Renal/Urology · PANCE / PANRE

Acute Kidney Injury (AKI)

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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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

Index	Prerenal	ATN (intrarenal)	Postrenal
BUN:Cr ratio	>20:1	10-15:1	Variable
FENa	<1%	>2%	Variable (>1% if chronic)
FEUrea	<35%	>50%	Variable
Urine Na (mEq/L)	<20	>40	Variable
Urine osmolality	>500	<350 (isosthenuric)	<350
Urine sediment	Bland, hyaline casts	Muddy brown granular casts	Bland or hematuria
Response to fluids	Cr improves	No change	No 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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