到整个肾小管坏死。肾小管内血红蛋白管型和RTE细胞内血红蛋白滴很少出现。肾小球未见明显组织学变化。RTE细胞的超微结构病变包括核膜染色质增多、核固缩、核溶解、线粒体肿胀或塌陷伴嵴断裂以及内质网和微绒毛的空泡 - 水样变性。还观察到核水肿。许多呈现坏死的RTE细胞塌陷。肾小球和间质毛细血管内皮也观察到空泡 - 水样变性和坏死。本研究中描述的严重急性肾小管坏死可能是肾缺氧损伤的结果。导致肾脏血管收缩的全身性低血压可能是犬巴贝斯虫感染中肾缺氧的最重要原因，但贫血也可能导致氧合不足。在有肾脏受累可能的患者中，在获得关于其对犬潜在肾毒性的进一步数据之前，应谨慎使用双丙酸咪唑苯脲。
