Nephrology · USMLE Step 1 and Step 2

AKI song

Acute Kidney Injury - Prerenal vs Intrinsic vs Postrenal, as a song. Hear the short teaser here. The full song is on YouTube and Spotify.

AKI

Full song on YouTube ↗Spotify ↗

Key points in this song10

Prerenal AKI is caused by decreased renal perfusion (hypovolemia, heart failure, sepsis) and is characterized by a BUN:Creatinine ratio greater than 20:1 and a fractional excretion of sodium (FENa) less than 1%.
In prerenal AKI, the kidneys are structurally intact and respond by avidly reabsorbing sodium and water, producing concentrated urine with osmolality greater than 500 mOsm/kg and urine sodium less than 20 mEq/L.
Intrinsic AKI most commonly results from acute tubular necrosis (ATN), caused by ischemia (prolonged prerenal state) or nephrotoxins (aminoglycosides, myoglobin, contrast, cisplatin), with FENa greater than 2% and muddy brown granular casts on urinalysis.
Acute interstitial nephritis (AIN), a cause of intrinsic AKI, classically presents with the triad of fever, rash, and eosinophilia after exposure to NSAIDs, penicillins, or rifampin, and shows WBC casts and eosinophiluria on urinalysis.
Rapidly progressive glomerulonephritis (RPGN) causes intrinsic AKI with RBC casts and dysmorphic red cells on urinalysis, and biopsy reveals crescents formed by parietal epithelial cell proliferation in Bowman's space.
Postrenal AKI results from urinary tract obstruction (BPH, bilateral ureteral obstruction, bladder outlet obstruction) and is the most common reversible cause of AKI in elderly men; renal ultrasound showing hydronephrosis is the key diagnostic step.
After relief of bilateral obstruction, post-obstructive diuresis can cause severe electrolyte disturbances including hyponatremia, hypokalemia, and hypomagnesemia, requiring careful IV fluid replacement.
Contrast-induced nephropathy, a form of ATN, is prevented by pre-hydration with isotonic saline and avoiding NSAIDs and nephrotoxins; N-acetylcysteine use is controversial but may be considered in high-risk patients.
Indications for emergent dialysis in AKI are recalled by the mnemonic AEIOU: Acidosis (refractory metabolic), Electrolyte abnormalities (refractory hyperkalemia), Ingestions (toxic), Overload (refractory pulmonary edema), and Uremia (encephalopathy, pericarditis, bleeding).
Myoglobinuria from rhabdomyolysis causes pigment-induced ATN; urinalysis shows heme-positive dipstick with no RBCs on microscopy, and serum creatine kinase greater than 5,000 U/L with a CK exceeding 15,000–20,000 U/L significantly increases AKI risk.