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) |
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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