A 65-year-old man comes to the emergency department due to acute-onset, severe right flank pain; nausea; and vomiting for the past hour. His medical conditions include prostate cancer and membranous nephropathy. Blood pressure is 148/60 mm Hg and pulse is 95/min. On physical examination, the patient appears to be in moderate distress due to pain and is diaphoretic. There is right costovertebral angle tenderness. Urinalysis shows hematuria. Contrast-enhanced CT scan reveals a wedge-shaped perfusion defect in the right kidney. The affected renal tissue is most likely to develop which of the following histologic changes over the next several days?

Question

A 65-year-old man comes to the emergency department due to acute-onset, severe right flank pain; nausea; and vomiting for the past hour.  His medical conditions include prostate cancer and membranous nephropathy.  Blood pressure is 148/60 mm Hg and pulse is 95/min.  On physical examination, the patient appears to be in moderate distress due to pain and is diaphoretic.  There is right costovertebral angle tenderness.  Urinalysis shows hematuria.  Contrast-enhanced CT scan reveals a wedge-shaped perfusion defect in the right kidney.  The affected renal tissue is most likely to develop which of the following histologic changes over the next several days?

Quizplus · Accepted Answer

11ec160b_39f9_1844_9249_97f67c83b054_MD0001_00 This patient with multiple risk factors for hypercoagulability (ie, malignancy, membranous nephropathy) has flank pain, hematuria, and a wedge-shaped perfusion defect in the right kidney. This presentation is consistent with a renal infarction, likely from thromboembolic disease. Prolonged ischemia (as seen in infarcted tissue) results in irreversible cellular injury and cellular necrosis. Necrosis is an uncontrolled process of cell death that results in denaturation of cellular proteins and enzymatic digestion of cellular components. Unlike apoptosis, necrosis leads to a loss of membrane integrity and leakage of proinflammatory intracellular material that can injure the surrounding tissue. Necrosis occurs in several distinct morphologic patterns. In most organs, irreversible ischemic injury typically results in coagulative necrosis. Because the digestive enzymes denature before they can significantly disrupt tissue integrity, the cellular architecture is maintained but nuclei are absent. A major exception is tissue within the CNS, in which ischemia (eg, stroke) causes liquefactive necrosis with digestion of cellular constituents and liquefaction of necrotic tissue (Choice E). (Choice A) Caseous necrosis is a pattern of necrosis seen with mycobacterial or certain fungal (eg, Histoplasma, Cryptococcus) infections. Collections of epithelioid macrophages and giant cells surround white, friable, cheese-like material made up of cell fragments and proteinaceous debris (ie, caseating granulomas). (Choice C) Fat necrosis occurs in areas with high numbers of adipocytes (eg, pancreas, breast, subcutaneous fat) and is frequently seen in pancreatitis. Enzymes released from damaged cells break down triglycerides into free fatty acids, which combine with calcium to form soaps; anucleated adipocytes with calcium deposits are visible on microscopy. (Choice D) Fibrinoid necrosis is a histologic pattern of injury seen in the walls of blood vessels affected by vasculitis or malignant hypertension. It results from immune complexes and/or plasma proteins (eg, fibrin) leaking through the damaged intima and depositing within the vessel wall; the deposits appear histologically as a circumferential ring of pink, amorphous material surrounding the vascular lumen. (Choice F) Dystrophic calcification occurs in areas of tissue injury or necrosis that escape removal by phagocytes. Phosphate ions in the necrotic tissue bind calcium to form salts, which can appear grossly as white granules and microscopically as amorphous, basophilic material on hematoxylin and eosin stain. However, the calcification develops slowly over the months and years following the initial injury. Educational objective: Lethal tissue ischemia causes coagulative necrosis in most tissues (eg, kidney, myocardium); cellular architecture is maintained but nuclei are absent. The exception is ischemic cell death in the CNS, which causes liquefactive necrosis.

A 65-Year-Old Man Comes to the Emergency Department Due to Acute-Onset