Pathologies of acute tubular necrosis

Perazella MA. Clinical Approach to Diagnosing Acute and Chronic Tubulointerstitial Disease. Adv Chronic Kidney Dis. 2017 Mar;24(2):57-63. Full-text for Emory users.

Abbreviations: ATIN, acute tubulointerstitial nephritis; CTIN, chronic
tubulointerstitial nephritis; NSAIDs, nonsteroidal anti-inflammatory
drugs; PPIs, proton pump inhibitors; SLE, systemic lupus erythematosis;
TIN, tubulointerstitial nephritis; TINU, tubulointerstitial nephritis
uveitis; DRESS, drug related eosinophilia systemic syndrome. (Perazella, p. 59)

Leah Haseley L, Jefferson JA. (2019). Pathophysiology and Etiology of Acute Kidney Injury. In: Comprehensive Clinical Nephrology, 6th ed.: p. 786-801.e1.

Fig. 66.5. Vascular factors contributing to the development of acute tubular necrosis. Renal vasoconstriction and endothelial injury promote renal ischemia and tubular injury. eNOS, endothelial nitric oxide synthase; GFR, glomerular filtration rate; ICAM-1, intercellular adhesion molecule 1; NO, nitric oxide.
Fig. 66.6. Tubular factors in the development of acute tubular necrosis. Loss of cell polarity results in weakening of cell-to-cell and cell matrix adhesion resulting in cast obstruction and backleak of tubular fluid.

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