Acute Kidney Injury (AKI)
Definition
Acute kidney injury (AKI) refers to a sudden decline in renal function resulting in retention of nitrogenous waste products (BUN, creatinine) and disturbance in fluid, electrolyte, and acid-base balance.
The loss of renal function develops over hours to days and can progress to uremia if untreated.
Diagnostic Criteria (KDIGO)
AKI is diagnosed if any of the following are present:
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↑ Serum creatinine by ≥ 0.3 mg/dL (26.5 μmol/L) within 48 hours
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↑ Serum creatinine to ≥ 1.5× baseline within 7 days
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Urine output < 0.5 mL/kg/h for ≥ 6 hours
Etiologic Classification
1. Prerenal AKI (~60%)
Caused by decreased renal perfusion without intrinsic damage.
If uncorrected, it can progress to ischemic tubular necrosis.
Common causes:
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Hypovolemia: Hemorrhage, diarrhea, vomiting, burns, diuretics, dehydration, hypercalcemia
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Hypotension: Sepsis, anaphylaxis, cardiogenic shock
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Decreased effective circulating volume: CHF (cardiorenal), cirrhosis (hepatorenal), nephrotic syndrome
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Renal vasoconstriction: NSAIDs, cyclosporine, tacrolimus
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Reduced glomerular perfusion: ACEIs/ARBs, renal artery stenosis
Pathophysiology:
↓ Renal perfusion → ↓ GFR → RAAS activation → Na⁺ and H₂O retention → ↑ urine osmolality, ↑ BUN:creatinine ratio (>20:1)
2. Intrinsic (Renal) AKI (~35%)
Due to direct injury to renal parenchyma — glomeruli, tubules, interstitium, or vasculature.
Major causes:
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Acute tubular necrosis (ATN) – ischemic or nephrotoxic (most common)
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Acute interstitial nephritis (AIN) – usually drug-induced (NSAIDs, antibiotics, PPIs)
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Glomerulonephritis – post-infectious, lupus nephritis, RPGN
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Vascular disorders: TTP, HUS, malignant hypertension, vasculitis, scleroderma crisis
Pathophysiology:
Tubular cell necrosis → obstruction by casts → back-leak of filtrate → ↓ GFR → impaired reabsorption → ↑ FENa (>2%) and ↓ urine osmolality.
3. Postrenal AKI (~5%)
Caused by bilateral obstruction of urinary outflow at any point from renal pelvis to urethra.
Common causes:
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BPH (most common in males)
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Ureteric or bladder stones
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Tumors (prostate, cervix, bladder)
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Blood clots, fibrosis
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Neurogenic bladder
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Congenital defects (e.g., posterior urethral valves)
Pathophysiology:
Obstruction → ↑ tubular hydrostatic pressure → ↓ GFR → tubular ischemia → azotemia.
Clinical Features
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Early stages: Often asymptomatic
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Oliguria (<400 mL/day) or anuria (<100 mL/day)
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Volume depletion signs (prerenal): hypotension, tachycardia, dry mucosa, ↓ skin turgor
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Volume overload (post/intrinsic): edema, hypertension, pulmonary crackles
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Uremic symptoms: anorexia, nausea, asterixis, pericarditis, confusion
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Postrenal: suprapubic fullness, flank pain, bladder distention
Phases of AKI
| Phase | Features | Duration |
|---|---|---|
| Initiation | Kidney insult; mild rise in creatinine | Hours–days |
| Oliguric | ↓ GFR, oliguria/anuria, ↑ BUN/Cr, hyperkalemia, acidosis | 1–3 weeks |
| Diuretic | ↑ urine output but impaired concentrating ability → dehydration, electrolyte loss | 1–2 weeks |
| Recovery | Renal function normalizes | Weeks–months |
Diagnostic Approach
1. Clinical Evaluation
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Assess volume status (dry mucosa, JVP, edema)
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Review medication list for nephrotoxins
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Check for obstruction symptoms (hesitancy, weak stream)
2. Laboratory Evaluation
| Test | Purpose |
|---|---|
| CMP | Assess electrolytes (Na⁺, K⁺, Ca²⁺, phosphate) |
| CBC | Identify infection or hemolysis |
| ABG/VBG | Detect metabolic acidosis |
| Urinalysis + Microscopy | Evaluate sediment (casts, cells, crystals) |
| Urine sodium, urea, creatinine, osmolality | Differentiate prerenal vs intrinsic |
| Calculate FENa and FEUrea | Assess tubular handling of sodium/urea |
Interpretation summary:
| Finding | Prerenal | Intrinsic | Postrenal |
|---|---|---|---|
| BUN:Cr ratio | >20:1 | <15:1 | Variable |
| FENa | <1% | >2–3% | Variable |
| FEUrea | <35% | >50% | Variable |
| Urine Osm | >500 mOsm/kg | <350 mOsm/kg | <350 mOsm/kg |
| Urine sediment | Hyaline casts | Muddy brown/RBC/WBC casts | Variable |
3. Imaging
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Bladder POCUS: assess for urinary retention
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Renal ultrasound: evaluate for hydronephrosis
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Non-contrast CT: if stones or obstruction suspected but not seen on ultrasound
4. Specialized Tests
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Autoantibodies: ANA, ANCA, anti-GBM (for GN)
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Complement levels: low in lupus or post-strep GN
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CPK: elevated in rhabdomyolysis
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Serum/urine protein electrophoresis: myeloma
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Renal biopsy: if unclear cause or intrinsic disease suspected
Management Overview
General Principles
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Identify and treat the underlying cause.
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Hold nephrotoxic agents (NSAIDs, ACEIs, ARBs, contrast).
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Renally dose all essential medications.
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Maintain euvolemia and adequate renal perfusion.
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Monitor I/O, daily weights, BP, electrolytes.
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Treat hyperkalemia, acidosis, and fluid overload as needed.
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Provide nutritional support and VTE prophylaxis.
Specific Management by Type
| Type | Management |
|---|---|
| Prerenal | Restore perfusion: isotonic IV fluids (normal saline), treat shock, stop RAAS inhibitors/NSAIDs |
| Intrinsic | Remove offending drugs, treat underlying cause, maintain perfusion, avoid overload |
| Postrenal | Relieve obstruction (catheterization, stent, nephrostomy), urology consult |
Indications for Nephrology Consult
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AKI stage 3
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Intrinsic AKI (esp. glomerulonephritis or interstitial nephritis)
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Inadequate response to treatment
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History of kidney transplant
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CKD stage G4+
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Need for dialysis or biopsy
Indications for Dialysis (AEIOU)
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Acid-base disturbance (refractory acidosis)
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Electrolyte abnormality (refractory hyperkalemia)
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Ingestions (toxic substances)
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Overload (refractory volume overload)
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Uremic complications (pericarditis, encephalopathy)
Prognosis
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Reversible if treated early (esp. prerenal and postrenal).
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Intrinsic AKI (esp. ATN) may take weeks to recover.
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Risk of progression to CKD or ESRD increases with delayed management.
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