ATLAS OF RENAL PATHOLOGY

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Thrombotic Microangiopathy

Pathology Editor: Agnes Fogo, MD
Medical Photographer: Brent Weedman

 
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Fig 1. Thrombotic microangiopathy is a lesion seen in many conditions, including hemolytic uremic syndrome, radiation nephritis, toxicity related to various drugs, and hereditary forms. The morphological lesions in these various conditions are the same. The lesion consists of fibrin thrombi within glomeruli, which may extend to arterioles. In this patient with hemolytic uremic syndrome, the thrombotic microangiopathy was confined to glomeruli, with extensive fibrin thrombi and platelet plugs filling up the capillary loops. (Jones' silver stain, original magnification X200).
 
 
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Fig 2. In this case of thrombotic microangiopathy, the fibrin thrombi extend from the glomerular capillary loop to the arteriolar vascular pole, a finding associated with worse prognosis. If the vascular lesions are extensive, cortical necrosis may even ensue. (Jones' silver stain, original magnification X200).
 
 
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Fig 3. In chronic stages of injury after thrombotic microangiopathy, organization of the injury may result in a split appearance of the basement membrane, simulating a membranoproliferative-like lesion. However, no immune complexes are present, and the differential diagnosis is easily resolved by ancillary immunofluorescence and electron microscopic studies. (Jones' silver stain, original magnification X200).
 
 
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Fig 4. In severe cases of thrombotic microangiopathy, cortical necrosis may occur, especially when lesions extend to larger vessels, as in this case. Both tubules and glomeruli are necrotic, with fibrin filling the glomerulus and an interlobular vessel, with early signs of chronic injury with intimal fibrosis and fibrin occluding the lumen. (Jones' silver stain, original magnification X200).
 
 
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Fig 5. Fibrin tactoids can also be visualized by electron microscopy in cases of thrombotic microangiopathy, along with endothelial cell swelling and expansion of the lamina rara interna. (Transmission electron microscopy, original magnification X6,000).
 
 
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Fig 6. In thrombotic microangiopathy, no deposits are seen by electron microscopy or immunofluorescence. In more chronic stages, new basement membrane may be formed after the endothelial injury and early interposition with expansion of the lamina rara interna can occur, as illustrated in this case. (Transmission electron microscopy, original magnification X3,000).
 

From the Department of Pathology, Vanderbilt University Medical Center, Nashville, TN.
Address author queries to Agnes Fogo, MD, Department of Pathology, Vanderbilt University Medical Center, MCN C-3310, Nashville, TN 37232. E-mail:Agnes.Fogo@vanderbilt.edu
Am J Kidney Dis 34(3):E7, 1999 (available www.ajkd.org)
 Copyright 1999 by the National Kidney Foundation, Inc.

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