STEPTRACKERRENAL | PATHOLOGY + PHYSIOLOGY | HIGH-YIELD REVIEW

Acute Kidney Injury

A sudden fall in GFR — before the kidney, in the kidney, or after it — read through BUN:Cr, FENa and the urine sediment.

FOCUS ON
Prerenal: tubules intact → they save Na⁺ and urea → BUN:Cr > 20, FENa < 1%, concentrated urine. ATN: tubules dead → FENa > 2%, dilute urine, muddy brown granular casts. Postrenal: hydronephrosis. Ischemia hits the proximal tubule and thick ascending limb first.
TYPE · CAUSE
MECHANISM
FINDINGS
CLUE
Prerenal azotemia
↓ renal perfusion: hypovolemia, heart failure, cirrhosis, NSAIDs/ACE inhibitors in low flow
BUN:Cr > 20, FENa < 1%, Uosm > 500; bland urine (hyaline casts)
Reversible if perfusion restored
Ischemic ATN
most common intrinsic
Prolonged hypoperfusion → necrosis of proximal tubule and medullary thick ascending limb
Muddy brown granular casts; FENa > 2%; Uosm < 350; BUN:Cr < 15
Patchy necrosis, sloughed cells block tubules
Nephrotoxic ATN
Direct tubular toxins (proximal tubule)
Aminoglycosides, IV contrast, cisplatin, amphotericin B, myoglobin, hemoglobin, ethylene glycol, uric acid
Aminoglycoside ATN: nonoliguric, 5–10 days in
ATN phases
Injury → loss of function → regeneration
Initiation → maintenance (oliguria, hyperkalemia, acidosis, uremia) → recovery (polyuria, hypokalemia)
Polyuric phase: watch K⁺ and volume
Rhabdomyolysis
Myoglobin → tubular toxicity, casts, vasoconstriction
↑↑ CK; urine dipstick ⁺ for blood but no RBCs; ↑ K⁺, ↑ PO₄³⁻, ↓ Ca²⁺
Crush, seizures, statins, exertion · aggressive IV fluids
Ethylene glycol
Metabolized to glycolate and oxalate
↑ anion and osmolar gap; envelope-shaped calcium oxalate crystals
Antifreeze · fomepizole
Tumor lysis syndrome
Cell breakdown → uric acid and phosphate crystals in tubules
↑ K⁺, ↑ PO₄³⁻, ↑ uric acid, ↓ Ca²⁺ after chemo (leukemia, lymphoma)
Prevent: fluids, allopurinol, rasburicase
Postrenal (obstructive)
Bilateral outflow block: BPH, stones, cervical/prostate cancer, neurogenic bladder, retroperitoneal fibrosis
Early: prerenal-like (BUN:Cr > 15); later: tubular damage (FENa ↑); hydronephrosis
Bladder ultrasound / catheter
Renal cortical necrosis
DIC or severe vasospasm infarcts the cortex
Anuria; obstetric emergencies (abruptio placentae), septic shock
Often irreversible
Uremia & dialysis
Retained toxins, K⁺, acid, fluid
Pericarditis, encephalopathy, asterixis, platelet dysfunction, nausea
Urgent dialysis: AEIOU — acidosis, electrolytes (K⁺), ingestions, overload, uremia

Mechanism — why the indices separate

PrerenalTubules healthy
→
RAAS + ADHAvid Na⁺, water, urea reabsorption
→
Low FENa, high BUN:CrConcentrated urine
ATNTubules dead
→
Can't reabsorb Na⁺ or concentrate
→
High FENa, BUN:Cr < 15Dilute urine, granular casts

The medulla works with little oxygen and high transport demand — so the thick ascending limb dies early.

Reading AKI indices

INDEX
PRERENAL
INTRINSIC (ATN)
POSTRENAL
BUN:Cr
> 20
< 15
> 15 (early)
FENa
< 1%
> 2%
> 2% (late)
Uosm
> 500
< 350
< 350 (late)
UNa
< 20
> 40
> 40 (late)
Sediment
Bland, hyaline casts
Muddy brown casts
Variable

How it's tested

COMMON CONFUSIONDiuretics raise FENa even in prerenal states. Use the fractional excretion of urea (FEUrea < 35% = prerenal) in a patient on diuretics.
THE TRAPDipstick strongly positive for blood with no RBCs under the microscope means myoglobin or hemoglobin — rhabdomyolysis or hemolysis — not glomerular bleeding.
YOUR APPROACHHistory (fluid loss, drugs, contrast, crush, obstruction) → BUN:Cr, FENa, osmolality → sediment → ultrasound if obstruction possible.

If you see… think…

Vomiting for 3 days, BUN:Cr 30, FENa 0.4% → prerenal azotemia
Septic shock, then muddy brown casts, FENa 4% → ischemic ATN
Rising creatinine a week into gentamicin → aminoglycoside ATN
Found down for 2 days, ↑ CK, dark urine, no RBCs → rhabdomyolysis
Envelope-shaped crystals + anion gap acidosis → ethylene glycol
Lymphoma chemo, then ↑ K⁺, ↑ uric acid, ↓ Ca²⁺ → tumor lysis syndrome
Old man with BPH, anuria, bilateral hydronephrosis → postrenal AKI
Polyuria and hypokalemia two weeks after ATN → recovery phase
Uremic patient with a friction rub → uremic pericarditis — dialysis
Placental abruption with DIC and anuria → renal cortical necrosis