5.5 Irradiation

Definition: Renal damage resulting from exposure to ionizing radiation

Radiation Nephropathy

Aetiology

• Abdominal irradiation for tumortherapy
• Radionuclide therapy (see Octreoide)
• Total body irradiation

Minimal dose (>1000 to 2000 rad) (>10 to 20 Gy)

Clinical findings

• Acute, chronic nephropathy (formerly called „nephritis“), proteinuria, hypertension, renal dysfunction
• Manifestation of disease: highly variable (weeks to more than one decade) after therapy.

Pathology

There are no systematic biopsy or autopsy studies. The morphologic picture, described below  is a mosaic composed of random biopsy findings.

Radiation nephropathy is best classified as a variant of „Thrombotic microangiopathy (TMA)“.
Macroscopy: normal kidneys to highly reduced kidney size, granular surface, reduced width of the cortex
Microscopy:

All renal compartments may be involved: glomeruli, vessels, tubulo-interstitial space.
The glomerular lesions are mostly in the foreground.

Glomerular lesions:

1. Endothelial cell damage (swelling, degeneration, necrosis), podocytic foot process effacement,
2. Fibrin thrombi
3. Mesangiolysis and loop aneurysms
4. Capillary wall thickening (subendothelial widening with matrix increase, basement membrane doubling)
5. Mesangial matrix increase, decrease of glomerular cells,
6. Segmental and or global glomerular obsolescence with hyaline deposits.
7. Fibrin in glomeruli is often found by ICH, even if thrombi  are absent by light microscopy.

The points 1-6 may be considered as morphogenetic steps in the development of glomerular damage. However, all may be found in one biopsy, side by side.

Arteries and Arterioles

Arterioles and interlobular arteries are most severly affected by fibrin thrombi and/ or massive circular and often transmural protein deposits (arteriolar hyalinosis). The arteries may show a mucoid widening of the intimal layer and, rarely, foam cells. Endateritis is not a feature of radiation nephropathy, thrombi and arerial changes are.

Tubulo-interstitial space

Tubular cell swelling and degeneration, tubular cell necrosis, polymorphism of tubular nuclei and tubular giant cells. Finally tubular atrophy.

Interstital edema and later fibrosis.

Tubular atrophy and interstitial fibrosis  may be primary and also secondary, due to glomerular and vascular lesions.