ACUTE TUBULAR INJURY/NECROSIS or ACUTE KIDNEY INJURY - Pathology

Tubulointerstitial disorders:1- ACUTE TUBULAR INJURY/NECROSIS

Tubular and Interstitial Diseases • (1) ischemic or toxic tubular injury, leading to acute kidney injury (AKI) or ATN and acute renal failure, and • (2) inflammatory reactions of the tubules and interstitium (tubulointerstitial nephritis).
ACUTE KIDNEY INJURY (AKI) (ACUTE TUBULAR NECROSIS, ATN) ATN is a clinicopathologic entity characterized clinically by Acute reduction of renal function and often, but not invariably, morphologic evidence of tubular injury.
ATI / ATN • It is the most common cause of acute renal failure, which signifies rapid reduction of renal function and urine flow
Causes of AKI 1. Ischemia due to decreased or interrupted blood flow, 2. Direct toxic injury to the tubules 3. Acute tubulointerstitial nephritis 4. Urinary obstruction
Types of ATN1. Ischemic 2. Nephrotoxic 3. Mixed
Pathogenesis
Tubular injury and (2)Disturbances in blood flow
Morphology Ischemic AKI
• focal tubular epithelial necrosis at multiple points along the nephron, with large skip areas in between, often accompanied by
• rupture of basement membranes (tubulorrhexis) and
• occlusion of tubular lumens by casts.
There is also evidence of epithelial regeneration: Flattened epithelial cells with hyperchromatic nuclei and mitotic figures are often present. In the course of time this regeneration repopulates the tubules so that, no residual evidence of damage is seen.
Clinical Course 1.initiation, 2. maintenance, and 3.recovery stages.
The initiation phase Lasting for about 36 hours, is dominated by the inciting medical, surgical, or obstetric event in the ischemic form of AKI.
The Initiation Phase • The only indication of renal involvement is a slight decline in urine output with a rise in BUN. • At this point, oliguria could be explained on the basis of a transient decrease in blood flow and declining GFR.
The maintenance phase • is characterized by sustained decreases in urine output to between 40 and 400 mL/day (oliguria), salt and water overload, rising BUN concentrations, hyperkalemia, metabolic acidosis, and other manifestations of uremia.
The recovery phase • a steady increase in urine volume that may reach up to 3 L/day. • The tubules are still damaged, so large amounts of water, sodium, and potassium are lost in the flood of urine.
The recovery phase •Hypokalemia, rather than hyperkalemia, becomes a clinical problem. There is a peculiar increased vulnerability to infectionat this stage.

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