Renal parenchyma with few sclerosed glomeruli and mild interstitial fibrosis (see attached sheet)
The attached sheet shows following report: LEFT KIDNEY: Number of glomeruli: 67 (permanents - 72) Number of sclerosed glomeruli: 6 (permanents - 0) Percentage of glomerular sclerosis: 9% (permanents - 0%) Tubular interstitial fibrosis/tubular atrophy: 1+ Vessel Arteriosclerosis: 1+ Vessel Hyalinosis: 0 (permanent - "occasional")
COMMENT: Both the biopsies are subcapsular and may be more fibrotic than the remainder of the kidney.
Permanent: KIDNEY (DONOR, LEFT), WEDGE BIOPSY (NEOB ADKY401): CHRONIC GLOMERULAR ENDOTHELIAL INJURY WITH MINIMAL MESANGIAL DEPOSITS, Note: Permanent and deeper sections from A show a wedge of frozen cortical tissue with about 72 glomeruli, of which none is globally sclerotic. Many glomeruli show segmental thickening of capillary walls, one with global duplication. All glomeruli show intracapillary mononuclear cells. There is mild to moderate mesangial expansion in most glomeruli. Adhesions, crescents, necrosis and thrombi are not present. Fibrosis and tubular atrophy affect about 5-10% of the cortical area. The remainder of the tubules is back to back. There is no interstitial inflammation. Many arteries are present, a few with mild intimal fibrosis. Arterioles show occasional hyalinosis. Vasculitis and thrombi are not present.
Permanent and deeper sections from B show a wedge of frozen cortical tissue with about 80 glomeruli, of which 4 are globally sclerotic. Many glomeruli show segmental thickening of capillary walls, some with segmental duplication. All glomeruli show intracapillary mononuclear cells. There is mild to moderate mesangial expansion in most glomeruli. Adhesions, crescents, necrosis and thrombi are not present. Fibrosis and tubular atrophy affect about 10% of the cortical area. The remainder of the tubules is back to back. A few tubules contain intratubular protein casts. Focal subcapsular inflammation is present. Many arteries are present, a few with mild intimal fibrosis. Arterioles show occasional hyalinosis. Vasculitis and thrombi are not present.
One slide labeled S16-78415 NEOB, ADKY401 FX showed similar findings as in frozen biopsy report.
Frozen tissue re-processed for electron microscopy shows segmental effacement of podocyte foot processes. There is segmental basement membrane duplication associated with wrinkling of capillary loops, new membrane formation and mesangial cell interposition. Evaluation of endothelial areas is limited by artifact. Minimal mesangial and para-mesangial electron dense deposits are present.
In summary, the biopsy shows chronic glomerular endothelial injury characterized by basement membrane duplication. In addition, there are minimal mesangial deposits by electron microscopy. These findings suggest chronic endothelial injury from chronic thrombotic microangiopathy or mild chronic immune complex glomerular disease. Correlation with clinical findings including prothrombotic or coagulopathic states is recommended.
