# Acute Tubular Necrosis > Acute tubular necrosis for NEET-PG Medicine: ischaemic versus nephrotoxic causes, muddy-brown casts, FENa and urine sodium, and supportive management. - Canonical URL: https://prepelephant.com/topics/neet-pg/medicine/acute-tubular-necrosis - Exam / course: NEET-PG · Subject: Medicine - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-08 - Last updated: 2026-10-08 - Reference basis: Harrison's Principles of Internal Medicine; KDIGO Clinical Practice Guideline for Acute Kidney Injury; Brenner and Rector's The Kidney - How to cite: "Acute Tubular Necrosis", PrepElephant, https://prepelephant.com/topics/neet-pg/medicine/acute-tubular-necrosis ## Direct answer Acute tubular necrosis is damage to renal tubular epithelial cells, most often from renal ischaemia or nephrotoxins, causing intrinsic acute kidney injury. Its hallmark is muddy-brown granular casts in the urine, a urine sodium above about 40 mmol/L and a fractional excretion of sodium above 2 per cent. Treatment is supportive: restore perfusion, stop nephrotoxins, correct electrolytes and start dialysis only for standard indications. ## What you must remember - **Ischaemic ATN:** hypotension, sepsis, major surgery and haemorrhage cause the commonest form, often with patchy tubular injury. - **Nephrotoxic ATN:** aminoglycosides, cisplatin, iodinated contrast, amphotericin B and pigments from rhabdomyolysis or haemolysis. - **Muddy-brown casts:** the granular casts of ATN, often accompanied by renal tubular epithelial cell casts, though they may be absent in some cases. - **FENa:** above 2 per cent favours ATN and below 1 per cent favours prerenal azotaemia, but diuretics make FENa unreliable, and then a fractional excretion of urea below 35 per cent favours a prerenal cause. - **Urine sodium and osmolality:** urine sodium above about 40 mmol/L and urine osmolality close to plasma, in contrast with concentrated urine in prerenal states. - **Recovery phases:** initiation, maintenance with oliguria, and recovery with polyuria that carries a risk of hypokalaemia and dehydration. - **Renal replacement:** started for AEIOU indications, not by a creatinine level alone. ## Septic shock after a course of gentamicin Consider a 55-year-old man admitted after an abdominal operation complicated by septic shock. He has received gentamicin for three days, and within 48 hours his creatinine has risen from 0.9 to 2.6 mg/dL, with urine output falling to about 0.3 mL/kg/h. 1. **Exclude obstruction:** The first step is a bladder scan and renal ultrasound, which show no hydronephrosis. 2. **Restore perfusion:** Resuscitation is guided by fluid responsiveness, with a mean arterial pressure of about 65 mmHg as the aim and vasopressors as needed, since sustained hypotension perpetuates tubular ischaemia. 3. **Stop the nephrotoxin:** Gentamicin is stopped, and other renally cleared drugs are dosed against levels with adjustment for renal function. 4. **Confirm the pattern:** A spot urine sodium of 52 mmol/L and a fractional excretion of sodium of about 3 per cent point towards ATN, and microscopy shows muddy-brown granular casts. 5. **Watch potassium and fluid:** Potassium is monitored closely because hyperkalaemia is the common threat, and fluid overload is treated with diuretics once the patient is perfused. 6. **Start dialysis only for indications:** Dialysis is started only if a standard indication emerges, such as refractory hyperkalaemia, acidosis or pulmonary oedema. Recovery often takes one to three weeks, and the patient may then pass large volumes that need careful fluid and electrolyte replacement. ## Where the examiner tries to catch you Three traps recur here. - **Trap:** reading a low FENa as prerenal after furosemide. — **Correct:** diuretics raise sodium excretion and mislead the index, so fractional excretion of urea below 35 per cent is the better alternative in that setting. - **Trap:** misreading urinary casts. — **Correct:** muddy-brown granular casts point to ATN, red-cell casts to glomerulonephritis, white-cell casts with eosinophils to interstitial nephritis, and waxy broad casts to chronic kidney disease. - **Trap:** confusing pigment nephropathy with ischaemic ATN. — **Correct:** in rhabdomyolysis the urine dipstick is strongly positive for blood while microscopy shows few red cells, and the CK is markedly raised. Indian examiners add the snake bite and leptospirosis scenarios, where ATN follows haemolysis, rhabdomyolysis or vasculotoxic injury, and management still rests on supportive care and timely dialysis when indicated. ## Frequently asked questions ### Which urinary finding is characteristic of acute tubular necrosis? Muddy-brown granular casts are the characteristic urinary finding in acute tubular necrosis, reflecting degenerated tubular epithelium. They are usually accompanied by renal tubular epithelial cell casts and a urine sodium above about 40 mmol/L, which together point to intrinsic tubular injury rather than a prerenal cause. ### What does a fractional excretion of sodium above 2 per cent indicate? A fractional excretion of sodium above 2 per cent in acute kidney injury favours acute tubular necrosis over prerenal azotaemia. It is less reliable in patients who have received diuretics, and in that setting a fractional excretion of urea below 35 per cent suggests a prerenal cause. ### Which drugs most commonly cause nephrotoxic acute tubular necrosis? Aminoglycosides, cisplatin, iodinated contrast media, amphotericin B and vancomycin are the commonest drugs causing nephrotoxic acute tubular necrosis. Risk rises with dehydration, concurrent nephrotoxins and pre-existing chronic kidney disease, so stopping the offending agent is the first step. ### What are the phases of acute tubular necrosis? Acute tubular necrosis passes through an initiation phase, a maintenance phase with oliguria, and a recovery phase with polyuria. The recovery phase is the one where dehydration, hypokalaemia and hypomagnesaemia can occur, so fluid and electrolyte balance must be watched carefully. ### How does rhabdomyolysis cause acute tubular necrosis? Rhabdomyolysis causes acute tubular necrosis through myoglobin pigment cast formation and direct tubular toxicity, and the risk is higher with volume depletion and acidic urine. The urine dipstick shows blood with few red cells on microscopy, and the CK is markedly raised, which helps distinguish it from ischaemic injury.