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Acute Tubular Necrosis (ATN)

Intrinsic acute kidney injury from ischaemic or toxic tubular cell damage.

Written by: Saygı Hospital Health Guide Editorial Board
Last updated:

This content has been compiled by the Saygı Hospital Health Guide Editorial Board and is periodically reviewed by a specialist physician.

References (5)

This content is for informational purposes only and does not constitute medical advice. You can book an appointment at our Dahiliye (İç Hastalıkları) department. Book Appointment →

What is Acute Tubular Necrosis (ATN)?

ATN occurs when prolonged hypoperfusion or nephrotoxic exposure injures the proximal tubule and the medullary thick ascending limb of Henle.

Ischaemic ATN follows shock from sepsis, haemorrhage, cardiac surgery, prolonged hypotension or major trauma.

Nephrotoxic ATN results from contrast media, aminoglycosides, vancomycin, amphotericin B, cisplatin, NSAIDs, calcineurin inhibitors, intravenous immunoglobulin, ethylene glycol or pigment nephropathy from rhabdomyolysis or massive haemolysis.

Symptoms

Rising serum creatinine and reduced urine output (oliguria) following a recognised insult
Some patients are non-oliguric, with maintained urine output but rising creatinine
Pigmented muddy-brown granular casts and renal tubular epithelial cells on urinalysis
Urine sodium typically over 40 mEq/L and fractional excretion of sodium over 2%
Urine osmolality close to plasma osmolality (300-350 mOsm/kg)
Hyperkalaemia, metabolic acidosis, fluid overload and uraemia
BUN-to-creatinine ratio under 20:1 (in contrast to prerenal injury)

Risk Factors

Sepsis and septic shock
Major surgery, especially cardiac and vascular
Massive haemorrhage and prolonged hypotension
Iodinated contrast administration in patients with chronic kidney disease, diabetes or heart failure
Use of aminoglycosides, vancomycin, amphotericin B, cisplatin or calcineurin inhibitors
Rhabdomyolysis (crush injury, statins, prolonged immobilisation, seizures)
Massive haemolysis (transfusion reaction, malaria, autoimmune haemolysis)

When to See a Doctor?

If you experience any of the following symptoms, seek medical attention promptly:

  • Patients with a rising creatinine of 0.3 mg/dL or more in 48 hours need urgent nephrology assessment
  • Anuria, severe oliguria or signs of fluid overload require immediate hospital admission
  • Hyperkalaemia with ECG changes, severe acidosis or uraemic encephalopathy is a medical emergency
  • All patients with new acute kidney injury require ultrasound to exclude obstruction and a thorough drug review

Treatment Methods

01
Identify and treat the precipitating cause (source control of sepsis, withdrawal of nephrotoxins, treatment of rhabdomyolysis)
02
Optimise haemodynamics and renal perfusion with appropriate intravenous fluids guided by clinical assessment
03
Discontinue all nephrotoxic agents and adjust drug doses to renal function
04
Manage hyperkalaemia (calcium gluconate, insulin-dextrose, beta-agonists, potassium-binding resins, dialysis)
05
Correct severe metabolic acidosis with bicarbonate or dialysis
06
Renal replacement therapy for refractory hyperkalaemia, severe acidosis, fluid overload, uraemic complications or progressive azotaemia
07
Nutritional support (protein 0.8-1 g/kg/day, salt and potassium restriction)

Which Department to Visit?

You can visit our Dahiliye (İç Hastalıkları) department for these complaints. Our specialist physicians will create the most suitable treatment plan for you.

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Health Disclaimer: The information on this page is prepared for general informational purposes only. It does not replace medical diagnosis and treatment. Please consult your physician for your complaints. Saygı Hospital does not accept responsibility for actions taken based on the information on this page.