Contrast-Associated AKI (Contrast Nephropathy) & Acute Tubular Necrosis vs Pre-Renal AKI

Meet the patient

A 71-year-old man with type 2 diabetes and stage 3b CKD, baseline creatinine 160 micromol/L and eGFR 38, has a CT coronary angiogram for new-onset chest pain. No one checks his eGFR on the day, no one holds his metformin, and he goes home a little dry. Three days later he is back: creatinine 240, oliguric, potassium 6.4.^[1]

Two questions now decide his stay, and they decide this whole page: is this pre-renal or ATN, and could it have been prevented?^[1]

The spine — one face-off, one confession

This topic is one face-off and one confession. The face-off is pre-renal versus ATN at the bedside, settled by urine sodium, FENa, osmolality and the sediment. The confession is that contrast AKI has no treatment — prevention is everything, and PRESERVE buried the two agents (N-acetylcysteine and bicarbonate) everyone used to reach for.^[1][3]

Define AKI the KDIGO way — any one of: creatinine up by 0.3 mg/dL (26.5 micromol/L) or more within 48 hours; creatinine 1.5 times baseline or more within 7 days; or urine output under 0.5 mL/kg/h for 6 hours or more.^[8]

Contrast-associated AKI (CA-AKI) — ESUR's preferred label is post-contrast AKI (PC-AKI): renal function deterioration after iodinated contrast. Trial definitions are concrete: a creatinine rise of 0.5 mg/dL (44 micromol/L) or more within 48 hours, or 25 per cent or more within 2 days of contrast. The ACR-NKF consensus deliberately separates contrast-associated (AKI coincident to contrast) from contrast-induced (AKI caused by contrast), because attribution is usually impossible.^{[9][12][13][11]}

Why "associated", not "induced". Patients given contrast are usually also septic, hypotensive, post-operative or nephrotoxic — causality is hard to prove, so the name changed. Mechanistically, though, CA-AKI is a textbook acute tubular necrosis.^[1][11]

The face-off — the table that earns the mark

Memorise this table as a single discriminator: a kidney that still grabs sodium is pre-renal; a kidney that has stopped grabbing sodium is ATN.^[1]

The one-line discriminator is FENa. Under 1 per cent is pre-renal; over 2 per cent is ATN; the band in between is grey, so read it with the sediment and the fluid response, never alone.^[2]

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ATN sorts by cause into three buckets that direct the history and the management.^[1]

• Ischaemic ATN — prolonged hypoperfusion: haemorrhagic or septic shock, sustained hypotension, major surgery (especially cardiac and aortic), pancreatitis, an uncorrected pre-renal state.
• Nephrotoxic ATN — direct tubular toxins: aminoglycosides (gentamicin, tobramycin, amikacin), radiocontrast, amphotericin B, cisplatin, tenofovir, high-dose aciclovir (crystalline), vancomycin, NSAIDs, ethylene glycol.
• Pigment nephropathy — myoglobin (rhabdomyolysis: crush, statin, immobility, seizure, heat stroke) and haemoglobin (haemolysis); the tell is dipstick-positive blood with no red cells on microscopy.^[2]

Why pre-renal recovers in hours and ATN takes weeks

The timetable is the mechanism. Pre-renal is a perfusion problem in an intact kidney; ATN is structural damage the tubule must regrow from scratch.^[1]

Pre-renal — the kidney is intact, the plumbing is dry. Glomerular filtration rides on glomerular pressure, defended by prostaglandins (dilating the afferent arteriole) and angiotensin II (constricting the efferent). When perfusion drops, intact tubules avidly reclaim sodium and water to defend circulating volume — hence urine sodium under 20, osmolality over 500, FENa under 1 per cent, BUN/creatinine over 20. Restore the perfusion and the kidney bounces back in hours. Leave it, and ischaemic ATN follows within hours to days.^[1]

ATN — the tubule is broken. Ischaemia or a nephrotoxin depletes ATP, and the S3 proximal segment and the medullary thick ascending limb (the most oxygen-starved strips of nephron) die first. Four mechanisms lock together to drop the GFR:^[2]

1. Cell injury and sloughing — the brush border is lost and cells detach into the lumen.
2. Cast obstruction — sloughed cells plus Tamm-Horsfall protein form muddy brown granular casts that plug the tubule.
3. Back-leak of filtrate — the tight junctions fail, so filtered solute seeps back into the interstitium.
4. Afferent vasoconstriction — tubuloglomerular feedback (adenosine at the macula densa) constricts the afferent arteriole.^[2]

The lost sodium reabsorption is the biochemical signature. The injured tubule cannot reclaim sodium, so urine sodium climbs over 40 and FENa exceeds 2 per cent, with isosthenuric urine (osmolality under 350).^[2]

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ATN runs in phases — initiation, maintenance, recovery. Recovery tubules cannot yet concentrate urine, so a polyuric phase of 3 to 5 L per day for several days precedes the return of GFR. Warn the family, or they will think you broke the kidney — and replace the urine millilitre for millilitre, watching sodium, potassium and magnesium.^[1]

The dual mechanism of contrast AKI

Contrast hits the same vulnerable cells twice. Iodinated contrast drives outer-medullary vasoconstriction and hypoxia while being directly cytotoxic to proximal tubular cells — which is why it behaves like every other ATN.^[1][2]

First — medullary hypoxia. The outer medulla lives permanently on the edge of hypoxia. Contrast gives a brief flow rise, then a sustained fall, mediated by adenosine (A1 receptors constrict the afferent arteriole), endothelin and reactive oxygen species, with loss of prostaglandin-driven vasodilation. The S3 segment and the thick ascending limb die first — this is medullary hypoxic ATN.^[1]

Second — direct cytotoxicity. The iodinated benzene ring injures mitochondria and drives oxidative stress and apoptosis; proximal cells internalise and concentrate the agent, prolonging exposure. High-osmolar agents (diatrizoate) raise tubular pressure and diuresis; the very viscous iso-osmolar iodixanol slows transit — both prolong contact, which is why neither class is clearly superior.^[2]

The timing is the fingerprint. Creatinine peaks at 48 to 72 hours and the uncomplicated case resolves within 7 to 10 days, usually non-oliguric, transient and self-limiting.^[1]

Who breaks first — risk and the Mehran score

A vulnerable kidney fails first; contrast just finds it. CA-AKI is the third commonest cause of hospital-acquired AKI, after hypoperfusion and surgery or drugs — and hospital AKI complicates about 1 in 5 admissions and up to half of ICU stays.^[1]

The incidence rises steeply with baseline renal function.^[1]

• Normal renal function — under 2 per cent.
• CKD stage 3 (eGFR 30 to 59) — 5 to 10 per cent.
• CKD stage 4 to 5 (eGFR under 30) or diabetes — 20 to 50 per cent.
• Mehran very-high-risk PCI — over 50 per cent.^[1]

The patient risk factors worth running on autopilot: pre-existing CKD (the single strongest predictor, especially eGFR under 45 to 60), diabetes (additive with CKD), dehydration, age over 75, heart failure (NYHA III to IV), acute MI within 24 hours, hypotension or an intra-aortic balloon pump, anaemia (haematocrit under 36 per cent women, 39 per cent men), multiple myeloma, concurrent nephrotoxins (NSAIDs, aminoglycosides, cisplatin, amphotericin B, calcineurin inhibitors), high contrast volume (over 3 to 5 times the eGFR in mL), and the intra-arterial route (highest in intra-renal or intra-cardiac).^[1]

The Mehran score (2004) — eight weighted variables, reproduce it verbatim.^[7]

• Hypotension (with inotropes or an intra-aortic balloon pump) and congestive heart failure — the circulatory variables
• Chronic kidney disease — graded by eGFR band
• Age over 75
• Anaemia
• Diabetes
• Volume of contrast — the only modifiable variable: keep it as low as possible

Each variable carries a weighted integer from the original paper (assigned from its odds ratio); the sum is the patient's risk score.^[7]

Risk bands: a low score (5 or under) carried a 7.5 per cent CIN rate in the development set and a very high score (over 16) 57.3 per cent, rising exponentially in between — discrimination in validation had a c statistic of 0.67.^[7]

Modern re-appraisal — the risk was oversold. With low- and iso-osmolar agents, smaller volumes and selective hydration, the absolute risk is far lower than the historical tables suggest, and you must not withhold essential contrast imaging for fear of AKI. AMACING drove that home.^[6]

The poor man's biopsy — urine biochemistry and sediment

Your first move in any AKI is to place it: pre-renal, intrinsic (and which compartment), or post-renal. Use the history, the urine chemistries and the sediment together — no single test is definitive.^[1]

FENa — the formula. FENa (per cent) equals (urine sodium times serum creatinine) divided by (serum sodium times urine creatinine), times 100, on a simultaneous spot urine and serum pair.^[2]

The classic trap — FENa after diuretics. A loop or thiazide forces natriuresis regardless of cause, so a genuinely pre-renal patient who just got furosemide shows a falsely high FENa and urine sodium. Switch to fractional excretion of urea: FEurea under 35 per cent supports pre-renal. FEurea is diuretic-independent, and so is the BUN/creatinine ratio (over 20 for pre-renal) — both bail you out when FENa is confounded.^[2]

More FENa traps. It is also falsely high in sepsis, bicarbonaturia (sodium dragged with bicarbonate), established CKD and salt-wasting states, and falsely low early in pigment nephropathy and early contrast AKI. Read it with the sediment.^[1]

What you hear and see at the bedside

Most AKI is silent and turns up on the biochemistry. When it speaks, it speaks in uraemia, fluid overload and electrolyte disturbance, layered onto whatever caused it.^[1]

AKI itself: oliguria or anuria, fluid overload (dyspnoea, raised JVP, basal crackles, S3, oedema, hypertension), and the uraemic syndrome — anorexia, nausea, hiccups, metallic taste, pruritus, easy bruising, pericarditic chest pain and rub, asterixis, confusion, seizures.^[1]

Cause-specific clues to hunt actively:^[1]

• Pre-renal — thirst, dry mucosae, slow capillary refill, postural drop, oliguria; a story of vomiting, diarrhoea, haemorrhage, burns, diuretics, heart failure or sepsis.
• Ischaemic ATN — a clear episode of prolonged hypotension (cardiac arrest, septic or haemorrhagic shock, major surgery), then oliguria within 24 to 72 hours.
• Nephrotoxic ATN — gentamicin day 5 to 7, amphotericin B, cisplatin, tenofovir, high-dose aciclovir, or iodinated contrast within 48 to 72 hours.
• Pigment nephropathy — swollen tender muscle, cola-coloured urine, a story of trauma, immobility, statin, seizure or heat stroke; dipstick positive for blood with no red cells on microscopy is myoglobin.
• AIN — a new drug (beta-lactam, PPI, NSAID, sulphonamide, rifampicin) with fever, rash and eosinophilia (the classic triad, often incomplete).^[1]

Contrast AKI versus cholesterol atheroembolism — the post-catheter trap. CA-AKI hits at 48 to 72 hours and resolves in 7 to 10 days. Atheroembolism arrives 1 to 4 weeks after catheter manipulation with livedo reticularis, blue toes, eosinophilia and low complement, and is often irreversible. They are not the same disease, and examiners love the distinction.^[1]

Investigations — first-line, then cause-directed

First-line, in every AKI:^[1][8]

• Urea, creatinine, eGFR — establish baseline and trend (dig out an old result; the single most useful number on the chart).
• Venous gas or bicarbonate — metabolic acidosis; the severity of the acidosis, with refractory hyperkalaemia and fluid overload, is what escalates care towards dialysis.
• Sodium, potassium, chloride, calcium, phosphate, magnesium, glucose, albumin.
• Full blood count (anaemia, eosinophilia in AIN or atheroemboli), CRP, blood cultures, lactate if sepsis is likely.
• Creatine kinase if any hint of rhabdomyolysis — a peak of 5000 U/L or more carried 83 per cent sensitivity for AKI requiring renal replacement therapy in cohort data.^[15]
• Urinalysis and microscopy — the single most useful bedside test.
• Urine electrolytes with a simultaneous serum sample for FENa (or FEurea if on diuretics).
• ECG for hyperkalaemia (peaked T waves, flattened P, prolonged PR, wide QRS, sine wave).
• Renal ultrasound to exclude obstruction and judge CKD versus AKI (small echogenic kidneys favour chronic).
• Chest X-ray for overload or a sepsis source.^[1][8]

Second-line is cause-directed. Serum immunoglobulins, free light chains and electrophoresis (myeloma); ANA, ANCA, anti-GBM and complement (GN or vasculitis); hepatitis B, C and HIV serology; and renal biopsy for unexplained intrinsic AKI, especially suspected rapidly progressive GN.^[1]

Prevention dominates — the four pillars

There is no drug that reverses established contrast AKI. Prevention is the entire strategy, in four pillars.^[3]

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Pillar 1 — risk-stratify. Measure eGFR before contrast in everyone. CKD, diabetes, dehydration, age over 75, heart failure, anaemia, myeloma and concurrent nephrotoxins raise the risk; apply the Mehran score in PCI. Low-risk patients (eGFR over 60, no risk factors) need no special prophylaxis.^[1]

Pillar 2 — isotonic saline. The single best-proven measure: isotonic (0.9 per cent) saline beats half-isotonic hydration, ESUR holds intravenous normal saline and sodium bicarbonate to be equally effective prophylaxis, and PRESERVE found no benefit of bicarbonate over saline. A trial-validated regimen is 3 mL/kg/h for 1 hour before contrast, then 1 mL/kg/h for 6 hours after. In heart failure, judge the rate against overload — AMACING recorded hydration-related complications in 5.5 per cent of hydrated patients.^{[12][10][3][13][6]}

Pillar 3 — minimise the contrast. Lowest possible volume (a practical rule: keep it under 3 to 5 times the eGFR in mL), use iso-osmolar (iodixanol) or low-osmolar (iohexol, iopamidol, ioversol) agents in preference to high-osmolar, prefer the intravenous to the intra-arterial route when feasible, and avoid repeat contrast within 72 hours.^[1]

Pillar 4 — hold the nephrotoxins. Stop NSAIDs (including over-the-counter), reconsider ACE inhibitors and ARBs (hold if hyperkalaemic or volume-deplete), and review aminoglycosides, amphotericin B, cisplatin, tenofovir and vancomycin.^[1]

PRESERVE killed NAC and bicarbonate

PRESERVE (Weisbord, NEJM 2018) randomised 5177 high-risk angiography patients to bicarbonate versus saline and N-acetylcysteine versus placebo in a 2 by 2 factorial. Neither agent reduced CA-AKI, dialysis or 90-day mortality. Routine NAC and bicarbonate are dead — isotonic saline and dose minimisation are what actually work. Statins, ascorbic acid, theophylline and fenoldopam are not recommended either.^[3]

AMACING — routine IV hydration is not always needed

AMACING (Nijssen, Lancet 2017) randomised 660 moderate-risk patients (eGFR 30 to 59) to no prophylactic hydration versus IV hydration. No prophylaxis was non-inferior for CA-AKI and dialysis, and avoided the cost and complications of hydration. In well-selected moderate-risk patients oral water is reasonable — but high-risk patients still get saline.^[6]

The metformin rule — precise, and everyone gets it wrong

The point examiners test: you hold metformin if AKI develops, not because contrast interacts with metformin, but because AKI lets metformin accumulate and risk lactic acidosis.^[1]

Resuscitation and the hyperkalaemia ladder

Contrast AKI is supportive care — but hyperkalaemia kills these patients before anything else does, so the potassium ladder is the real bedside skill.^[1]

Treat the cause in parallel: fluids for the dry pre-renal patient (a measured balanced-crystalloid challenge, then reassess), the Surviving Sepsis hour-1 bundle for septic ATN — blood cultures before antibiotics, broad-spectrum antimicrobials within 1 hour, 30 mL/kg crystalloid for hypotension or lactate of 4 mmol/L or more, and noradrenaline as first-line vasopressor to a mean arterial pressure of 65 mmHg or more — and a catheter or nephrostomy for obstruction (watch for post-obstructive diuresis).^[22][23][24]

Universal AKI measures — apply to all types:^[1]

• Stop all nephrotoxins — NSAIDs, ACE inhibitors, ARBs, aminoglycosides, amphotericin B, cisplatin, tenofovir, iodinated contrast; review herbal and AYUSH agents.
• Re-dose every drug for the current eGFR (loading doses usually unchanged; maintenance doses adjusted).
• Optimise perfusion — target MAP over 65 mmHg.
• Monitor — urine output (catheterise if oliguric), potassium, bicarbonate, creatinine and fluid balance every 6 to 12 hours.^[1]

The hyperkalaemia ladder — reproduce the doses verbatim.^[17][18]

Membrane stabilisation first, then shift potassium into cells, then remove it:^[18]

• Calcium gluconate 10 per cent, 10 mL IV — stabilises the myocardial membrane; it does NOT lower potassium. Indicated with ECG changes or potassium of 6.5 mmol/L or more; repeat if ECG changes persist.^[18][17]
• Insulin 10 units IV with dextrose 25 g — shifts potassium into cells; hypoglycaemia is the frequent complication, so watch the glucose (a 5-unit or 0.1 units/kg insulin dose, or 50 g of dextrose, are validated ways to reduce it).^[19][20]
• Salbutamol 10 to 20 mg nebulised — beta-2 agonist; the 20 mg dose lowers potassium further than 10 mg, and it is additive with insulin-dextrose.^[21][17]
• Potassium binders — sodium polystyrene sulfonate is no longer recommended (questionable efficacy, gastrointestinal harm); the modern options are patiromer and sodium zirconium cyclosilicate, which act over hours.^[17][18]
• Dialysis if refractory — the definitive and most efficient way to remove potassium.^[17]

Why not colloids. Hydroxyethyl starch and synthetic colloids increase AKI and RRT need (6S, CHEST, CRISTAL); albumin is not superior to crystalloid; balanced crystalloids beat 0.9 per cent saline at volume (SMART). Fluid overload itself worsens AKI via venous congestion — fluids are not a blanket prescription.^[1]

AEIOU — when to dialyse, and when not to start early

Dialyse for AEIOU — and only for AEIOU or persistent severe AKI.^[1]

The timing question is settled. AKIKI and STARRT-AKI showed no mortality benefit from early, prophylactic dialysis in severe AKI — and in AKIKI nearly half the delayed group never needed dialysis at all. Start for AEIOU, for AKI that is not recovering, or for clinical deterioration — not for a biochemical number alone.^[4][5]

• AKIKI (Gaudry, NEJM 2016): 620 critically ill Stage 3 AKI patients, immediate versus delayed RRT — no difference in 60-day mortality, and almost half the delayed group never needed dialysis.^[4]
• STARRT-AKI (Bagshaw, NEJM 2020): 3019 severe AKI patients, accelerated versus standard RRT — no mortality difference, and more adverse events with the accelerated strategy.^[5]

The named traps — what costs marks and lives

Everyone forgets: FENa is junk after diuretics — use FEurea under 35 per cent. The classic trap: a post-catheter creatinine 1 to 4 weeks out, with livedo, blue toes and eosinophilia, is cholesterol atheroembolism, not contrast nephropathy.^[1]

• Missing obstruction — always ultrasound an unexplained AKI, especially anuria or a single kidney.
• Re-prescribing nephrotoxins — NSAIDs, ACE inhibitors or aminoglycosides on a recovering kidney.
• Over-resuscitation — pulmonary oedema and worse AKI from venous congestion.
• FENa after diuretics — it misleads: only 48 per cent of diuretic-treated pre-renal patients keep a FENa under 1 per cent, but 89 per cent have a FEurea under 35 per cent — use FEurea.^[14]
• Missing rapidly progressive GN — needs urgent immunosuppression within days, not supportive care.
• Atheroembolism mislabelled as contrast AKI — livedo, blue toes, eosinophilia; in a dialysis-requiring series the renal failure arrived about 5 weeks after the trigger (58 per cent after coronary angiography), with high mortality.^[25]
• Treating pigment nephropathy as fluid-responsive pre-renal — rhabdomyolysis needs high-volume fluid resuscitation, not a token bolus.^[15]

Prognosis and disposition

Pre-renal recovers in hours; ATN over days to weeks; obstruction recovers after relief. Hospital-acquired AKI mortality is around 10 per cent when uncomplicated and over 50 per cent in ICU multi-organ failure. CA-AKI itself is usually transient — it peaks at 48 to 72 hours and resolves in 7 to 10 days; dialysis is needed in under 1 per cent of unselected patients but in over 5 to 12 per cent of Mehran very-high-risk PCI.^[1]

Disposition. Stage 1 stays with the primary team; nephrology for Stage 2 to 3, persistent AKI, suspected GN or AIN, or an RRT need; ICU for multi-organ failure, vasopressors or dialysis. Most CA-AKI is managed on the ward.^[1]

An AKI episode is not benign even when it recovers — survivors carry more long-term CKD and more cardiovascular events, so follow up renal function after discharge.^[2]

Special situations

CKD and diabetes are the highest-risk kidneys — and you still image them. Maximise the four pillars, consider an alternative modality (ultrasound, MRI without contrast, CT without contrast), use iso-osmolar contrast in the highest-risk intra-arterial settings, and do not withhold clinically essential imaging — the risk of missing the diagnosis exceeds the risk of CA-AKI in modern practice.^[1]

Emergency imaging is never delayed for AKI prevention. In trauma, stroke, aortic dissection, pulmonary embolism or ACS for PCI, apply pragmatic hydration and dose minimisation and deal with the primary threat first.^[1]

Gadolinium (MRI contrast) and nephrogenic systemic fibrosis. Avoid gadolinium at eGFR under 30 unless essential, because of nephrogenic systemic fibrosis — a fibrosing disorder of skin and viscera. Use group II macrocyclic agents (gadoteridol, gadobutrol), which carry a risk under 0.01 per cent; the risk has fallen sharply since the group I agents (gadodiamide, gadopentetate) were restricted.^[2]

Patients already on dialysis can usually receive iodinated contrast without extra prophylaxis — the kidneys are not at risk, and there is no need to time dialysis around contrast.^[1]

Evidence and regional deltas

KDIGO 2012 is the international standard for AKI definition, staging and contrast prevention: isotonic saline or balanced crystalloid for high-risk patients, lowest possible contrast dose, low- or iso-osmolar agents, and NAC and bicarbonate not recommended for routine prophylaxis.^[1]

Exam pearls

• FENa under 1 per cent equals pre-renal; after diuretics use FEurea under 35 per cent — urea handling is diuretic-independent.^[14]
• Muddy brown granular casts equal ATN — biopsy-verified as specific for tubular injury; RBC casts equal GN; WBC casts and eosinophiluria equal AIN; broad waxy casts equal CKD.^[16]
• Dipstick blood positive with no red cells equals myoglobin or haemoglobin — check CK: a peak of 5000 U/L or more flags RRT-level AKI risk.^[15]
• CA-AKI: trial definitions are a creatinine rise of 0.5 mg/dL or more within 48 hours, or 25 per cent or more within 2 days of contrast.^[12][13]
• PRESERVE: N-acetylcysteine and bicarbonate do NOT prevent CA-AKI — use isotonic saline.^[3]
• AMACING: no prophylactic hydration is non-inferior in moderate-risk elective patients.^[6]
• Mehran score: eight variables; 5 or under is low (7.5 per cent), over 16 is very high (57.3 per cent).^[7]
• Hyperkalaemia ladder: calcium gluconate 10 per cent 10 mL IV, then insulin 10 units with dextrose 25 g, then salbutamol 10 to 20 mg nebulised, then patiromer or SZC, then dialysis.^[18][19][21]
• AEIOU equals dialysis indications: Acidosis, Electrolytes, Ingestion, Overload, Uraemia.^[1]
• AKIKI and STARRT-AKI: no mortality benefit of early dialysis — start for AEIOU or persistent Stage 3.^[4][5]
• Post-catheter creatinine rising weeks later with livedo, blue toes and eosinophilia is cholesterol atheroembolism, not contrast nephropathy.^[25]

Ward-round test

Stem 1 — the post-angiogram creatinine. A 68-year-old with CKD and diabetes has a creatinine rise from 150 to 200 micromol/L 48 hours after coronary angiography. FENa 2.4 per cent, urine sodium 44, sediment with muddy brown granular casts. What is this, and what do you do?^[1]

Stem 2 — the diuretic trap. A heart-failure patient on IV furosemide develops AKI, and FENa comes back 2.8 per cent. Is this ATN, and if not, how do you tell?^[2]

Stem 3 — the post-catheter trap. Three weeks after a cardiac catheter, a 74-year-old has a rising creatinine, livedo reticularis, blue toes and eosinophilia. Diagnosis, and is this contrast nephropathy?^[1]

Stem 4 — potassium 6.9 with ECG changes. An AKI patient has peaked T waves and a wide QRS, potassium 6.9. What is the first drug, the dose, and what does it actually do?^[1]

Rapid viva checklist

1. KDIGO AKI definition and the ESUR/ACR CA-AKI definition
2. Pre-renal versus ATN face-off (FENa, urine sodium, osmolality, BUN/creatinine, sediment)
3. FEurea-under-35 trap after diuretics
4. Dual mechanism of contrast AKI (medullary vasoconstriction plus cytotoxicity)
5. Risk bands and the Mehran score with its bands
6. Four prevention pillars; PRESERVE killed NAC and bicarb; AMACING on hydration
7. Metformin rule (hold if AKI develops)
8. Hyperkalaemia ladder with doses; calcium gluconate 10 per cent 10 mL
9. AEIOU dialysis indications; AKIKI and STARRT-AKI timing
10. Three exam traps (FENa after diuretics; cholesterol atheroembolism; dipstick blood with no red cells)^[1]

Coverage self-check

If you cannot answer any ward-round stem from this page alone, re-read the matching section. The page is built to be self-sufficient for final-prof, NEET-PG, INICET, USMLE and PLAB questions on Contrast-Associated AKI and ATN versus Pre-Renal AKI.^[1]