Autopsy Findings in Essential Hypertension: Renal Pathology

Chronic hypertension produces characteristic renal changes at autopsy.

Gross Findings

• Kidneys: symmetrically reduced size (late), or enlarged (early); firm, pale cortex.
• Capsule: adherent, strips with cortical tissue.
• Cut surface: cortical thinning, granular surface (fine granularity = arteriolosclerosis).
• Arteries: intimal thickening, “onion-skin” hyperplasia (nephrosclerosis).

Microscopic (Light Microscopy)

• Vascular: Hyaline arteriolosclerosis (homogeneous pink deposits in afferent/efferent arterioles); hyperplastic arteriolosclerosis (onion-skin, in malignant HTN).
• Glomeruli: Global sclerosis (ischemic), periglomerular fibrosis, hyalinosis.
• Tubules: Atrophy, thyroidization (dilated atrophic tubules with protein casts).
• Interstitium: Fibrosis, chronic inflammatory infiltrate.

Immunofluorescence

• Non-specific: IgM, C3 in sclerotic glomeruli (trapping, not immune complex disease).
• No linear or granular deposits typical of immune GN.

Electron Microscopy

• GBM: wrinkling, duplication (secondary to ischemia).
• Podocyte foot process effacement (non-specific).
• Endothelial swelling, subendothelial flocculent material.

Terminology

Nephrosclerosis = hypertensive renal vascular disease. Benign = chronic, gradual. Malignant = accelerated, with fibrinoid necrosis, TMA.

These changes correlate with duration/severity of hypertension and predict renal functional decline.