What is the primary pathophysiological mechanism in acute tubular necrosis (ATN) following prolonged hypotension?

Acute tubular necrosis (ATN) primarily occurs due to ischemic injury to renal cells, particularly following prolonged hypotension. When blood flow to the kidneys is significantly reduced, such as in cases of severe dehydration, shock, or prolonged low blood pressure, the renal tubular cells receive insufficient oxygen and nutrients, leading to cellular injury and necrosis.

Ischemic conditions cause a depletion of ATP in the renal tubular cells, impairing their ability to maintain essential functions, including ion transport, and results in cell swelling and death. The proximal tubular cells are particularly vulnerable because they have high metabolic activity and are reliant on oxygen for ATP production.

This pathophysiological mechanism is critical for understanding the progression of ATN, as the damaged renal tubules can't effectively filter waste from the blood, leading to the accumulation of toxins and electrolyte imbalances in the body. Therefore, the primary pathophysiological mechanism in ATN following prolonged hypotension is indeed ischemic injury to renal cells.