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Renal cholesterol embolism: analysis of two spontaneous autopsy cases.

Authors
  • Ehara, Takashi
  • Yazawa, Masanobu
  • Konishi, Kounosuke
  • Hora, Kazuhiko
  • Shigematsu, Hidekazu
Type
Published Article
Journal
Nephrology (Carlton, Vic.)
Publication Date
Feb 01, 2005
Volume
10
Issue
1
Pages
90–96
Identifiers
PMID: 15705188
Source
Medline
License
Unknown

Abstract

Two cases of spontaneous cholesterol embolism, which followed different clinical courses, acute and chronic renal failure, are presented and histopathological lesions are compared. Both cases were diagnosed as cholesterol embolism post-mortem. Case 1 (a 66-year-old man) had acute onset of illness with fever, leucocytosis and renal failure, diagnosed as vasculitis, and died of rupture of an abdominal aortic aneurysm. Case 2 (an 84-year-old man) had eosinophilia of unknown aetiology for 7 years with intermittent worsening of renal function and died of sepsis. Case 1 had diffuse cholesterol crystal emboli in the interlobular arteries and arterioles of the kidney, but case 2 had patchy cholesterol emboli in the interlobular arteries of the kidney. The aorta of case 1 was diffusely ulcerated, which is in contrast to that of case 2, who had limited ulceration in thoracic aorta, which might have contributed to the long duration of illness. Immunohistochemically, the number of macrophages and T cells that infiltrated around cholesterol emboli in the arteries was more in case 1 (macrophages 27.7, T cells 36.1/mm(2)) than in case 2 (2.7, 1.38/mm(2)). Focal interstitial inflammation occurred in both cases. In case 1, marked tubulitis was observed. Case 2 had rather severe atrophy of the tubules and fibrotic interstitium where mast cells were rich (31.9/mm(2)). The number of B cells and eosinophils was few in case 2 (11.35, 0.7/mm(2)) compared with case 1 (101.9, 16.15/mm(2)). These results suggest that in acute lesions of renal cholesterol embolism, macrophages and T cells accumulate around cholesterol crystals and cause tubulointerstitial inflammatory lesions with other inflammatory cells. In chronic lesions, macrophages, T cells and mast cells are the major inflammatory cells present in the interstitium.

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