Chapter title |
Assessment of In Vivo Kidney Cell Death: Acute Kidney Injury
|
---|---|
Chapter number | 13 |
Book title |
Programmed Necrosis
|
Published in |
Methods in molecular biology, January 2018
|
DOI | 10.1007/978-1-4939-8754-2_13 |
Pubmed ID | |
Book ISBNs |
978-1-4939-8753-5, 978-1-4939-8754-2
|
Authors |
Wulf Tonnus, Moath Al-Mekhlafi, Christian Hugo, Andreas Linkermann |
Abstract |
The kidney has been studied as an organ to investigate cell death in vivo for a number of reasons. The unique vasculature that does not contain collateral vessels favors the kidney over other organs for the investigation of ischemia-reperfusion injury. Unilateral uretic obstruction has become the most prominently studied model for fibrosis with impact far beyond postrenal kidney injury. In addition, the tubular elimination mechanisms render the kidney susceptible to toxicity models, such as cisplatin-induced acute kidney injury. During trauma of skeletal muscles, myoglobulin deposition causes tubular cell death in the model of rhabdomyolysis-induced acute kidney injury. Here, we introduce these clinically relevant in vivo models of acute kidney injury (AKI) and critically review the protocols we use to effectively induce them. |
Mendeley readers
Geographical breakdown
Country | Count | As % |
---|---|---|
Unknown | 7 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
---|---|---|
Unspecified | 1 | 14% |
Student > Bachelor | 1 | 14% |
Researcher | 1 | 14% |
Lecturer | 1 | 14% |
Unknown | 3 | 43% |
Readers by discipline | Count | As % |
---|---|---|
Unspecified | 1 | 14% |
Biochemistry, Genetics and Molecular Biology | 1 | 14% |
Nursing and Health Professions | 1 | 14% |
Medicine and Dentistry | 1 | 14% |
Unknown | 3 | 43% |