Radiation-induced kidney toxicity: molecular and cellular pathogenesis

Radiation nephropathy (RN) is a kidney injury induced by ionizing radiation. In a clinical setting, ionizing radiation is used in radiotherapy (RT). The use and the intensity of radiation therapy is limited by normal-tissue damage including kidney toxicity. Different thresholds for kidney toxicity e...

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Published inRadiation oncology (London, England) Vol. 16; no. 1; p. 43
Main Authors Klaus, Richard, Niyazi, Maximilian, Lange-Sperandio, Bärbel
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 25.02.2021
BioMed Central
BMC
Subjects
Aldosterone
Anemia
Angiotensin
Animal models
Antioxidants
Apoptosis
Cancer therapies
Care and treatment
Cell cycle
Cell death
Cellular senescence
Chemotherapy
Complications and side effects
Deoxyribonucleic acid
Development and progression
DNA
DNA damage
Drugs
Fibrosis
Hypertension
Ionizing radiation
Kidney diseases
Kidneys
Metabolites
Necrosis
Nephropathy
Oxidative stress
Pathogenesis
Radiation damage
Radiation effects
Radiation nephropathy
Radiation therapy
Radiotherapy
Renal fibrosis
Renin
Review
Senescence
Signal transduction
Statins
Total body irradiation
Toxicity
Germany
Renal inflammation
Total body irradiation
Renal fibrosis
DNA damage
Cellular senescence
Radiotherapy
Radiation nephropathy
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Abstract Radiation nephropathy (RN) is a kidney injury induced by ionizing radiation. In a clinical setting, ionizing radiation is used in radiotherapy (RT). The use and the intensity of radiation therapy is limited by normal-tissue damage including kidney toxicity. Different thresholds for kidney toxicity exist for different entities of RT. Histopathologic features of RN include vascular, glomerular and tubulointerstitial damage. The different molecular and cellular pathomechanisms involved in RN are not fully understood. Ionizing radiation causes double-stranded breaks in the DNA, followed by cell death including apoptosis and necrosis of renal endothelial, tubular and glomerular cells. Especially in the latent phase of RN oxidative stress and inflammation have been proposed as putative pathomechanisms, but so far no clear evidence was found. Cellular senescence, activation of the renin-angiotensin-aldosterone-system and vascular dysfunction might contribute to RN, but only limited data is available. Several signalling pathways have been identified in animal models of RN and different approaches to mitigate RN have been investigated. Drugs that attenuate cell death and inflammation or reduce oxidative stress and renal fibrosis were tested. Renin-angiotensin-aldosterone-system blockade, anti-apoptotic drugs, statins, and antioxidants have been shown to reduce the severity of RN. These results provide a rationale for the development of new strategies to prevent or reduce radiation-induced kidney toxicity.
AbstractList Radiation nephropathy (RN) is a kidney injury induced by ionizing radiation. In a clinical setting, ionizing radiation is used in radiotherapy (RT). The use and the intensity of radiation therapy is limited by normal-tissue damage including kidney toxicity. Different thresholds for kidney toxicity exist for different entities of RT. Histopathologic features of RN include vascular, glomerular and tubulointerstitial damage. The different molecular and cellular pathomechanisms involved in RN are not fully understood. Ionizing radiation causes double-stranded breaks in the DNA, followed by cell death including apoptosis and necrosis of renal endothelial, tubular and glomerular cells. Especially in the latent phase of RN oxidative stress and inflammation have been proposed as putative pathomechanisms, but so far no clear evidence was found. Cellular senescence, activation of the renin-angiotensin-aldosterone-system and vascular dysfunction might contribute to RN, but only limited data is available. Several signalling pathways have been identified in animal models of RN and different approaches to mitigate RN have been investigated. Drugs that attenuate cell death and inflammation or reduce oxidative stress and renal fibrosis were tested. Renin-angiotensin-aldosterone-system blockade, anti-apoptotic drugs, statins, and antioxidants have been shown to reduce the severity of RN. These results provide a rationale for the development of new strategies to prevent or reduce radiation-induced kidney toxicity.
Abstract Radiation nephropathy (RN) is a kidney injury induced by ionizing radiation. In a clinical setting, ionizing radiation is used in radiotherapy (RT). The use and the intensity of radiation therapy is limited by normal-tissue damage including kidney toxicity. Different thresholds for kidney toxicity exist for different entities of RT. Histopathologic features of RN include vascular, glomerular and tubulointerstitial damage. The different molecular and cellular pathomechanisms involved in RN are not fully understood. Ionizing radiation causes double-stranded breaks in the DNA, followed by cell death including apoptosis and necrosis of renal endothelial, tubular and glomerular cells. Especially in the latent phase of RN oxidative stress and inflammation have been proposed as putative pathomechanisms, but so far no clear evidence was found. Cellular senescence, activation of the renin–angiotensin–aldosterone-system and vascular dysfunction might contribute to RN, but only limited data is available. Several signalling pathways have been identified in animal models of RN and different approaches to mitigate RN have been investigated. Drugs that attenuate cell death and inflammation or reduce oxidative stress and renal fibrosis were tested. Renin–angiotensin–aldosterone-system blockade, anti-apoptotic drugs, statins, and antioxidants have been shown to reduce the severity of RN. These results provide a rationale for the development of new strategies to prevent or reduce radiation-induced kidney toxicity.
Radiation nephropathy (RN) is a kidney injury induced by ionizing radiation. In a clinical setting, ionizing radiation is used in radiotherapy (RT). The use and the intensity of radiation therapy is limited by normal-tissue damage including kidney toxicity. Different thresholds for kidney toxicity exist for different entities of RT. Histopathologic features of RN include vascular, glomerular and tubulointerstitial damage. The different molecular and cellular pathomechanisms involved in RN are not fully understood. Ionizing radiation causes double-stranded breaks in the DNA, followed by cell death including apoptosis and necrosis of renal endothelial, tubular and glomerular cells. Especially in the latent phase of RN oxidative stress and inflammation have been proposed as putative pathomechanisms, but so far no clear evidence was found. Cellular senescence, activation of the renin-angiotensin-aldosterone-system and vascular dysfunction might contribute to RN, but only limited data is available. Several signalling pathways have been identified in animal models of RN and different approaches to mitigate RN have been investigated. Drugs that attenuate cell death and inflammation or reduce oxidative stress and renal fibrosis were tested. Renin-angiotensin-aldosterone-system blockade, anti-apoptotic drugs, statins, and antioxidants have been shown to reduce the severity of RN. These results provide a rationale for the development of new strategies to prevent or reduce radiation-induced kidney toxicity. Keywords: Radiation nephropathy, Total body irradiation, Radiotherapy, Renal fibrosis, Cellular senescence, DNA damage, Renal inflammation
Abstract Radiation nephropathy (RN) is a kidney injury induced by ionizing radiation. In a clinical setting, ionizing radiation is used in radiotherapy (RT). The use and the intensity of radiation therapy is limited by normal-tissue damage including kidney toxicity. Different thresholds for kidney toxicity exist for different entities of RT. Histopathologic features of RN include vascular, glomerular and tubulointerstitial damage. The different molecular and cellular pathomechanisms involved in RN are not fully understood. Ionizing radiation causes double-stranded breaks in the DNA, followed by cell death including apoptosis and necrosis of renal endothelial, tubular and glomerular cells. Especially in the latent phase of RN oxidative stress and inflammation have been proposed as putative pathomechanisms, but so far no clear evidence was found. Cellular senescence, activation of the renin–angiotensin–aldosterone-system and vascular dysfunction might contribute to RN, but only limited data is available. Several signalling pathways have been identified in animal models of RN and different approaches to mitigate RN have been investigated. Drugs that attenuate cell death and inflammation or reduce oxidative stress and renal fibrosis were tested. Renin–angiotensin–aldosterone-system blockade, anti-apoptotic drugs, statins, and antioxidants have been shown to reduce the severity of RN. These results provide a rationale for the development of new strategies to prevent or reduce radiation-induced kidney toxicity.
ArticleNumber 43
Audience Academic
Author Niyazi, Maximilian
Lange-Sperandio, Bärbel
Klaus, Richard
Author_xml – sequence: 1
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  surname: Klaus
  fullname: Klaus, Richard
  organization: Division of Pediatric Nephrology, Department of Pediatrics, Dr. v. Hauner Children's Hospital, University Hospital, LMU Munich, Lindwurmstr. 4, 80337, Munich, Germany
– sequence: 2
  givenname: Maximilian
  surname: Niyazi
  fullname: Niyazi, Maximilian
  organization: German Cancer Consortium (DKTK), Partner Site Munich, Munich, Germany
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  givenname: Bärbel
  orcidid: 0000-0001-8898-3459
  surname: Lange-Sperandio
  fullname: Lange-Sperandio, Bärbel
  email: baerbel.lange-sperandio@med.uni-muenchen.de
  organization: Division of Pediatric Nephrology, Department of Pediatrics, Dr. v. Hauner Children's Hospital, University Hospital, LMU Munich, Lindwurmstr. 4, 80337, Munich, Germany. baerbel.lange-sperandio@med.uni-muenchen.de
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Issue 1
Keywords Renal inflammation
Total body irradiation
Renal fibrosis
DNA damage
Cellular senescence
Radiotherapy
Radiation nephropathy
Language English
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PublicationTitle Radiation oncology (London, England)
PublicationTitleAlternate Radiat Oncol
PublicationYear 2021
Publisher BioMed Central Ltd
BioMed Central
BMC
Publisher_xml – name: BioMed Central Ltd
– name: BioMed Central
– name: BMC
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Snippet Radiation nephropathy (RN) is a kidney injury induced by ionizing radiation. In a clinical setting, ionizing radiation is used in radiotherapy (RT). The use...
Abstract Radiation nephropathy (RN) is a kidney injury induced by ionizing radiation. In a clinical setting, ionizing radiation is used in radiotherapy (RT)....
Abstract Radiation nephropathy (RN) is a kidney injury induced by ionizing radiation. In a clinical setting, ionizing radiation is used in radiotherapy (RT)....
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SubjectTerms Aldosterone
Anemia
Angiotensin
Animal models
Antioxidants
Apoptosis
Cancer therapies
Care and treatment
Cell cycle
Cell death
Cellular senescence
Chemotherapy
Complications and side effects
Deoxyribonucleic acid
Development and progression
DNA
DNA damage
Drugs
Fibrosis
Hypertension
Ionizing radiation
Kidney diseases
Kidneys
Metabolites
Necrosis
Nephropathy
Oxidative stress
Pathogenesis
Radiation damage
Radiation effects
Radiation nephropathy
Radiation therapy
Radiotherapy
Renal fibrosis
Renin
Review
Senescence
Signal transduction
Statins
Total body irradiation
Toxicity
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Title Radiation-induced kidney toxicity: molecular and cellular pathogenesis
URI https://www.ncbi.nlm.nih.gov/pubmed/33632272
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https://pubmed.ncbi.nlm.nih.gov/PMC7905925
https://doaj.org/article/eedf83ad64194297a3082da0721671ac
Volume 16
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