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| Renal Infarct |
| Etiology |
•Most renal infarcts are the result of embolized thrombi that lodge in renal arterial vessels. |
| Pathogenesis |
•Vascular occlusion by embolized thrombi causes infarctive, coagulative type necrosis. |
| Epidemiology |
•The epidemiology is that of the primary disease process affecting the heart, i.e, atherosclerotic cardiovascular disease, infectious endocarditis. |
| Clinical |
•Since many
cases are caused by thrombi that form in the left heart, the clinical
picture may be dominanted by the cardiac problems. •Flank pain may be present and a direct reflection of the renal infarct. |
| General Gross Description |
•On cut section, renal infarcts are
triangular with the base at the cortical surface and the apex
pointing towards the medulla and the occluded artery. •A day or so after
occlusion, the infarct appears pale compared to adjacent parenchyma. •Old resolved infarcts on cut section show a V shape absence of renal parenchyma. |
| General Micro Description |
•Recent infarcts show coagulative necrosis where the native
renal architecture is discernible but the tissue is necrotic.
•Heal by scarring. |
| Reference |
• Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 982.
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