Which of the following is a common cause of intrinsic (intrarenal) AKI?

• A. Acute tubular necrosis due to ischemia
• B. Glomerulonephritis
• C. Acute interstitial nephritis
• D. Prerenal AKI

Answer: (A)

Intrinsic kidney injury happens when the damage is inside the kidney itself, not from weak blood flow or obstruction outside. Among the intrinsic causes, ischemia leading to acute tubular necrosis is one of the most common. When perfusion drops severely or for a prolonged period, tubular epithelial cells—especially in the proximal tubule and thick ascending limb—become energy-deprived, lose their structure, slough off, and form casts that clog tubules. This tubular damage disrupts reabsorption, impairs filtration, and leads to oliguria and azotemia. Ischemic ATN is especially common after events like shock, major surgery, or severe sepsis, which is why it’s a frequent intrinsic AKI culprit in clinical practice.

Lab clues often include a higher sodium loss in the urine, with a fractional excretion of sodium above 2%, urine sodium commonly over 40 mEq/L, and urine osmolality around 300–350 mOsm/kg, sometimes with muddy brown granular casts. These findings help differentiate intrinsic ATN from prerenal AKI, where perfusion is reduced but kidney tissue remains structurally intact and the urine is typically more concentrated with a low FeNa.

Other intrinsic causes exist, such as glomerulonephritis, which targets the glomeruli, and acute interstitial nephritis, which involves the kidney interstitium and is often drug-related. However, ischemic acute tubular necrosis remains the most frequent intrinsic mechanism in many patients.