Renal/Urology · PANCE / PANRE

Acute Tubular Necrosis (ATN)

Most common cause of intrinsic AKI; tubular epithelial injury from ischemia or nephrotoxins.

Also known as: ATN, acute tubular necrosis, ischemic ATN, nephrotoxic ATN

Overview

Intrinsic AKI characterized by injury and necrosis of renal tubular epithelial cells, most often from ischemic insult (prolonged hypoperfusion) or direct nephrotoxic exposure. The most common cause of hospital-acquired AKI.

Epidemiology

Accounts for ~50% of hospital-acquired AKI and ~75% of AKI in critically ill patients. Mortality 40-60% in ICU patients requiring RRT.

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Risk factors

Ischemic: sepsis, hemorrhage, prolonged hypotension, cardiac/aortic surgery
Nephrotoxic medications: aminoglycosides (gentamicin, tobramycin, amikacin), vancomycin, amphotericin B, cisplatin, foscarnet
Iodinated contrast (especially CKD, diabetes, dehydration)
Endogenous toxins: myoglobin (rhabdomyolysis), hemoglobin (hemolysis), uric acid (tumor lysis), light chains (myeloma)
Underlying CKD, advanced age, volume depletion

Pathophysiology

Ischemic or toxic injury depletes tubular ATP, disrupts apical brush borders, and causes epithelial cell death and desquamation. Sloughed cells obstruct the tubular lumen → backleak of filtrate, tubuloglomerular feedback, and reduced GFR. Three phases: initiation (hours-days), maintenance (days-weeks of established oliguric AKI), and recovery (polyuric phase as tubules regenerate).

Clinical presentation

Symptoms

Often asymptomatic AKI discovered on labs in ICU or postoperative setting
Oliguria or anuria common; nonoliguric ATN in 30-50% (better prognosis)
Symptoms of underlying cause: sepsis, shock, recent surgery, exposure to nephrotoxin
Uremic symptoms if severe: nausea, confusion, dyspnea

Signs / physical exam

Volume status variable — euvolemic, overloaded, or depleted depending on cause and management
Findings of underlying critical illness
Skin findings in atheroemboli (livedo, blue toes)
Bladder not distended; no obstruction

Classic findings

Muddy brown granular casts in urine sediment are pathognomonic for ATN.

Differential diagnosis

Prerenal AKI — BUN:Cr >20:1, FENa <1%, bland sediment; responsive to volume — distinguish before fluid challenge
Acute interstitial nephritis — Drug exposure (PPI, NSAID, beta-lactam), fever, rash, eosinophilia, WBC casts
Glomerulonephritis — Dysmorphic RBCs, RBC casts, proteinuria, hypertension — biopsy-driven diagnosis
Postrenal obstruction — Hydronephrosis on US, distended bladder, anuria; rapid reversal with drainage
Renal atheroembolic disease — Days-weeks after vascular procedure; livedo reticularis, blue toes, eosinophilia, eosinophiluria
Contrast-induced nephropathy — Cr rise within 24-72 h of IV contrast; typically resolves by day 7-10

Diagnostic workup

Diagnostic criteria

Clinical diagnosis: AKI meeting KDIGO criteria with characteristic sediment (muddy brown casts), FENa >2%, recent ischemic or nephrotoxic event, and exclusion of prerenal/postrenal/other intrinsic causes. Biopsy rarely needed.

Labs

BMP — rise in creatinine and BUN, often with hyperkalemia, acidosis
Urinalysis with microscopy — muddy brown granular casts, renal tubular epithelial cells, FENa >2%
Urine sodium >40 mEq/L, urine osmolality <350 (isosthenuria — inability to concentrate)
CK if rhabdomyolysis suspected; LDH and haptoglobin if hemolysis suspected
SPEP/UPEP with free light chains if multiple myeloma suspected

Imaging

Renal ultrasound to exclude obstruction; kidneys typically normal-sized and echotexture
CT only if specific cause suspected (atheroembolic disease, masses)

Diagnostic algorithm

Phase	Duration	Features	Management Priority
Initiation	Hours-days	Reversible injury; Cr rising	Identify cause; remove nephrotoxin; optimize perfusion
Maintenance	1-3 weeks	Established AKI; oliguria; peak Cr	Supportive care; RRT if AEIOU criteria; avoid further insults
Recovery	Days-weeks	Polyuria; tubular regeneration	Replace losses; monitor K, Mg, PO4; gradual return of function

Three phases of acute tubular necrosis with management priorities at each stage.

Treatment

First-line

Remove or treat underlying cause: stop offending nephrotoxin, treat sepsis, restore perfusion
Optimize hemodynamics: target MAP ≥65 with isotonic crystalloid and vasopressors (norepinephrine first-line) as needed
Adjust renally cleared medications (vancomycin, gabapentin, opioids, DOACs)
Avoid further insults: NSAIDs, ACEi/ARB during acute phase, iodinated contrast, aminoglycosides
Conservative management — no specific therapy reverses established ATN; focus is supportive while tubules regenerate

Second-line / adjunct

Loop diuretic — furosemide, bumetanide — for volume overload only; does not change ATN course or improve mortality
Renal replacement therapy for KDIGO indications (AEIOU): refractory acidosis, hyperkalemia, ingestion of dialyzable toxin, volume overload, uremic complications
Modality choice: CRRT preferred in hemodynamically unstable ICU patients; intermittent HD in stable patients
Nutrition support: avoid protein restriction (associated with worse outcomes)
During recovery (polyuric phase): replace urinary losses; monitor for hypokalemia, hypomagnesemia, hypophosphatemia

Complications

Volume overload, pulmonary edema
Hyperkalemia with cardiac arrhythmia
Metabolic acidosis (high anion gap from retained acids)
Uremic complications: pericarditis, encephalopathy, bleeding
Failure to recover, transition to CKD/ESRD (~25% of severe ATN)
Death — especially in septic ATN (40-60% in ICU)

PANCE pearls

Muddy brown granular casts + renal tubular epithelial cells = ATN sediment.
Three phases: initiation (insult), maintenance (oliguria, peak Cr, 1-3 weeks), recovery (polyuria, watch electrolytes).
Diuretics do not change outcome but help volume management. 'Furosemide stress test' (no response to 1-1.5 mg/kg) predicts severe AKI.
Nonoliguric ATN has better prognosis than oliguric.
No medication has been shown to reverse or shorten ATN. Dopamine, fenoldopam, mannitol, and 'renal-dose' dopamine are not recommended.

References

KDIGO 2012 — KDIGO Clinical Practice Guideline for Acute Kidney Injury
ADQI — Acute Disease Quality Initiative consensus statements on AKI biomarkers and management

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