Everything You Need to Know About Prerenal vs intrinsic vs postrenal AKI for Step 1

Acute kidney injury (AKI) questions are everywhere on Step 1 and Step 2 because they reward pattern recognition: volume status + urine studies + obstruction clues. If you can quickly separate prerenal vs intrinsic vs postrenal AKI, you’ll get the diagnosis, the next best step, and the classic lab patterns—often in under 30 seconds.

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AKI: the core definition (what Step expects)

AKI = abrupt decline in GFR over hours to days leading to:

• ↑ BUN and ↑ creatinine
• Often ↓ urine output (but patients can be non-oliguric)

KDIGO-style thresholds (don’t memorize every number, but recognize the concept):

• Creatinine rise $\ge 0.3$ mg/dL in 48 hours or
• $\ge 1.5\times$ baseline within 7 days or
• Urine output $< 0.5$ mL/kg/hr for 6 hours

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The big 3: where the problem is

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Pathophysiology you should actually visualize

Prerenal AKI: “Kidney is structurally fine”

• Decreased renal perfusion → ↓ GFR
• Tubules respond appropriately:
  • RAAS on → Na+ reabsorption
  • ADH on → water reabsorption
  • Urea reabsorbed (proximal tubule) → BUN rises more than Cr

Key concept: If you restore perfusion early, function returns because the tubules aren’t dead—yet.

First Aid cross-ref: Renal—AKI section (prerenal azotemia; FeNa concept; BUN:Cr changes).

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Intrinsic AKI: “The kidney is injured”

Different subtypes show up on exams; ATN is the workhorse.

Acute Tubular Necrosis (ATN)

• Tubular epithelial injury → sloughing → obstruction + back-leak of filtrate
• Tubules can’t reabsorb Na+ effectively → salt wasting

Two classic etiologies:

• Ischemic ATN: prolonged prerenal state, shock
• Nephrotoxic ATN: aminoglycosides, amphotericin B, cisplatin, radiocontrast, ethylene glycol, myoglobin (rhabdo)

Urine hallmark: muddy brown granular casts
Course: often oliguric; recovery phases are testable (maintenance → recovery with diuresis).

First Aid cross-ref: Renal—ATN; casts table; nephrotoxic drugs.

Acute Interstitial Nephritis (AIN)

• Hypersensitivity reaction (often drug-induced)
• Classic triad (not always all present):
  fever + rash + eosinophilia
• Urine eosinophils and WBC casts

Common causes (high-yield):

• NSAIDs
• Penicillins/cephalosporins
• PPIs
• Rifampin
• Also infections (e.g., pyelonephritis) and autoimmune (e.g., Sjögren)

First Aid cross-ref: Renal—interstitial nephritis; urine findings.

Glomerulonephritis (GN) / nephritic syndrome

• Inflammation damages glomerular capillaries → RBCs leak
• Hematuria + proteinuria + HTN + periorbital edema
• RBC casts = extremely high-yield

Think about causes like post-strep GN, IgA nephropathy, RPGN patterns (Step 1 heavy).

First Aid cross-ref: Renal—nephritic syndromes; RBC casts.

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Postrenal AKI: “The plumbing is blocked”

• Obstruction increases hydrostatic pressure in Bowman space → ↓ net filtration pressure
• Early: kidney may look prerenal-ish on labs
• Later: tubular injury leads to intrinsic-like salt wasting

High-yield clue: Hydronephrosis on ultrasound (except sometimes early obstruction or retroperitoneal fibrosis).

First Aid cross-ref: Renal—postrenal azotemia; hydronephrosis.

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Clinical presentation: how stems hint at each category

Prerenal clues

• History of vomiting/diarrhea, poor PO, hemorrhage
• Diuretics, burns, pancreatitis (third spacing)
• CHF exacerbation (JVP up, edema), cirrhosis (ascites)
• Orthostasis, dry mucous membranes
• Often oliguria that improves with fluids (if not overloaded)

Intrinsic clues

• Recent:
  • contrast study
  • aminoglycoside use
  • prolonged hypotension/sepsis
• Rash/fever/arthralgias (AIN)
• Hematuria, cola-colored urine (GN)
• Systemic findings: vasculitis, SLE, infection

Postrenal clues

• BPH symptoms: hesitancy, weak stream, incomplete emptying
• Anuria or fluctuating urine output
• Suprapubic fullness, distended bladder
• Pelvic malignancy, stones, neurogenic bladder

Pearl: Postrenal AKI often needs bilateral obstruction (or obstruction of a solitary kidney) to cause significant AKI.

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Diagnosis: the Step-friendly algorithm (fast and safe)

Step 1: Confirm AKI + assess severity

• BMP (BUN/Cr, K+, HCO₃⁻)
• Urinalysis + microscopy
• Strict I/Os

Step 2: Rule out obstruction early (especially Step 2)

• Renal/bladder ultrasound is commonly the “best next step” when the cause isn’t obvious.
• Look for hydronephrosis and bladder retention.

Step 3: Use urine studies to separate prerenal vs intrinsic

Key tests:

• FeNa (fractional excretion of sodium)
• Urine sodium
• Urine osmolality
• BUN:Cr ratio
• Urine sediment (casts)

High-yield lab patterns table

Important caveat (testable): If patient is on diuretics, FeNa can be falsely elevated. Use FeUrea instead:

• FeUrea < 35% suggests prerenal.
• FeUrea > 50% suggests intrinsic.

First Aid cross-ref: Renal—FeNa; prerenal vs ATN table; casts.

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Urine casts: rapid-fire recognition (super high-yield)

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Treatment: what changes by category (and what never changes)

Universal first steps in any AKI

• Stop nephrotoxins: NSAIDs, ACEi/ARB (often held temporarily), aminoglycosides, IV contrast if possible
• Dose-adjust meds cleared by kidney
• Monitor:
  • K+ (arrhythmia risk)
  • Volume status
  • Acid-base
• Consider emergent dialysis when indicated (see below)

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Prerenal AKI treatment

Goal: restore renal perfusion.

• Hypovolemia: isotonic fluids (e.g., normal saline or lactated Ringer’s)
• Hemorrhage: blood products as needed
• CHF: optimize forward flow (careful—may need diuresis, not fluids)
• Cirrhosis/hepatorenal physiology: albumin + vasoconstrictors in select scenarios (Step 2 nuance)

Step trap: Giving fluids to a volume-overloaded CHF patient can worsen everything—look at JVP, lungs, edema.

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Intrinsic AKI treatment (by subtype)

ATN

• Mostly supportive
• Optimize perfusion (avoid hypotension)
• Avoid further nephrotoxins
• Manage electrolytes; dialysis if needed
• If rhabdo: aggressive IV fluids; treat cause

AIN

• Stop offending drug
• Supportive care
• Steroids sometimes used if severe/persistent (more Step 2-level management)

GN / RPGN

• Often needs targeted therapy (e.g., steroids, immunosuppression, plasmapheresis depending on cause)
• Recognize the pattern; consult nephrology early

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Postrenal AKI treatment

Goal: relieve obstruction.

• Suspected urinary retention: Foley catheter
• Stones: analgesia, tamsulosin; urology interventions if obstructing/infected
• BPH: alpha-1 blockers; catheterization; definitive management later
• Malignancy/stricture: stent or nephrostomy

Pearl: After obstruction relief, watch for post-obstructive diuresis → can cause volume depletion and electrolyte derangements (replace fluids carefully).

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Dialysis indications (memorize this for exams)

Use AEIOU:

• Acidosis (severe, refractory)
• Electrolytes: hyperkalemia refractory to medical therapy
• Ingestions: toxic alcohols (ethylene glycol, methanol), lithium, salicylates (context-dependent)
• Overload: pulmonary edema refractory to diuretics
• Uremia: encephalopathy, pericarditis, bleeding (platelet dysfunction), severe symptoms

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High-yield associations & classic Step vignettes

Prerenal AKI

• NSAIDs → afferent arteriole constriction (↓ PGE₂) → ↓ GFR
• ACE inhibitors/ARBs → efferent arteriole dilation → ↓ GFR
• Renal artery stenosis (bilateral or solitary kidney) + ACEi → acute rise in creatinine
• BUN:Cr > 20:1 from increased urea reabsorption

First Aid cross-ref: Renal—autoregulation (afferent/efferent), NSAIDs vs ACEi.

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Intrinsic AKI (ATN)

• Aminoglycosides → nephrotoxicity (also ototoxicity)
• Radiocontrast injury after imaging
• Pigment nephropathy: rhabdo (myoglobin), hemolysis (hemoglobin)

Urine: muddy brown casts
Lab: FeNa > 2%, urine Na+ high

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Intrinsic AKI (AIN)

• New medication + fever/rash/eosinophilia
• Eosinophils in urine (Hansel stain)

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Postrenal AKI

• Older male + LUTS → BPH → hydronephrosis
• Anuria with pelvic malignancy or bilateral obstruction
• Step 2 “next step” often: bladder scan or renal ultrasound, then relieve obstruction

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Quick “one-liner” differentiators (what to recall under time pressure)

• Prerenal: kidney is conserving → low FeNa, concentrated urine, hyaline casts
• Intrinsic (ATN): tubules are broken → high FeNa, dilute urine, muddy brown casts
• Postrenal: think hydronephrosis/retention, variable urine indices, fix obstruction

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Mini self-check (3 classic prompts)

1. CHF patient, JVP up, crackles, rising Cr, FeNa < 1%
   → Prerenal physiology (low effective arterial blood volume), treat underlying CHF.

2. After contrast CT, Cr rises, FeNa 3%, muddy brown casts
   → ATN.

3. Elderly man with weak stream, suprapubic fullness, hydronephrosis on US
   → Postrenal; catheterize/decompress.