Radiation Nephritis

What is radiation nephritis?

Radiation nephritis is classified into two categories based on the onset of symptom presentation: (1) acute radiation nephritis and (2) chronic radiation nephritis.

Acute radiation nephritis usually presents within 6 to 12 months of exposure to radiation. Patients may present with edema, hypertension (may be malignant), proteinuria, and anemia. Often, this progresses to secondary chronic radiation nephritis. Angiotensin-converting enzyme inhibitors (ACE-I) are the antihypertensive agents of choice for treatment of hypertension associated with radiation nephritis.

Primary chronic radiation nephritis presents after more than 18 months of radiation exposure and is characterized by proteinuria, hypertension, and progression of CKD.

Although the exact pathogenesis remains elusive, it is believed that exposure of the kidneys to greater than 1500 to 2500 rad leads to endothelial cell injury. Radiation can also cause direct injury to the tubular epithelial cells. Furthermore, patients receiving radiation therapy for some underlying malignancy also receive concomitant chemotherapy, which may potentiate radiation’s toxic effects on the kidneys.

Histopathologically, there is characteristic thickening of the capillary walls, which may also demonstrate “splitting.” Interposition of deposits between the split layers of the glomerular basement membrane is noticeably similar to that seen in hemolytic uremic syndrome and thrombotic thrombocytopenic purpura.

Proper shielding of the kidneys, especially in those with preexisting CKD, should be pursued when possible. Fractionizing the total irradiation dose into several small doses over several days may also be protective.

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