Book contents
- Frontmatter
- Contents
- Contributors
- Part I General Principles of Cell Death
- Part II Cell Death in Tissues and Organs
- 11 Cell Death in Nervous System Development and Neurological Disease
- 12 Role of Programmed Cell Death in Neurodegenerative Disease
- 13 Implications of Nitrosative Stress-Induced Protein Misfolding in Neurodegeneration
- 14 Mitochondrial Mechanisms of Neural Cell Death in Cerebral Ischemia
- 15 Cell Death in Spinal Cord Injury – An Evolving Taxonomy with Therapeutic Promise
- 16 Apoptosis and Homeostasis in the Eye
- 17 Cell Death in the Inner Ear
- 18 Cell Death in the Olfactory System
- 19 Contribution of Apoptosis to Physiologic Remodeling of the Endocrine Pancreas and Pathophysiology of Diabetes
- 20 Apoptosis in the Physiology and Diseases of the Respiratory Tract
- 21 Regulation of Cell Death in the Gastrointestinal Tract
- 22 Apoptosis in the Kidney
- 23 Physiologic and Pathological Cell Death in the Mammary Gland
- 24 Therapeutic Targeting Apoptosis in Female Reproductive Biology
- 25 Apoptotic Signaling in Male Germ Cells
- 26 Cell Death in the Cardiovascular System
- 27 Cell Death Regulation in Muscle
- 28 Cell Death in the Skin
- 29 Apoptosis and Cell Survival in the Immune System
- 30 Cell Death Regulation in the Hematopoietic System
- 31 Apoptotic Cell Death in Sepsis
- 32 Host–Pathogen Interactions
- Part III Cell Death in Nonmammalian Organisms
- Plate section
- References
22 - Apoptosis in the Kidney
from Part II - Cell Death in Tissues and Organs
Published online by Cambridge University Press: 07 September 2011
- Frontmatter
- Contents
- Contributors
- Part I General Principles of Cell Death
- Part II Cell Death in Tissues and Organs
- 11 Cell Death in Nervous System Development and Neurological Disease
- 12 Role of Programmed Cell Death in Neurodegenerative Disease
- 13 Implications of Nitrosative Stress-Induced Protein Misfolding in Neurodegeneration
- 14 Mitochondrial Mechanisms of Neural Cell Death in Cerebral Ischemia
- 15 Cell Death in Spinal Cord Injury – An Evolving Taxonomy with Therapeutic Promise
- 16 Apoptosis and Homeostasis in the Eye
- 17 Cell Death in the Inner Ear
- 18 Cell Death in the Olfactory System
- 19 Contribution of Apoptosis to Physiologic Remodeling of the Endocrine Pancreas and Pathophysiology of Diabetes
- 20 Apoptosis in the Physiology and Diseases of the Respiratory Tract
- 21 Regulation of Cell Death in the Gastrointestinal Tract
- 22 Apoptosis in the Kidney
- 23 Physiologic and Pathological Cell Death in the Mammary Gland
- 24 Therapeutic Targeting Apoptosis in Female Reproductive Biology
- 25 Apoptotic Signaling in Male Germ Cells
- 26 Cell Death in the Cardiovascular System
- 27 Cell Death Regulation in Muscle
- 28 Cell Death in the Skin
- 29 Apoptosis and Cell Survival in the Immune System
- 30 Cell Death Regulation in the Hematopoietic System
- 31 Apoptotic Cell Death in Sepsis
- 32 Host–Pathogen Interactions
- Part III Cell Death in Nonmammalian Organisms
- Plate section
- References
Summary
Normal kidney structure and function
The kidneys maintain the homeostasis of electrolyte, fluid, and acid–base balance; eliminate waste products; and have an endocrine-metabolic function. They secrete hormones such as erythropoietin, Klotho, and 1,25-(OH)2-vitamin D and clear other hormones and cytokines. Each kidney contains 1 million basic functional units, or nephrons. Each nephron is composed of a glomerulus and a renal tubule. The glomerulus is a tightly woven, highly permeable capillary bed, surrounded by differentiated, very specialized cells, the podocytes. The mesangium contains mesangial cells and holds the capillaries together. Every day, 180 L of plasma is filtered through the glomeruli. Podocytes prevent the filtration of proteins, and their injury will lead to pathological urinary protein excretion (proteinuria). Podocytes do not divide, and podocyte loss causes podocytopenia, an early event in progressive glomerular scarring. Tubular cells reabsorb most of the filtered fluid and nutrients, and only 1 to 2 L of urine is excreted. Proximal tubular cells are responsible for the bulk of reabsorption. They are rich in mitochondria, consume high amounts of energy, and express a variety of transporters that favor the uptake of nephrotoxins. Thus they are prime targets in toxic and ischemic renal injury.
- Type
- Chapter
- Information
- ApoptosisPhysiology and Pathology, pp. 240 - 249Publisher: Cambridge University PressPrint publication year: 2011
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