Temporary warm ischaemia, 5/6 nephrectomy and single uranylnitrate administration — comparison of three models intended to cause renal fibrosis in rats

Appenroth, Dorothea; Lupp, Amelie; Kriegsmann, Jörg; Sawall, Stefan; Splinther, J.; Sommer, Manfred; Stein, G; Fleck, Christian

doi:10.1078/0940-2993-00197

Cited by 17 publications

(12 citation statements)

References 27 publications

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“…After 20 weeks, fibrotic areas containing atrophic tubules with a thickened tubular basement membrane and mild lymphocytic infiltration were identified. Uranyl nitrate administration induced renal fibrosis in a dose-dependent manner (29). In another study, uranyl nitrate administration of 10 mg/kg in rats for a period of 2 months appeared to cause chronic injuries, as demonstrated by increased interstitial fibrosis, atrophic proximal tubules and mononuclear cell infiltrates.…”

Section: Mercuric Chloride (Hgcl 2 )mentioning

confidence: 95%

“…These authors suggest that the administration of uranyl nitrate in rats induced renal failure with a slow recovery phase and longterm pathological lesions (56). Uranyl nitrate appears to be an optimal model of interstitial fibrosis and is useful for investigating molecular mediators of kidney damage (29).…”

Section: Mercuric Chloride (Hgcl 2 )mentioning

confidence: 99%

“…Epithelial-mesenchymal transition, a process by which differentiated epithelial cells give rise to the matrixproducing fibroblasts and myofibroblasts, is increasingly documented as an integral part of tissue fibrogenesis after renal injury (13,35,41). In this sense, tubular epithelial cells are also important in the pathogenesis of tubulointerstitial fibrosis (29). Thus, epithelial-mesenchymal transition, such as occurs in common glomerular diseases, could be a primary pathway leading to podocyte dysfunction, proteinuria, and glomerulosclerosis (13).…”

Section: Fibroblastsmentioning

confidence: 99%

“…Renal fibrosis is one of the consequences of kidney injury and is associated with renal dysfunction that may culminate in renal collapse (25,26). Renal fibrosis, particularly associated with glomerulosclerosis and renal interstitial fibrosis (5,10,27,28) that is characterised by tubular atrophy, tubular dilatation, increased fibrogenesis (29) and deposition of collagen and ECM (15), can progress in humans as a consequence of chronic infection, obstruction of the ureters, hypertension, diabetic nephropathy and chronic exposure to heavy metals (25).…”

Section: Impact Of Renal Fibrosis On Human Healthmentioning

confidence: 99%

“…It is important to emphasize that these changes are clearly different from the compensatory changes that occur after reduction of renal mass (42). To study renal fibrosis, induced models (surgical and chemical), spontaneous models, genetic models and in vitro models (29,(43)(44)(45)(46)(47)(48) can be used.…”

Section: Animal Models Of Renal Fibrosismentioning

confidence: 99%

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Pathophysiological Mechanisms of Renal Fibrosis: A Review of Animal Models and Therapeutic Strategies

2017

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Abstract. Chronic kidney disease (CKD) is a long-term condition in which theChronic kidney disease (CKD) represents a serious hazard to human health, and has a high prevalence. In developed countries, it is estimated that more than 10% of adults present some degree of CKD (1). Despite a varied initial evolution, which is related to the diversity of its aetiologies -namely genetics, autoimmune-related infections, environmental factors, diet, and drugs -progressive renal disease frequently results in renal fibrosis and finally in renal failure. The mechanisms implicated in renal fibrosis are still poorly understood, and existing therapies are ineffective or only slightly successful, hence it is essential to understand the pathophysiological mechanisms underlying the usual development of CKD, and to discover and better understand new strategies for treating this disease. In order to study the biopathology of this disease and to evaluate new treatments, animal models are required. The perfect animal model for renal disease research should have human-like renal anatomy, haemodynamics and physiology, as well as enabling the determination of relevant renal, biochemical and haemodynamic parameters. In all probability, no species can consistently meet all these requirements, and the experimental plan and other constraints often determine the choice of animal models for particular research applications. With this in mind, this review aims to describe and analyze animal models of renal fibrosis and suggest new areas of research. Renal Fibrosis: Aetiology and PathophysiologyDiabetes and hypertension are currently the two principal causes of CKD (2), among other causes such as infectious glomerulonephritis, renal vasculitis, ureteral obstruction, genetic alterations, autoimmune diseases (1) and drugs (3, 4). In general, diabetes causes glomerular hypertension by reducing the afferent arteriolar resistance while stimulating the efferent arterioles (2). Thus, elevated glomerular capillary pressure is one of the major factors in progressive renal sclerosis (5). Diabetes and hypertension gradually lead to glomerular expansion, which causes endothelial dysfunction and haemodynamic changes: loss of the glomerular basement membrane electric charge and its thickening, a decreased number of podocytes, foot-process effacement and mesangial distension have been shown to 1

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Section: Mercuric Chloride (Hgcl 2 )mentioning

confidence: 95%

Section: Mercuric Chloride (Hgcl 2 )mentioning

confidence: 99%