This is the microscopic appearance of an acute renal infarct.
At the far right is normal kidney,
then to the left of that hyperemic kidney that is dying, then to the left of that pale pink infarcted kidney in which both tubules and glomeruli are dead. This is an ascending bacterial infection leading to acute pyelonephritis. Numerous PMN's are seen filling renal tubules across the center and right of this picture. The tubular vacuolization and dilation here is a result of ethylene glycol poisoning. This is representative of acute tubular necrosis (ATN), which has many causes. ATN resulting from toxins usually has diffuse tubular involvement, whereas ATN resulting from ischemia (as in profound hypotension from cardiac failure) has patchy tubular involvement. Here is a vasculitis of a renal arterial branch. Lymphocytes are scattered in and around the vessel. This happens to be polyarteritis nodosa, a systemic vasculitis that most often affects the kidneys. The P-ANCA serology is usually positive The microscopic appearance of the "end stage kidney" is similar regardless of cause, which is why a biopsy in a patient with chronic renal failure yields little useful information. The cortex is fibrotic, the glomeruli are sclerotic, there are scattered chronic inflammatory cell infiltrates, and the arteries are thickened. Tubules are often dilated and filled with pink casts and give an appearance of "thyroidization." Malignant hypertension:
A: Fibrinoid necrosis of afferent arteriole
B: Hyperplastic arteriolitis (onio-skin lesion)
Courtesy of : Dr. H. Rennke, Dept Pathology, Brigham and Woman’s Hospital
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