Renal/Urology · PANCE / PANRE

Acute Kidney Injury (AKI)

Written & clinically reviewed by Ryan Busch, PA-C · Updated August 2026 · Report an error

Abrupt decline in renal function categorized as prerenal, intrarenal, or postrenal.

Also known as: AKI, acute renal failure, ARF, prerenal azotemia, intrarenal AKI, postrenal AKI

Overview

An abrupt (within hours to days) decline in kidney function defined by KDIGO criteria: rise in serum creatinine ≥0.3 mg/dL within 48 h, ≥1.5× baseline within 7 days, or urine output <0.5 mL/kg/h for ≥6 h. Categorized by mechanism into prerenal (hypoperfusion), intrarenal (parenchymal injury), and postrenal (obstruction).

Epidemiology

Affects up to 20% of hospitalized adults and >50% of ICU patients. Prerenal causes account for ~60% of community-acquired AKI; ATN dominates hospital-acquired AKI.

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Question 1RenalMedium
A 75-year-old male has acute kidney injury with creatinine rising from 1.0 to 2.5 over 3 days during hospitalization for pneumonia. BUN/Cr ratio is 25:1. Fractional excretion of sodium (FENa) is 0.5%. Urine sodium is 15 mEq/L. Which of the following types of acute kidney injury (AKI) does this best fit?
  • AAcute interstitial nephritis
  • BPre-renal AKI
  • CPost-renal AKI from urinary obstruction
  • DIntrinsic AKI from acute tubular necrosis
Reveal answer & full explanation
Correct answer: B — Pre-renal AKI
  • AAcute interstitial nephritis
  • BPre-renal AKI✓
  • CPost-renal AKI from urinary obstruction
  • DIntrinsic AKI from acute tubular necrosis

Why Pre-renal AKI is correct

  • BUN:Cr ratio >20:1 (here 25:1) reflects urea reabsorption in the setting of reduced renal perfusion
  • Fractional excretion of sodium (FENa) <1% (here 0.5%) indicates intact tubular sodium reabsorption, consistent with pre-renal state
  • Urine sodium <20 mEq/L (here 15 mEq/L) further supports pre-renal AKI
  • Additional pre-renal features: urine osmolality >500 (concentrating ability preserved) and bland urinary sediment
  • Causes include volume depletion, sepsis, heart failure, hepatorenal syndrome

Why the others are wrong

  • Acute interstitial nephritis — Acute interstitial nephritis (AIN) is drug-induced (NSAIDs, proton pump inhibitors (PPIs), antibiotics especially beta-lactams), often with eosinophiluria, fever, and rash; FENa would typically be elevated
  • Post-renal AKI from urinary obstruction — Post-renal AKI presents with hydronephrosis on ultrasound; indices may vary but the urinary findings here do not suggest obstruction
  • Intrinsic AKI from acute tubular necrosis — Acute tubular necrosis (ATN) shows BUN:Cr 10-15:1, FENa >2%, urine Na >40 mEq/L, urine osmolality <350, and muddy brown granular casts — the opposite of this patient's findings

Additional high-yield points

  • Pre-renal AKI can progress to ATN if the underlying cause is not treated
  • Treatment: address the underlying cause; pre-renal responds to fluids; ATN is managed supportively
Question 2RenalMedium
A 72-year-old man is admitted with acute kidney injury after several days of poor oral intake and vomiting. He is orthostatic with dry mucous membranes. Labs show a serum BUN:creatinine ratio of 28:1, urine sodium of 12 mEq/L, fractional excretion of sodium of 0.6%, and urine osmolality of 580 mOsm/kg. Urine microscopy shows hyaline casts without cellular elements. Which category of acute kidney injury do these findings indicate?
  • APrerenal acute kidney injury
  • BAcute tubular necrosis
  • CPostrenal obstructive injury
  • DAcute glomerulonephritis
Reveal answer & full explanation
Correct answer: A — Prerenal acute kidney injury
  • APrerenal acute kidney injury✓
  • BAcute tubular necrosis
  • CPostrenal obstructive injury
  • DAcute glomerulonephritis

Why Prerenal acute kidney injury is correct

  • Prerenal AKI results from hypovolemia; when renal perfusion falls, the tubules are intact and respond to angiotensin II, aldosterone, and ADH by avidly reabsorbing sodium and water
  • Characteristic lab pattern: urine sodium <20 mEq/L, fractional excretion of sodium (FENa) <1%, urine osmolality >500 mOsm/kg (concentrated), and a disproportionate rise in BUN relative to creatinine (>20:1) because reabsorbed urea follows water
  • Bland urine with only hyaline casts is expected in prerenal AKI
  • This patient's values (urine Na 12 mEq/L, FENa 0.6%, urine osm 580 mOsm/kg, BUN:Cr 28:1) all fit the prerenal pattern

Why the others are wrong

  • B) Acute tubular necrosis — Injured tubules cannot reabsorb sodium or concentrate urine, producing urine Na >40, FENa >2%, isosthenuric urine osmolality near 300 mOsm/kg, BUN:Cr around 10–15:1, and muddy-brown granular casts
  • C) Postrenal obstructive injury — Postrenal AKI is suggested by hydronephrosis on imaging and does not produce this avid-sodium-retention index pattern
  • D) Acute glomerulonephritis — Glomerulonephritis causes an active sediment with dysmorphic RBCs, RBC casts, and proteinuria rather than the bland, concentrated, sodium-avid urine seen here
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Risk factors

  • Age >65, baseline CKD, diabetes, heart failure, cirrhosis
  • Volume depletion: vomiting, diarrhea, diuretics, hemorrhage, sepsis
  • Nephrotoxins: NSAIDs, ACEi/ARB, aminoglycosides, vancomycin, IV contrast, cisplatin
  • Major surgery (especially cardiac), critical illness, rhabdomyolysis

Pathophysiology

Prerenal: reduced renal perfusion preserves tubular integrity; reversible with restored flow. Intrarenal: direct parenchymal damage (tubular, glomerular, interstitial, or vascular) — most commonly acute tubular necrosis from ischemia or toxins. Postrenal: bilateral obstruction (or unilateral with single functioning kidney) raises intratubular pressure and reduces GFR.

Clinical presentation

Symptoms

  • Often asymptomatic; detected on routine labs
  • Reduced urine output or change in urine appearance
  • Volume overload symptoms: dyspnea, edema, orthopnea (if oliguric)
  • Uremic symptoms in advanced injury: nausea, anorexia, pruritus, confusion

Signs / physical exam

  • Volume status assessment is the central physical finding
  • Prerenal: dry mucous membranes, flat JVP, orthostasis, poor skin turgor
  • Intrinsic/oliguric: hypervolemia with edema, crackles, elevated JVP
  • Postrenal: distended bladder, suprapubic tenderness, enlarged prostate on DRE

Classic findings

Asterixis, pericardial friction rub, and uremic frost suggest advanced uremia requiring urgent dialysis evaluation.

Differential diagnosis

  • Prerenal azotemia — Volume depletion or low effective arterial volume; BUN:Cr >20:1, FENa <1%, urine Na <20, bland sediment; reverses with fluid challenge
  • Acute tubular necrosis — Recent ischemic insult or nephrotoxin; FENa >2%, urine Na >40, muddy brown granular casts
  • Acute interstitial nephritis — Recent drug (PPI, NSAID, beta-lactam), fever, rash, eosinophilia, WBC casts and eosinophils in urine
  • Glomerulonephritis — Hematuria with dysmorphic RBCs, RBC casts, proteinuria, hypertension
  • Postrenal obstruction — Anuria or fluctuating output, distended bladder, hydronephrosis on ultrasound — relieved by catheter or stent
  • Hepatorenal syndrome — Advanced cirrhosis with ascites, no response to volume, urine Na <10, normal sediment
  • Cardiorenal syndrome — Decompensated heart failure with congestion; improves with decongestion despite low forward flow
  • Contrast-associated AKI — Cr rise within 24-72 h of iodinated contrast; usually peaks day 3-5 and resolves by day 7-10

Diagnostic workup

Diagnostic criteria

KDIGO AKI: Stage 1 (Cr 1.5-1.9× baseline or +0.3 mg/dL; UOP <0.5 mL/kg/h × 6-12 h). Stage 2 (Cr 2.0-2.9× baseline; UOP <0.5 mL/kg/h × ≥12 h). Stage 3 (Cr ≥3× baseline, ≥4 mg/dL, or RRT initiation; UOP <0.3 mL/kg/h × ≥24 h or anuria ≥12 h).

Labs

  • BMP with serum creatinine and BUN — establish baseline and trajectory
  • Urinalysis with microscopy — sediment is the single most useful test to localize injury
  • Urine electrolytes for FENa or FEUrea (FEUrea more reliable on diuretics)
  • CBC, urine protein-to-creatinine ratio
  • If glomerular: ANA, ANCA, anti-GBM, complement (C3/C4), hepatitis serologies, SPEP/UPEP

Imaging

  • Renal ultrasound — rules out obstruction (hydronephrosis) and assesses kidney size/echogenicity
  • Bladder scan — postvoid residual >150-200 mL suggests outlet obstruction
  • CT without contrast if stones suspected

Diagnostic algorithm

IndexPrerenalATN (intrarenal)Postrenal
BUN:Cr ratio>20:110-15:1Variable
FENa<1%>2%Variable (>1% if chronic)
FEUrea<35%>50%Variable
Urine Na (mEq/L)<20>40Variable
Urine osmolality>500<350 (isosthenuric)<350
Urine sedimentBland, hyaline castsMuddy brown granular castsBland or hematuria
Response to fluidsCr improvesNo changeNo change (relieve obstruction)
Laboratory discrimination of prerenal vs intrarenal (ATN) vs postrenal AKI.

Treatment

First-line

  • Identify and treat underlying cause (volume, sepsis, obstruction, nephrotoxin withdrawal)
  • Prerenal: isotonic crystalloid (lactated Ringer's or normal saline) — balanced solutions preferred
  • Postrenal: relieve obstruction with Foley catheter, percutaneous nephrostomy, or ureteral stent
  • Stop nephrotoxins: NSAIDs, ACEi/ARB (if hemodynamically driven), aminoglycosides, contrast
  • Adjust renally cleared medications and avoid further insults

Second-line / adjunct

  • Loop diuretic — furosemide, torsemide, bumetanide — for volume overload (does not change AKI course)
  • Vasopressor — norepinephrine, vasopressin — for septic shock with target MAP ≥65
  • Renal replacement therapy (RRT) for AEIOU: refractory Acidosis, Electrolyte derangement (hyperkalemia), Ingestion (dialyzable toxin), Overload (volume), Uremia (pericarditis, encephalopathy, bleeding)

Complications

  • Hyperkalemia with cardiac arrhythmia
  • Metabolic acidosis (high anion gap)
  • Volume overload, pulmonary edema
  • Uremic encephalopathy, pericarditis, platelet dysfunction
  • Transition to CKD; 25-30% have incomplete recovery after severe AKI

PANCE pearls

  • FENa <1% with BUN:Cr >20:1 = prerenal; FENa >2% = ATN. FENa is unreliable on diuretics — use FEUrea (<35% prerenal).
  • Muddy brown granular casts = ATN. RBC casts = GN. WBC casts = pyelonephritis or AIN. Eosinophils = AIN (low sensitivity).
  • Always check a bladder scan or place a Foley early — postrenal causes are easy to miss and rapidly reversible.
  • ACEi/ARB can cause functional AKI in bilateral renal artery stenosis or volume-depleted states; hold and rechallenge after recovery.
  • Contrast-associated AKI is overdiagnosed; recent data suggest IV contrast in stable patients with eGFR >30 carries minimal risk.

References

  • KDIGO 2012 — KDIGO Clinical Practice Guideline for Acute Kidney Injury (Kidney Int Suppl 2012)
  • KDIGO 2024 — KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of CKD (Kidney Int 2024)
  • ADQI — Acute Disease Quality Initiative consensus on contrast-associated AKI (Mehran et al., NEJM 2019)

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Commonly confused with

vs Acute Tubular Necrosisvs Chronic Kidney Disease

Related Renal/Urology diagnoses

Chronic Kidney Disease (CKD)End-Stage Renal Disease and DialysisNephrotic SyndromeNephritic SyndromeIgA NephropathyAcute Tubular Necrosis (ATN)Acute Interstitial Nephritis (AIN)Post-Streptococcal Glomerulonephritis (PSGN)Autosomal Dominant Polycystic Kidney Disease (ADPKD)Urolithiasis (Kidney Stones)Acute Cystitis (Uncomplicated UTI)Acute PyelonephritisRenal Cell Carcinoma (RCC)Bladder Cancer

Educational use only. This outline is a study aid for PA students and is not medical advice or a substitute for clinical judgment. FirstPassPA is an independent study tool and is not affiliated with, endorsed by, or sponsored by NCCPA or PAEA. PANCE® and PANRE® are registered trademarks of the National Commission on Certification of Physician Assistants; End of Rotation™ is a program of the Physician Assistant Education Association.