Comparative Biomedical Sciences, The Royal Veterinary College, Royal College Street, London NW1 0TU, UK.
Comparative Biomedical Sciences, The Royal Veterinary College, Royal College Street, London NW1 0TU, UK.
Vet J. 2021 Aug;274:105714. doi: 10.1016/j.tvjl.2021.105714. Epub 2021 Jul 9.
There is mounting evidence that kidney ischaemia/hypoxia plays an important role in feline chronic kidney disease (CKD) development and progression, as well as in human disease and laboratory animal models. Ischaemic acute kidney injury is widely accepted as a cause of CKD in people and data from laboratory species has identified some of the pathways underlying this continuum. Experimental kidney ischaemia in cats results in morphological changes, namely chronic tubulointerstitial inflammation, tubulointerstitial fibrosis, and tubular atrophy, akin to those observed in naturally-occurring CKD. Multiple situations are envisaged that could result in acute or chronic episodes of kidney hypoxia in cats, while risk factors identified in epidemiological studies provide further support that kidney hypoxia contributes to spontaneously occurring feline CKD. This review evaluates the evidence for the role of kidney ischaemia/hypoxia in feline CKD and the proposed mechanisms and consequences of kidney hypoxia. As no effective treatments exist that substantially slow or prevent feline CKD progression, there is a need for novel therapeutic strategies. Targeting kidney hypoxia is one such promising approach, with therapies including those that attenuate the hypoxia-inducible factor (HIF) pathway already being utilised in human CKD.
越来越多的证据表明，肾脏缺血/缺氧在猫慢性肾脏病（CKD）的发展和进展中以及在人类疾病和实验动物模型中起着重要作用。缺血性急性肾损伤被广泛认为是人类 CKD 的病因，来自实验物种的数据已经确定了这一连续体的一些潜在途径。在猫中进行的实验性肾脏缺血会导致形态学变化，即慢性肾小管间质性炎症、肾小管间质性纤维化和肾小管萎缩，类似于在自然发生的 CKD 中观察到的变化。可以设想多种情况会导致猫的急性或慢性肾脏缺氧发作，而流行病学研究中确定的危险因素进一步支持肾脏缺氧导致自发性猫 CKD。本综述评估了肾脏缺血/缺氧在猫 CKD 中的作用以及肾脏缺氧的拟议机制和后果。由于目前尚无有效治疗方法能显著减缓或预防猫 CKD 的进展，因此需要新的治疗策略。靶向肾脏缺氧是一种很有前途的方法，已经在人类 CKD 中使用了包括减轻缺氧诱导因子（HIF）途径的治疗方法。
