IPLab:Lab 1:Kidney Infarction
This 48-year-old male died in a motor vehicle accident. An incidental finding at autopsy was a renal infarct which was reddish-tan in color, sharply delineated, and triangular in shape. The base of the infarct was located at the capsular surface and its apex at the corticomedullary junction.
A higher-power photomicrograph shows the edge of this reddish area, illustrating coagulation necrosis (1) compared to the normal tissue (2). The necrotic tissue in this hemorrhagic, red infarct is hypereosinophilic. Compare the tubules on the right with the normal tubules seen in the left-hand portion of the slide. Note the interstitial hemorrhage which is associated with vascular leakage within this necrotic region in the tissue.
This higher-power view of the infarct demonstrates retention of the tubular structure and cellular outlines. In the lower right-hand corner is a barely identifiable glomerulus (1). Note that, although the cellular architecture is retained, there are no nuclei within the renal tubular cells. The nuclei visible in this photomicrograph are the nuclei of inflammatory cells.
The shape of the infarct is due to the blood flow distribution of the renal circulation.
Remember that the interlobar arteries branch at 90 degrees to form the arcuate arteries at the level of the corticomedullary junction. This is a good place for thrombi to lodge. Also, the interlobular arteries branch off the arcuate arteries at 90 degrees, another good place for thrombi to lodge.
Ischemia means too little blood flow to maintain viability of the tissue. Blood flow can be decreased enough to result in necrosis of a metabolically active tissue like the kidney, but the blood flow does not necessarily have to be completely stopped. Also, blood can seep into an area of infarction through damaged blood vessels at the edge of the infarcted tissue.
- eMedicine Medical Library: Renal Cortical Necrosis
- eMedicine Medical Library: Acute Tubular Necrosis
- Merck Manual: Renal Cortical Necrosis
- Domanovits H, Paulis M, Nikfardjam M, Meron G, Kürkciyan I, Bankier AA, Laggner AN. Acute renal infarction: clinical characteristics of 17 patients. Medicine (Baltimore) 1999 Nov; 78(6): 386-94.
Related IPLab Cases
- Lab 4: Kidney: Atheromatous Emboli
- Lab 5: Kidney: Nodular Intercapillary Glomerulosclerosis
- Lab 6: Kidney: Glomerulonephritis
- Lab 6: Kidney: Acute Transplant Rejection
- Lab 6: Kidney: Chronic Transplant Rejection
The normal fibrinogen level is 184 to 412 mg/dL.