Kidney disease models: tools to identify mechanisms and potential therapeutic targets.

包寅武 包寅武,袁圆 袁圆,陈江华 陈江华,林伟强 林伟强,Yin-Wu Bao,Yuan Yuan,Jiang-Hua Chen,Wei-Qiang Lin

doi:10.24272/j.issn.2095-8137.2017.055

包寅武包寅武, 袁圆袁圆 + Show 6 more

Open Access

https://doi.org/10.24272/j.issn.2095-8137.2017.055

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Journal: Zoological Research	Publication Date: Jan 1, 2018
Citations: 96	License type: cc-by

Affiliation: Zhejiang University

Abstract

Acute kidney injury (AKI) and chronic kidney disease (CKD) are worldwide public health problems affecting millions of people and have rapidly increased in prevalence in recent years. Due to the multiple causes of renal failure, many animal models have been developed to advance our understanding of human nephropathy. Among these experimental models, rodents have been extensively used to enable mechanistic understanding of kidney disease induction and progression, as well as to identify potential targets for therapy. In this review, we discuss AKI models induced by surgical operation and drugs or toxins, as well as a variety of CKD models (mainly genetically modified mouse models). Results from recent and ongoing clinical trials and conceptual advances derived from animal models are also explored.

Highlights

Acute kidney injury (AKI) and chronic kidney disease (CKD) are linked to high morbidity and mortality
We focused on murine models of AKI and CKD (Figure 2)
The latest validated criteria are: (1) more than 50% decrease in glomerular filtration rate (GFR); (2) greater than 10fold increase in albuminuria compared with controls; and (3) pathological changes in kidneys including advanced mesangial matrix expansion±nodular sclerosis and mesangiolysis, glomerular basement membrane (GBM) thickening by >50% over baseline, arteriolar hyalinosis, and tubulointerstitial fibrosis

Summary

INTRODUCTION

Acute kidney injury (AKI) and chronic kidney disease (CKD) are linked to high morbidity and mortality. There is increasing recognition that AKI and CKD are closely linked and are regarded as an integrated clinical syndrome (Chawla & Kimmel, 2012) (Figure 1). Key biological processes such as cell death, cell proliferation, inflammation, and fibrosis, as well as common biomarkers, are detected in both kinds of nephropathy (Andreucci et al, 2017; Endre et al, 2011). Large sample size and long followup duration are essential in a multicenter clinical trial to Received: 15 July 2017; Accepted: 05 September 2017

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Findings

CONCLUSIONS