Pathophysiology of Acute Tubular Necrosis

What is the pathophysiology of Acute Tubular Necrosis?

Although Acute Tubular Necrosis is characterized by a profound decrease in GFR, the connection between the tubular injury and the loss of glomerular function is not entirely understood.

Three major mechanisms are thought to underlie the loss of kidney function in Acute Tubular Necrosis:

1. Intratubular obstruction: 

Following an ischemic or nephrotoxic injury, tubular epithelial cells and cellular debris are sloughed from the tubular epithelium and occlude the tubular lumen distally. These sloughed cells and debris form the granular casts seen in the urine sediment.

2. Tubular back leak: 

The sloughing of apoptotic and necrotic tubular epithelial cells results in denuding of the tubular basement membrane and unregulated back leak of glomerular filtrate. The combination of tubular obstruction and back leak results in decreased urine flow through the tubular lumen.

3. Vasoconstriction and microvascular injury: 

Although the pathognomonic injury in Acute Tubular Necrosis is damage to the tubular epithelium, there is both reactive vasoconstriction and endothelial injury in the microvasculature that results in decreased glomerular perfusion, directly reducing the GFR and contributing to the extension of the initial injury.

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