Acute tubular necrosis




Acute tubular necrosis

Renal system

Renal and ureteral disorders

Renal agenesis

Horseshoe kidney

Potter sequence











Renal tubular acidosis

Minimal change disease

Diabetic nephropathy

Focal segmental glomerulosclerosis (NORD)


Membranous nephropathy

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Membranoproliferative glomerulonephritis

Poststreptococcal glomerulonephritis

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Alport syndrome

Kidney stones


Acute pyelonephritis

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Prerenal azotemia

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Acute tubular necrosis

Postrenal azotemia

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Polycystic kidney disease

Multicystic dysplastic kidney

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Renal artery stenosis

Renal cell carcinoma


Nephroblastoma (Wilms tumor)

WAGR syndrome

Beckwith-Wiedemann syndrome

Bladder and urethral disorders

Posterior urethral valves

Hypospadias and epispadias

Vesicoureteral reflux

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Transitional cell carcinoma

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Renal system pathology review

Congenital renal disorders: Pathology review

Renal tubular defects: Pathology review

Renal tubular acidosis: Pathology review

Acid-base disturbances: Pathology review

Electrolyte disturbances: Pathology review

Renal failure: Pathology review

Nephrotic syndromes: Pathology review

Nephritic syndromes: Pathology review

Urinary incontinence: Pathology review

Urinary tract infections: Pathology review

Kidney stones: Pathology review

Renal and urinary tract masses: Pathology review


Acute tubular necrosis


0 / 17 complete

USMLE® Step 1 questions

0 / 2 complete

High Yield Notes

10 pages


Acute tubular necrosis

of complete


USMLE® Step 1 style questions USMLE

of complete

A 45-year-old man is brought to the emergency department for evaluation following a motor vehicle accident. Trauma chest/abdomen/pelvis CT-imaging demonstrates multiple bilateral fractures, a right humeral shaft fracture, as well as splenic and liver lacerations with ongoing internal hemorrhage. The patient is resuscitated with type O negative blood and is taken to the operating room for repair of the aforementioned injuries. His condition remains stable postoperatively. Following surgery, his temperature is 38.0°C (100.4°F), pulse is 95/min, respirations are 20/min, and blood pressure is 115/70 mmHg. On his second day of hospitalization, his urine output decreases. Urine microscopy demonstrates granular casts and a calculated fractional excretion of sodium (FENa) of 3%. On the patient’s eighth day of hospitalization, a significant increase in urine output is noted. Serum creatinine charting is shown:

 Laboratory value  Result 
  On admission  Day 2  Day 8 
Creatinine  1.1 mg/dL  3.5 mg/dL  2.3 mg/dL 
   In the coming days, this patient is at highest risk of developing which of the following findings? 

External References

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Acute tubular necrosis p. 626

Aminoglycosides p. 188

acute tubular necrosis p. 627

Cisplatin p. 449

acute tubular necrosis p. 627

Granular casts p. 618

acute tubular necrosis p. 627

Heart failure p. 318

acute tubular necrosis with p. 626


acute tubular necrosis and p. 627


acute tubular necrosis p. 627


acute tubular necrosis with p. 627

Ischemia p. 208, 691

acute tubular necrosis from p. 626

Lead poisoning p. 427, 432

acute tubular necrosis p. 626


acute tubular necrosis p. 627


acute tubular necrosis p. 627

Shock p. 319

acute tubular necrosis p. 627

Tubular necrosis p. 618, 626, 626


Acute tubular necrosis (ATN) is a type of acute kidney injury (AKI) that results in the sudden and rapid death of tubular cells in the kidneys. This can lead to a decrease in urine production and an increase in the levels of creatinine and urea in the blood.

ATN may be caused by sepsis leading to hypotension and renal hypoperfusion; ischemia due to renal hypoperfusion, like in hypovolemic shock; but it can also be due to exposure to toxins and nephrotoxic drugs which cause damage to the tubular cells. Such drugs include nephrotoxic antibiotics, contrast agents used during imaging studies, amphotericin B, and toxic heavy metals.


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