Mastering Medical
Renal & Acid-Base

Acute Kidney Injury: Step 1 review notes and self-test

Notes for the Acute Kidney Injury rapid review: the clue that separates each of its 5 confusion pairs, with timestamps and a self-test.

This video covers prerenal, intrinsic, and postrenal acute kidney injury. Watch it first, then use these notes to test yourself.

Acute Kidney Injury for USMLE Step 1: Prerenal, Intrinsic & Postrenal Made Easy

Prerenal azotemia vs Intrinsic AKI

Watch this part at 0:29

Think prerenal when you see FeNa under 1 percent, a BUN-to-creatinine ratio above 20:1, and bland sediment. Think intrinsic AKI when FeNa is above 2 percent with active sediment. Do not localize AKI from a rising creatinine alone, and remember that FeNa is unreliable with loop diuretics, so use FeUrea under 35 percent as the better substitute. If no clear cause emerges, exclude postrenal obstruction with renal ultrasound.

Prerenal azotemia vs Intrinsic AKI Prerenal: FeNa under 1 percent, BUN to creatinine above 20:1, bland sediment; intrinsic AKI: FeNa above 2 percent with active sediment. Open the comparison and video →

Postrenal AKI vs Intrinsic AKI

Watch this part at 1:51

Think postrenal AKI when urinary outflow obstruction causes hydronephrosis on ultrasound. Think intrinsic AKI when kidney parenchymal injury produces active urine sediment. Late obstruction can mimic intrinsic tubular injury, so image for hydronephrosis when obstruction is plausible.

Postrenal AKI vs Intrinsic AKI Postrenal AKI: outflow obstruction with hydronephrosis on ultrasound; intrinsic AKI: parenchymal injury with active urine sediment. Open the comparison and video →

Acute interstitial nephritis vs Acute tubular necrosis

Watch this part at 3:06

Think acute interstitial nephritis when you see WBC casts, eosinophils, and a recent drug, although fever, rash, and eosinophilia are often absent. Think acute tubular necrosis when muddy brown granular casts follow ischemia or toxin exposure, especially with FeNa above 2 percent. Do not assume that every medication-related injury is an allergy because some drugs directly injure tubules.

Acute interstitial nephritis vs Acute tubular necrosis AIN: WBC casts, eosinophils, and a recent drug; ATN: muddy brown granular casts after ischemia or a toxin. Open the comparison and video →

Drug-induced acute interstitial nephritis vs Autoimmune acute interstitial nephritis

Watch this part at 4:32

Think drug-induced acute interstitial nephritis when AKI with sterile pyuria and WBC casts follows a culprit medication. Think autoimmune acute interstitial nephritis when tubulointerstitial nephritis occurs with systemic immune clues or uveitis without drug timing. Both can cause sterile pyuria and WBC casts, so use exposure timing and extra-renal features to separate them.

Drug-induced acute interstitial nephritis vs Autoimmune acute interstitial nephritis Drug-induced AIN follows a culprit medication; autoimmune AIN follows systemic immune clues or uveitis without drug timing. Open the comparison and video →

Acute kidney injury vs Chronic kidney disease

Watch this part at 5:46

Think acute kidney injury when creatinine rises or urine output declines abruptly over hours to days. Think chronic kidney disease when kidney damage or reduced GFR persists for more than 3 months with chronic anemia, mineral-bone disease, small echogenic kidneys, or long-standing proteinuria. One high creatinine value cannot separate them, so check the baseline, duration, kidney size, and chronic complications.

Acute kidney injury vs Chronic kidney disease AKI is rapid and recent; CKD is persistent for months with chronic adaptation and scarring clues. Open the comparison and video →

Quick self-test

Name the diagnosis from the clue, then tap to check.

  1. AKI from urinary outflow obstruction, suggested by retention, suprapubic fullness, hydronephrosis, BPH, stones, pelvic tumor, or catheter blockage.

    Postrenal AKI · Postrenal AKI vs Intrinsic AKI

  2. AKI from direct kidney parenchymal injury such as ATN, glomerulonephritis, interstitial nephritis, vascular disease, or toxins.

    Intrinsic AKI · Postrenal AKI vs Intrinsic AKI

  3. AKI after NSAIDs, PPIs, beta-lactams, sulfonamides, or another new drug; fever/rash/eosinophilia can occur but are often absent.

    Acute interstitial nephritis · Acute interstitial nephritis vs Acute tubular necrosis

  4. AKI with sterile pyuria, WBC casts, and possible fever/rash/eosinophilia after NSAIDs, PPIs, beta-lactams, sulfonamides, or another drug.

    Drug-induced acute interstitial nephritis · Drug-induced acute interstitial nephritis vs Autoimmune acute interstitial nephritis

  5. Abrupt creatinine rise or urine output decline over hours to days, often after sepsis, hypotension, obstruction, drug exposure, or toxin.

    Acute kidney injury · Acute kidney injury vs Chronic kidney disease

  6. Volume loss or low effective arterial volume with concentrated urine and sodium retention.

    Prerenal azotemia · Prerenal azotemia vs Intrinsic AKI

  7. Kidney tissue injury with impaired concentrating ability and sodium wasting.

    Intrinsic AKI · Prerenal azotemia vs Intrinsic AKI

  8. AKI after ischemia or toxin exposure with muddy brown granular casts.

    Acute tubular necrosis · Acute interstitial nephritis vs Acute tubular necrosis

Keep going

Every pair in this review has a free page in the library with a side-by-side comparison and a practice question. Work through the ones you missed in the self-test first.