Radiation-induced kidney toxicity: molecular and cellular pathogenesis.

Area of Science:

• Nephrology
• Radiation Oncology
• Molecular Biology

Background:

• Radiation nephropathy (RN) is kidney injury caused by ionizing radiation during radiotherapy (RT).
• Kidney toxicity limits radiation therapy's use and intensity.
• Histopathology reveals vascular, glomerular, and tubulointerstitial damage in RN.

Purpose of the Study:

• To elucidate the molecular and cellular pathomechanisms of RN.
• To identify strategies for mitigating radiation-induced kidney toxicity.

Main Methods:

• Review of existing literature on RN pathomechanisms.
• Analysis of molecular signaling pathways identified in animal models.
• Evaluation of therapeutic approaches tested in preclinical studies.

Main Results:

• Ionizing radiation induces DNA damage, leading to cell death (apoptosis, necrosis) in renal cells.
• Oxidative stress, inflammation, cellular senescence, and renin-angiotensin-aldosterone-system activation are implicated in RN.
• Renin-angiotensin-aldosterone-system blockade, anti-apoptotic drugs, statins, and antioxidants show promise in reducing RN severity.

Conclusions:

• The precise pathomechanisms of RN require further investigation.
• Therapeutic strategies targeting cell death, inflammation, oxidative stress, and fibrosis may prevent or reduce RN.
• These findings support developing novel interventions to mitigate kidney toxicity from RT.