Acute Kidney Injury

Meet the patient

A 68-year-old man with heart failure and stage 3 CKD is admitted after three days of diarrhoea and vomiting. His GP added ibuprofen for aching joints two days ago; ramipril and furosemide are still on the drug chart. He is dry, oliguric, and his creatinine has doubled from 130 to 260 micromol/L. The potassium comes back at 6.7 mmol/L.[6]

Three exam questions are now live and you must answer them in order: what is the cause, what will kill him first, and when do you reach for dialysis? This whole topic is the answer to those three questions.[6]

What AKI actually is — and why 'failure' became 'injury'

Acute kidney injury is a syndrome, hours to days, in which the kidney stops keeping the inside of the body constant. Fluid, electrolytes and acid-base drift, and nitrogenous waste accumulates. The KDIGO 2012 definition (it retired the older RIFLE and AKIN schemes) is any one of the following:[6]

• Serum creatinine up by 0.3 mg/dL (26.5 micromol/L) or more within 48 hours; OR
• Serum creatinine 1.5 times the known or presumed baseline within the prior 7 days; OR
• Urine output under 0.5 mL/kg/h for 6 hours or more.[6]

The word changed from 'failure' to 'injury' on purpose. Even a small, reversible creatinine rise carries real prognostic weight — more mortality, more future CKD — and 'failure' implied an all-or-nothing state that hid the spectrum.[5]

The skill in AKI is not the diagnosis. A creatinine trend makes the diagnosis in a minute. The skill is finding and reversing the cause, spotting the life-threatening complication (hyperkalaemia, acidosis, overload, uraemia) and knowing when to dialyse. And remember the trap: a normal creatinine early does not exclude AKI. Creatinine is a late, lagging, muscle-mass-dependent marker — a frail elderly patient can lose half their GFR and still sit inside the laboratory 'normal' range.[6]

PIN — pre-renal, intrinsic, obstructioN

AKI sorts into three buckets, and the numbers are worth memorising: pre-renal about 60 per cent, intrinsic about 35 per cent, obstruction about 5 per cent. The framework drives everything downstream — the work-up, the fluid decision, the disposal. Run PIN on every patient.[6]

Pre-renal (about 60 per cent) is a perfusion problem in an intact kidney. The tubules still grab sodium and water, so it recovers in hours once you fix the perfusion. Causes: hypovolaemia (haemorrhage, vomiting, diarrhoea, burns, diuretics), low effective circulating volume (heart failure, cirrhosis, sepsis, nephrotic syndrome), and drugs that wreck autoregulation — NSAIDs constrict the afferent arteriole, ACE inhibitors and ARBs dilate the efferent arteriole.[6]

Intrinsic (about 35 per cent) is disease inside the kidney, sorted by compartment: vascular (renal artery thrombosis or embolism, atheroembolism, renal vein thrombosis, malignant hypertension, HUS/TTP, vasculitis); glomerular (acute GN, rapidly progressive GN); tubular — acute tubular necrosis, ATN, the single commonest intrinsic cause, from ischaemia or nephrotoxins; and interstitial (acute interstitial nephritis, AIN, drug-induced or infective).[6]

Post-renal (about 5 per cent) is obstruction below the renal pelvis, fully reversible if you relieve it early: BPH, prostate, cervical or bladder cancer, retroperitoneal fibrosis, bilateral stones, neurogenic bladder, a blocked catheter. Exclude it first — it is the easiest to miss and the fastest to fix.[6]

KDIGO stages severity on the creatinine and the urine output — reproduce it verbatim, it is a guaranteed viva mark.[6]

Stage by the worse of the two criteria. The baseline is the lowest known creatinine in the prior 7 days; if you do not have one, estimate from a stable older value.[6]

Acute or chronic? AKI and CKD coexist as acute-on-chronic, and the split changes the prognosis. Points towards chronic: small echogenic kidneys on ultrasound, normocytic anaemia, hyperphosphataemia with hypocalcaemia, raised parathyroid hormone, long-standing hypertension, and a creatinine that has been high for months in the old records. Acute shows a rising creatinine over days, normal or large kidneys, and usually an obvious precipitant. When you genuinely cannot tell, treat as AKI (potentially reversible) while you confirm.[6]

Rapidly progressive glomerulonephritis (RPGN) is the glomerular emergency inside the intrinsic bucket. Creatinine climbs over weeks to a few months with active sediment — dysmorphic RBCs and RBC casts. It needs urgent biopsy and immunosuppression (cyclophosphamide and glucocorticoids, plus plasma exchange for anti-GBM disease) because delayed treatment leaves irreversible scarring.[6]

How common, and who breaks first

AKI is not a niche nephrology problem — it is a ward-round default. Susantitaphong's meta-analysis of 318 cohorts pooled adult hospital incidence at 21.6 per cent (95 per cent CI 19.3 to 24.1) on KDIGO-equivalent definitions, with AKI-associated mortality of 23.9 per cent in adults. Incidence climbs past 50 per cent in septic shock in ICU and falls in the community. Screen every medical admission.[1]

A vulnerable kidney fails first. The risk factors worth running on autopilot:[6]

• Age over 65 — less renal reserve, more comorbidity, more polypharmacy
• Pre-existing CKD — the single strongest risk factor; a small insult on a damaged kidney tips it over
• Diabetes mellitus — nephropathy, autonomic neuropathy, volume depletion
• Heart failure — chronic low perfusion, RAAS activation
• Cirrhosis — hepatorenal physiology
• Sepsis — the commonest single cause of hospital-acquired AKI
• Hypovolaemia of any cause
• Myeloma or paraproteinaemia — cast nephropathy, light-chain toxicity
• Cancer — chemotherapy nephrotoxicity, tumour lysis, obstruction[6]

The nephrotoxin shelf — memorise it; you will prescribe off it for life.[6]

• NSAIDs — block prostaglandin-driven afferent arteriolar dilation in volume depletion
• ACE inhibitors and ARBs — dilate the efferent arteriole, dropping glomerular pressure
• Aminoglycosides (gentamicin, amikacin, tobramycin) — accumulate in proximal tubule cells; non-oliguric AKI after 5 to 7 days; watch trough levels
• Vancomycin — dose-related AKI, worse with piperacillin-tazobactam
• Amphotericin B — direct tubular toxicity; the deoxycholate form is worst
• Radiocontrast — iodinated contrast, risk within 24 to 72 hours
• Calcineurin inhibitors (ciclosporin, tacrolimus) — afferent vasoconstriction
• Chemotherapy (cisplatin, ifosfamide, methotrexate) and targeted agents
• Statins (rhabdomyolysis) and antivirals (aciclovir, tenofovir, foscarnet)[6]

Setting sets the likely cause. In the community, pre-renal volume depletion (gastroenteritis, diuretics, heart failure) and obstruction. On the ward, sepsis, perioperative hypotension, heart failure and nephrotoxic drugs. In ICU, septic shock, multi-organ failure and major surgery.[6]

Why pre-renal recovers in hours and ATN takes weeks

Every AKI ends in a falling GFR, but the mechanism decides the timetable. Understand the mechanism and you understand why pre-renal recovers in hours while ATN takes days to weeks.[6]

Pre-renal azotaemia — intact tubules, falling perfusion. GFR rides on glomerular capillary pressure, held steady by autoregulation: prostaglandins dilate the afferent arteriole, angiotensin II constricts the efferent arteriole. When perfusion drops, the tubules are intact and avidly reabsorb sodium and water to defend circulating volume — so you see low urine sodium (under 20), concentrated urine (osmolality over 500), FENa under 1 per cent and BUN/Cr over 20:1. Fix the perfusion and the kidney bounces back in hours. Leave it, and ischaemic ATN follows within hours to days.[6]

The 'triple whammy' — how a compensated kidney collapses. In a well-perfused kidney, NSAIDs and ACE inhibitors are harmless. In a volume-depleted patient whose GFR is hanging entirely on prostaglandins (afferent dilation) and angiotensin II (efferent constriction), blocking either one collapses glomerular pressure. NSAIDs constrict the afferent; ACE inhibitors and ARBs dilate the efferent. Add a diuretic to strip the volume further and you have the classic AKI precipitant: NSAID plus ACE inhibitor plus diuretic in a dry patient.[6]

ATN — structural tubular injury. ATN follows ischaemia (a prolonged pre-renal insult — haemorrhage, sepsis, hypotension, cardiac arrest) or a direct nephrotoxin (aminoglycosides, contrast, heavy metals, myoglobin, haemoglobin, tumour lysis products). Four mechanisms lock together to drop the GFR:[6]

1. Tubular cell injury and apoptosis — ischaemia depletes ATP. The proximal tubule's S3 segment in the outer medulla is the most metabolically active and least oxygenated strip of kidney, so it dies first. Cells lose their brush border, detach from the basement membrane and shed into the lumen.
2. Cast obstruction — shed cells and Tamm-Horsfall protein form muddy brown granular casts that plug the tubule, raising intratubular pressure against filtration.
3. Back-leak of filtrate — the damaged epithelium no longer holds, so glomerular filtrate seeps back into the interstitium; filtered solute never reaches the urine.
4. Intrarenal vasoconstriction — injured tubules release cytokines and trip tubuloglomerular feedback (adenosine at the macula densa), constricting the afferent arteriole and dropping GFR further. Endothelial injury and medullary congestion keep the cycle turning.[6]

ATN has a script — oliguric phase, then polyuric (diuretic) phase, then recovery. Tubular cells must regenerate, a job of days to weeks; recovering tubules cannot concentrate urine, so the diuresis precedes the recovery of GFR. Tell the family to expect it, or they will think you have broken the kidney.[6]

Pigment nephropathy — rhabdomyolysis and haemolysis. Myoglobin (crushed or injured muscle) and free haemoglobin (haemolysis) filter freely, get endocytosed by proximal tubule cells, release free iron, generate reactive oxygen species, deplete ATP and cast up with Tamm-Horsfall protein — worst when urine is acidic and the patient is dry. The trap that earns the mark: the dipstick reads positive for 'blood' but microscopy shows no red cells. That dissociation is myoglobin (or haemoglobin). CK over 5000 IU/L defines clinically significant rhabdomyolysis with high AKI risk.[10]

Contrast-induced AKI. Iodinated contrast causes medullary hypoxia (it raises blood viscosity and medullary oxygen demand) plus direct tubular toxicity and free-radical injury — ATN within 24 to 72 hours, usually non-oliguric.[7]

Tumour lysis syndrome. Rapid tumour cell kill — haematological malignancy after chemo, or a bulky treatment-sensitive tumour — dumps uric acid, potassium and phosphate. Urate and calcium-phosphate crystals obstruct and injure tubules; hyperkalaemia and hyperphosphataemia are the immediate threats.[17]

Why a 'normal' creatinine does not exclude AKI. Creatinine lags and depends on muscle mass. A small elderly patient can lose half their GFR and still read 'normal'. Urine output and trend beat any single creatinine.[6]

What you hear and see at the bedside

AKI is usually silent and found on the biochemistry. When it speaks, it speaks in uraemia, fluid overload and electrolyte disturbance — layered onto the story of whatever caused it.[6]

Features of AKI itself: oliguria (under 0.5 mL/kg/h) or anuria, fluid overload (dyspnoea, oedema, hypertension), and the uraemic syndrome — anorexia, nausea, vomiting, confusion, asterixis (the flap), pericarditic chest pain, a friction rub, pruritus, bruising, and at the severe end seizures and coma.[6]

The history and examination that crack the cause:[6]

• Hypovolaemia / pre-renal — thirst, dry mucosae, reduced skin turgor, tachycardia, hypotension or a postural drop, oliguria, cold peripheries, slow capillary refill. A story of vomiting, diarrhoea, haemorrhage, burns, diuretic overuse or DKA.
• Sepsis — fever or hypothermia, rigors, hypotension, warm or mottled peripheries, a source (pneumonia, pyelonephritis, peritonitis, line infection). Sepsis is the commonest single cause of hospital-acquired AKI.
• Obstructive (post-renal) — anuria or fluctuating output, a palpable bladder, an enlarged prostate on PR, a pelvic mass, a single kidney, prior pelvic or retroperitoneal surgery or radiotherapy, neurogenic bladder. Hesitancy, weak stream, straining and nocturia point to BPH.
• Nephrotoxin exposure — go through the drug chart line by line: recent contrast, NSAIDs, ACE inhibitors and ARBs, aminoglycosides, amphotericin, chemotherapy, tenofovir, aciclovir; recreational and occupational toxins.
• Acute interstitial nephritis — the classic triad of fever, rash and eosinophilia, often incomplete (only a minority show all three); onset days to weeks after a new drug (penicillin, PPI, NSAID, sulphonamide, rifampicin); may have arthralgia and eosinophiluria.
• Glomerulonephritis or vasculitis — haematuria (smoky or cola-coloured urine), oedema and hypertension (nephritic syndrome), proteinuria; systemic clues — rash, palpable purpura, arthralgia, mouth ulcers, sinusitis, haemoptysis or lung cavities (granulomatosis with polyangiitis), haemoptysis (anti-GBM or Goodpasture), abdominal pain and diarrhoea (HUS).
• Rhabdomyolysis — muscle pain, weakness, swelling, dark tea- or cola-coloured urine; a story of trauma, prolonged immobility, statin, cocaine, seizure, exertion, burns or electrical injury.
• Tumour lysis syndrome — high tumour burden (leukaemia, lymphoma, bulky solid tumour) within 48 to 72 hours of starting chemo or steroids; hyperkalaemia, hyperphosphataemia, hypocalcaemia, hyperuricaemia.
• Atheroembolism — after a vascular procedure (catheter, angiography, vascular surgery) or spontaneously; livedo reticularis, blue toes, eosinophilia, hypocomplementaemia; AKI that evolves over weeks.
• Hepatorenal syndrome — cirrhosis with ascites, jaundice, hypoalbuminaemia; AKI that does not improve after an albumin challenge.[6]

In the elderly, AKI wears a disguise. It shows as confusion, falls, functional decline, incontinence or drug toxicity rather than oliguria — less renal reserve, more polypharmacy, blunted thirst. Drop your threshold for a creatinine.[6]

Acute-on-chronic. A patient with known CKD tips into AKI from a small insult — one NSAID, a dehydrating illness, a contrast study — that would not scratch a normal kidney. Separate acute-on-chronic (potentially recoverable) from end-stage disease (small kidneys, anaemia, mineral bone disease).[6]

The poor man's biopsy — urine biochemistry and sediment

Your first job is to place the patient in pre-renal, intrinsic or post-renal, then refine within intrinsic. Use the history, the urine biochemistry (FENa, urine sodium, urine osmolality, BUN/Cr) and the sediment together — no single test is definitive.[6]

Pre-renal vs intrinsic (ATN) — the face-off table, with FENa as the discriminator:[6]

FENa — the formula and the trap. FENa (per cent) = (urine sodium times serum creatinine) / (serum sodium times urine creatinine) times 100, on a spot simultaneous urine and serum pair. The trap everyone falls into: FENa is invalid after recent diuretics, which force sodium out regardless of cause. In that setting switch to fractional excretion of urea (FEurea) — under 35 per cent supports pre-renal. FENa is also unreliable in CKD, glycosuria and salt-wasting states.[6]

The sediment is the poor man's biopsy — learn it as a one-line discriminator:[6]

• Muddy brown granular casts and renal tubular epithelial cells — ATN.
• Dysmorphic RBCs and RBC casts — glomerulonephritis (a glomerular bleed; RBC casts are pathognomonic of glomerular disease).
• WBC casts, eosinophiluria, sterile pyuria — acute interstitial nephritis (eosinophiluria is Hansel-stain positive; also think papillary necrosis, tuberculosis, UTI).
• Pigmented granular casts, dipstick-positive blood but no RBCs — rhabdomyolysis (myoglobin) or haemolysis (haemoglobin).
• Bland sediment with leucocytes — consider obstruction, atypical infection, or pre-renal disease.
• Crystals — urate (tumour lysis), calcium oxalate (ethylene glycol), envelope-shaped calcium phosphate (hyperparathyroidism).[6]

When you MUST actively exclude obstruction: anuria, a single kidney or transplant, recent pelvic or retroperitoneal surgery, prostate or pelvic malignancy, neurogenic bladder, bilateral flank pain with stones. Get a bladder scan and renal ultrasound within 24 hours — immediately if the patient is obstructed and infected, which is a urological emergency. Hydronephrosis on ultrasound confirms obstruction, but its absence does not exclude early obstruction, retroperitoneal fibrosis, or a ureter encased by tumour.[6]

Acute or chronic, revisited. Small echogenic kidneys, normocytic anaemia, hyperphosphataemia with hypocalcaemia, raised PTH and a long-standing stable creatinine favour chronic. A clear precipitant, a rising creatinine and normal-sized kidneys favour acute (or acute-on-chronic). Always hunt down an old creatinine in the records.[6]

Three questions at the bedside

The bedside exam answers three questions in order: is the patient dry or drowned, what is the cause, and is there a life-threatening complication?[6]

Volume status decides the fluid challenge.[6]

• Hypovolaemia (give fluid) — tachycardia, hypotension or a postural drop (systolic fall over 20 mmHg or diastolic over 10 on standing), cool peripheries, slow capillary refill (over 2 seconds), reduced skin turgor, dry axillae and mucosae, low JVP, sunken eyes, oliguria.
• Hypervolaemia (no fluid; think diuretic or dialysis) — raised JVP, bilateral basal crackles, peripheral and sacral oedema, ascites, gallop rhythm, hypertension, S3.[6]

Haemodynamic target. Restore a mean arterial pressure of 65 mmHg or more to keep the kidney perfused; aim higher in the chronically hypertensive or vasoconstricted. Judge perfusion, not pressure — lactate, capillary refill, mottling and urine output are what matter, and a normal blood pressure does not exclude shock.[6]

Targeted hunt for the cause.[6]

• Septic screen — temperature, source exam (chest, urine, abdomen, lines, wounds, meninges), blood cultures, lactate.
• Abdomen — palpable bladder (obstruction), renal masses (tumour, polycystic), ascites (cirrhosis or HRS), abdominal aortic aneurysm.
• Rectal or vaginal exam — enlarged prostate, pelvic mass, cervical or rectal malignancy.
• Skin — rash, purpura (vasculitis), livedo and blue toes (atheroembolism), petechiae, cellulitis (source).
• Drug chart — go through every drug: stop NSAIDs, hold ACE inhibitors and ARBs, check aminoglycoside levels, antifungals, chemotherapy, antivirals; ask about recent contrast and over-the-counter NSAIDs (patients forget ibuprofen and naproxen).
• Cardiac — heart failure (low-output pre-renal AKI), pericardial rub (uraemic pericarditis), new murmur (endocarditis).
• Neurology — confusion, asterixis (uraemic flap), seizures (uraemia or hypertensive encephalopathy).[6]

Always check the potassium with a venous gas and look at the ECG at presentation. Hyperkalaemia kills AKI patients before anything else does.[6]

Investigations — first-line, then cause-directed

First-line, in every AKI:[6]

• Urea, electrolytes, creatinine, eGFR — establish the baseline and the trend (dig out any old result; this is the single most useful number on the chart).
• Venous bicarbonate (or venous gas) — metabolic acidosis; pH under 7.1 to 7.15 or bicarbonate under 12 is severe.
• Sodium, potassium, chloride — hyperkalaemia, hyponatraemia, anion-gap acidosis.
• Calcium, phosphate, magnesium — hypocalcaemia, hyperphosphataemia.
• Full blood count — anaemia (haemolysis, CKD), eosinophilia (AIN), leucocytosis (sepsis), thrombocytopenia (HUS/TTP, sepsis, DIC), fragmented red cells and schistocytes (HUS/TTP).
• CRP, blood cultures, lactate — sepsis work-up.
• Creatine kinase (CK) — rhabdomyolysis (over 5000 is high risk).
• Urinalysis and microscopy — protein, blood, leucocytes, nitrites, glucose; sediment is the key discriminator.
• Urine electrolytes (sodium and creatinine) with a simultaneous serum sample — to calculate FENa (or FEurea if on diuretics).
• ECG — hyperkalaemia (peaked T waves, flattened or absent P waves, prolonged PR, widened QRS, sine wave), pericarditis (diffuse ST elevation, PR depression).
• Renal ultrasound — kidney size (small suggests CKD; large suggests obstruction, polycystic, infiltrative), hydronephrosis (obstruction), and to confirm two kidneys before biopsy.
• Bladder scan — post-void residual, retention.
• Drug levels — gentamicin and vancomycin troughs.
• Hepatic screen and clotting — coagulopathy, cirrhosis or HRS; group and save.[6]

Second-line is cause-directed — send it when intrinsic disease is on the table. Serum immunoglobulins, free light chains and electrophoresis (myeloma); complement C3/C4 (low in lupus, post-infectious GN, cryoglobulinaemia); autoantibodies — ANA, ANCA (MPO and PR3), anti-GBM — for GN and vasculitis; hepatitis B and C and HIV serology (related GN); antistreptolysin O and anti-DNase B (post-streptococcal GN); myoglobin, lactate dehydrogenase, haptoglobin, blood film (rhabdomyolysis or haemolysis); urine for eosinophils (Hansel stain, AIN); and renal biopsy — the definitive test for unexplained intrinsic AKI, especially suspected RPGN.[6]

FENa — formula and interpretation:[6]

FENa (per cent) = (Urine Na x Serum Cr) / (Serum Na x Urine Cr) x 100 [6]

• Under 1 per cent — pre-renal azotaemia (intact tubular sodium retention)
• Over 2 per cent — intrinsic (ATN; damaged tubules cannot hold sodium)
• Misleading after diuretics — use FEurea = (Urine Urea x Serum Cr) / (Serum Urea x Urine Cr) x 100, where under 35 per cent supports pre-renal.[6]

Sediment — the high-yield associations:[6]

• Muddy brown granular casts plus renal tubular epithelial cells → ATN
• Dysmorphic RBCs and RBC casts → glomerulonephritis
• WBC casts and eosinophiluria → acute interstitial nephritis
• Sterile pyuria → obstruction, tuberculosis, interstitial nephritis
• Pigmented casts, dipstick blood but no RBCs → rhabdomyolysis or haemolysis[6]

BUN/creatinine ratio. Over 20:1 supports pre-renal (the kidney reabsorbs urea with sodium and water); 10 to 20:1 favours intrinsic. The ratio is dimensionless, so the threshold is the same in SI units.[6]

Hyperkalaemia ECG changes — reproduce them in order of severity. These are the traces that precede arrest, so learn the sequence.[6]

1. Peaked (tented) T waves — earliest, pinched base, narrow
2. Flattening or loss of P waves
3. Prolonged PR interval
4. Widening of the QRS complex
5. Sine wave — pre-arrest; the ECG melts into a sinusoidal pattern
6. Ventricular fibrillation or asystole[6]

The urgent threshold is potassium over 6.0 mmol/L — or over 5.5 with ECG changes. Treat immediately; do not wait for a confirmatory repeat.[8][9]

KDIGO staging — verbatim

Stage by the worse of creatinine and urine output; creatinine uses the ratio to baseline, urine output is mL/kg/h.[6]

The universal bundle — and the potassium that kills first

Every AKI starts with an ABCDE primary survey, then a cause-directed resuscitation bundle that applies to all patients — with hyperkalaemia treated as its own emergency if it is there.[6]

Five things you do for EVERY AKI — the universal bundle:[6]

1. Stop nephrotoxic drugs — NSAIDs, ACE inhibitors, ARBs, aminoglycosides (unless essential, then with therapeutic drug monitoring), iodinated contrast, metformin (lactic acidosis risk); review herbal and over-the-counter agents.
2. Re-dose every drug for renal function — vancomycin, digoxin, low-molecular-weight heparins, morphine and its metabolites, beta-blockers, sulphonylureas, gabapentin and pregabalin; use a renal drug-dosing chart or ask the pharmacist.
3. Exclude and relieve obstruction — bladder scan; catheterise if in retention; renal ultrasound within 24 hours (immediately for septic obstruction — a urological emergency).
4. Optimise haemodynamics — target mean arterial pressure 65 mmHg or more; fluid if dry, vasopressors if vasodilated (sepsis).
5. Monitor — strict fluid balance, daily weights, hourly urine output (catheterise if oliguric or unstable), daily U&E and creatinine (more often if unstable or hyperkalaemic).[6]

Resuscitating pre-renal or hypovolaemic AKI. Give a fluid challenge with balanced crystalloid (Hartmann's or Plasma-Lyte) 250 to 500 mL over 15 to 30 minutes (10 to 15 mL/kg), then reassess fluid responsiveness — passive leg raise, pulse-pressure variation, IVC, JVP — and urine output before giving more. Avoid hydroxyethyl starch (CHESS-AKI and 6S showed more AKI and mortality) and avoid albumin outside cirrhosis; large volumes of 0.9 per cent saline cause hyperchloraemic acidosis and may worsen AKI, which is why balanced crystalloid wins.[6][11][12]

Septic AKI — the Surviving Sepsis hour-1 bundle:[13]

• Oxygen to saturation 94 to 98 per cent (88 to 92 per cent in COPD)
• Blood cultures before antibiotics — but never delay antibiotics for cultures
• Broad-spectrum IV antibiotics within 1 hour
• Lactate; remeasure if raised
• Balanced crystalloid 30 mL/kg bolus for septic shock or lactate over 4
• Noradrenaline (norepinephrine) first-line for fluid-refractory shock, titrated to MAP 65 mmHg or more; vasopressin second line[13]

Hyperkalaemia is the emergency inside the emergency. If potassium is over 6.0 mmol/L or any ECG change is present, treat immediately and in parallel:[8][9]

• Calcium gluconate 10 per cent, 10 mL IV over 5 to 10 minutes — stabilises the myocardial membrane (no effect on the potassium level; repeat if ECG changes persist). Calcium chloride is the alternative via a central line.
• Insulin-dextrose — 10 units of soluble (regular) insulin IV with 25 g (50 mL of 50 per cent) dextrose IV over 15 to 30 minutes; drives potassium into cells. Check glucose at 30 minutes, 1, 2, 3 and 6 hours (hypoglycaemia risk for up to 6 hours).
• Salbutamol 10 to 20 mg nebulised (or 0.5 mg IV) — adjunctive; shifts potassium into cells via beta-2 stimulation; useful if insulin-dextrose is contraindicated.
• Sodium bicarbonate — only if a significant metabolic acidosis coexists (pH under 7.1 to 7.15); slow to act and weak on potassium in isolation.
• Potassium removal — sodium polystyrene sulfonate 15 to 30 g orally or rectally (slow; hours to act); newer binders (patiromer, sodium zirconium cyclosilicate) are faster. Dialysis if refractory or potassium keeps climbing.[8]

Why fluid overload harms and colloids are out. A positive balance worsens AKI outcomes: pulmonary oedema, raised intra-abdominal and renal venous pressure, and it hides ongoing injury. Colloids (albumin, hydroxyethyl starch) offer no benefit over crystalloid here, and starch increases AKI and mortality (CHESS-AKI, 6S). Treat the volume status, not a number.[11][12]

The four-step ladder — and when to dialyse (AEIOU)

Definitive management is a four-step ladder; only stage 3 or dialysis-requiring AKI needs critical care.[6]

1. Treat the cause — fluids for pre-renal, antibiotics for sepsis, relieve obstruction, stop nephrotoxins, immunosuppression for RPGN, steroids for severe AIN, rasburicase for tumour lysis.
2. Optimise haemodynamics — fluid if depleted, vasopressors if vasodilated, target MAP over 65; inotropes if cardiogenic.
3. Manage complications — the hyperkalaemia ladder above, metabolic acidosis, fluid overload, nutrition.
4. Renal replacement therapy when indicated — AEIOU, below.[6]

The hyperkalaemia ladder — drug, dose, route, rationale, reproduced verbatim:[8]

• Calcium gluconate 10 per cent — 10 mL IV over 5 to 10 minutes — membrane stabilisation (no effect on K); repeat if ECG changes persist
• Insulin 10 units + 50 per cent dextrose 50 mL IV — shifts K into cells; onset 15 to 30 minutes, duration 4 to 6 hours; monitor glucose
• Salbutamol 10 to 20 mg nebulised — shifts K into cells (beta-2); adjunctive
• Sodium bicarbonate (1.26 per cent or 8.4 per cent) — for acidosis; slow, modest K-lowering
• Potassium binders — sodium polystyrene sulfonate 15 to 30 g orally or rectally; patiromer or sodium zirconium cyclosilicate (faster); slow onset
• Dialysis — definitive removal; for refractory hyperkalaemia[8][18]

Metabolic acidosis. Give sodium bicarbonate if pH is under 7.1 to 7.15 (or bicarbonate under 12) — target pH over 7.15 to 7.20; avoid it in volume overload (dialyse instead). Severe acidosis blunts cardiac contractility and vasopressor responsiveness.[6]

Fluid overload and pulmonary oedema. Sit the patient up, give oxygen, a loop diuretic (IV furosemide) if the kidney still responds — diuretics do not treat AKI but can flip oliguric to non-oliguric and ease fluid handling — and dialyse if refractory.[6]

Nutrition. Enteral nutrition early; adequate calories and protein, adjusted for whether the patient is on renal replacement therapy; restrict sodium, potassium and phosphate. Do not restrict protein — malnutrition raises mortality.[20]

Relieving obstruction. A urethral catheter for bladder-outlet obstruction; a percutaneous nephrostomy or retrograde ureteric stent for ureteric obstruction. Watch for post-obstructive diuresis — polyuria after relief as recovering tubules fail to concentrate; replace fluid and electrolytes to avoid hypovolaemia and a secondary AKI.[6]

Disease-directed therapy — the right drug for the right cause:[6]

• Acute interstitial nephritis — stop the offending drug; a short course of oral corticosteroids tapering over a few weeks if severe or biopsy-confirmed; biopsy if not recovering.[14]
• Rapidly progressive glomerulonephritis — urgent renal biopsy; high-dose IV methylprednisolone pulses then oral prednisolone plus cyclophosphamide (or rituximab for ANCA vasculitis); plasma exchange for anti-GBM disease and severe pulmonary haemorrhage. In the sick patient, do not delay immunosuppression for the biopsy.[15][16]
• Rhabdomyolysis — aggressive isotonic saline to keep the urine output high until CK falls; consider sodium bicarbonate to alkalinise urine (evidence mixed); treat compartment syndrome, hyperkalaemia and hypocalcaemia (only if symptomatic).[10]
• Tumour lysis syndrome — aggressive hydration before and during chemotherapy; rasburicase for established or high-risk hyperuricaemia (breaks uric acid to soluble allantoin; contraindicated in G6PD deficiency); allopurinol for prophylaxis; manage hyperkalaemia and hyperphosphataemia.[17]
• Hepatorenal syndrome — albumin challenge to confirm; treat with terlipressin plus albumin, or noradrenaline in ICU; definitive treatment is liver transplant.[19]
• Contrast-induced AKI — isotonic saline hydration (1 mL/kg/h for 6 to 12 hours pre- and post-procedure); hold metformin and nephrotoxins; use the lowest contrast volume, iso-osmolar or low-osmolar agents. N-acetylcysteine and bicarbonate are NOT effective (PRESERVE trial).[7][4]

AEIOU — the dialysis indications, reproduce verbatim:[2][3]

• A — Acidosis — severe, refractory metabolic acidosis (pH under 7.1 to 7.15)
• E — Electrolytes — refractory hyperkalaemia (K over 6.5 or persistently over 6.0 despite medical therapy)
• I — Ingestion — dialysable toxins: lithium, salicylate, methanol, ethylene glycol, metformin (in severe lactic acidosis), barbiturates
• O — Overload — refractory pulmonary oedema or fluid overload unresponsive to diuretics
• U — Uraemia — uraemic pericarditis, uraemic encephalopathy (seizures, coma), uraemic bleeding, or severe symptomatic uraemia[7]

(Add an extra I for intractable acidosis, or use AEIOU-H for severe drug toxicity — the core five are exam standard.)[7]

When to refer. Nephrology for stage 3 AKI, AKI not improving after 48 to 72 hours, a suspected intrinsic or obstructive cause, or anyone meeting AEIOU. Critical care or ICU for AKI with multi-organ failure, refractory hyperkalaemia, severe acidosis, fluid overload needing RRT, or a vasopressor requirement.[6]

The named subtypes that have their own drug

• Contrast-induced AKI (CI-AKI). KDIGO defines it as a creatinine rise of 0.3 mg/dL or more, or 1.5 times baseline, within 48 to 72 hours of contrast with no alternative cause. Risk factors: pre-existing CKD (especially eGFR under 30), diabetes, heart failure, hypovolaemia, high contrast volume, intra-arterial injection. Prevention is isotonic saline hydration; hold metformin (lactic acidosis risk) and nephrotoxins; use the lowest contrast volume, iso-osmolar or low-osmolar agents. N-acetylcysteine and sodium bicarbonate do NOT prevent CI-AKI (PRESERVE, NEJM 2018).[7][4]
• Rhabdomyolysis. CK over 5000 IU/L defines clinically significant disease; the biochemical picture is hyperkalaemia, hyperphosphataemia, hypocalcaemia, high anion-gap acidosis, raised CK and myoglobin, dipstick blood with no red cells, pigmented granular casts. Treat with aggressive isotonic saline (keep the urine output high) and manage compartment syndrome and electrolytes. Urine alkalinisation is controversial; mannitol is not routinely recommended.[10]
• Acute interstitial nephritis (AIN). Drugs cause most cases — penicillins (methicillin is the classic), proton-pump inhibitors, NSAIDs (often with nephrotic-range proteinuria), sulphonamides, rifampicin, 5-flucytosine, allopurinol, mesalazine; also infection and autoimmune. Urine shows WBC casts, eosinophiluria, sterile pyuria, haematuria, mild proteinuria. The classical fever-rash-eosinophilia triad is often absent. Management: stop the offending drug; a short course of oral corticosteroids if severe, biopsy-confirmed, or not recovering within a week.[14]
• Hepatorenal syndrome (HRS-AKI). Cirrhosis with ascites; AKI that fails to improve after 48 hours of albumin challenge without shock, nephrotoxins or structural kidney disease; terlipressin plus albumin is first-line vasoconstrictor therapy, noradrenaline in ICU; definitive treatment is liver transplant.[19]
• Tumour lysis syndrome. A metabolic emergency within 48 to 72 hours of cytotoxic therapy in high-burden haematological malignancy: hyperuricaemia, hyperkalaemia, hyperphosphataemia, hypocalcaemia, AKI. Prevention with hydration and rasburicase (high risk) or allopurinol (lower risk) is the standard of care.[17]
• Obstructive uropathy. Relieve with a catheter (bladder outlet) or nephrostomy or ureteric stent (ureteric); watch for post-obstructive diuresis (replace fluid and electrolytes).[6]
• Atheroembolic disease. After vascular procedures or spontaneously; livedo reticularis, blue toes, eosinophilia, hypocomplementaemia, AKI evolving over weeks; supportive care; renal recovery is poor.[6]
• Cancer-related AKI. Any combination of obstruction, direct infiltration, tumour lysis, chemotherapy toxicity (cisplatin, ifosfamide), immunotherapy (immune-checkpoint-inhibitor AIN and GN) and paraneoplastic GN; tailor treatment to the mechanism.[6]

What kills AKI patients — and the traps that cause it

Metabolic complications.[6]

• Hyperkalaemia — the leading cause of death in AKI; arrhythmia, asystole
• Metabolic acidosis — high anion gap from organic acid retention; worsens hyperkalaemia and hypotension
• Hyponatraemia — water retention with isosthenuria
• Hyperphosphataemia with hypocalcaemia — phosphate retention, reduced vitamin D activation; symptomatic hypocalcaemia (tetany, seizures) is rare unless rhabdomyolysis or tumour lysis
• Hyperuricaemia, hypermagnesaemia[6]

Volume complications. Pulmonary oedema (the commonest reason for emergent RRT), hypertension, peripheral and pulmonary oedema, ascites.[6]

Uraemic complications. Uraemic pericarditis (a dialysis indication; friction rub, chest pain, effusion), uraemic encephalopathy (confusion, asterixis, seizures, coma), bleeding (platelet dysfunction), nausea, anorexia, pruritus, anaemia (reduced erythropoietin).[6]

Life-threatening complications. Arrhythmia and cardiac arrest from hyperkalaemia; uraemic pericarditis with tamponade; seizures or coma from uraemic encephalopathy; severe acidosis with circulatory collapse; massive pulmonary oedema; and infection, the leading cause of death in AKI.[6]

Classic pitfalls — each one is an exam question:[6]

• Missing obstruction — always a bladder scan and renal ultrasound; anuria, a single kidney or pelvic malignancy are red flags
• Failing to stop nephrotoxins — NSAIDs, ACE inhibitors and ARBs, aminoglycosides, contrast; review every drug, including over-the-counter NSAIDs
• Over-resuscitation — causing pulmonary oedema; reassess responsiveness, do not chase a number
• Using FENa after diuretics — use FEurea (under 35 per cent for pre-renal) instead
• Calling CKD an AKI (or vice versa) — small echogenic kidneys, anaemia and mineral bone disease favour chronic
• Missing RPGN — dysmorphic RBCs and RBC casts need urgent biopsy and immunosuppression; delay causes irreversible scarring
• Missing rhabdomyolysis — dipstick positive for blood with no red cells is myoglobin (or haemoglobin)
• Treating the number, not the patient — furosemide to 'make urine' without fluid overload worsens outcome
• Forgetting to re-dose or stop drugs — LMWH, vancomycin, metformin and digoxin accumulate and harm[6]

AKI is not benign — disposition and follow-up

An AKI is not a benign lab abnormality. It independently raises short-term mortality, length of stay, CKD progression and cardiovascular events. Prognosis tracks the stage, the cause (pre-renal reversed quickly vs ATN vs RPGN), oliguria, the need for dialysis and comorbidity.[5]

KDIGO staging (reproduce exactly)

Disposition

• Ward with strict fluid balance and daily labs: a stable Stage 1 with a clear, reversible cause.
• HDU or ICU: hyperkalaemia emergencies, pulmonary oedema, severe acidosis, sepsis, need for emergency RRT, multi-organ failure.
• Nephrology referral early if intrinsic renal disease is suspected (active sediment, an RPGN pattern, systemic vasculitis or myeloma clues), the cause is unclear, or Stage 2 to 3 is progressing.[6]

Recovery and follow-up

Re-check creatinine 1 to 3 months after AKI — even 'recovered' AKI earns a CKD-risk label, a medication review, and blood-pressure and albuminuria follow-up. Avoid repeated nephrotoxic insults.[5]

Special populations

Elderly

Less reserve, more polypharmacy — ACE inhibitor or ARB plus diuretic plus NSAID is the triple whammy — obstructive uropathy from the prostate, and dehydration. Creatinine under-reflects injury because muscle mass is low, so small absolute rises matter.[6]

Pregnancy

Separate pre-renal AKI, pyelonephritis, pre-eclampsia or HELLP, thrombotic microangiopathy, acute fatty liver and obstruction from the gravid uterus (hydronephrosis is normal in pregnancy). Obstetric-led care; delivery may be the definitive therapy for pre-eclampsia-related injury.[6]

Heart failure (cardiorenal)

Congestion drives AKI through raised venous pressure; over-diuresis drives pre-renal injury. Use weights, JVP, lactate and haemodynamics — not creatinine alone — to set diuretic intensity. SGLT2 inhibitors remain beneficial long-term in HF and CKD when stable.[6]

Liver disease (HRS-AKI)

In cirrhosis with ascites, exclude hypovolaemia, shock, nephrotoxins and structural disease first. Terlipressin plus albumin protocols for hepatorenal syndrome where available; transplant is definitive for eligible patients.[19]

Tumour lysis, rhabdomyolysis, myeloma

• TLS: hydration, urate lowering (allopurinol or rasburicase), monitor K, phosphate and calcium.[17]
• Rhabdomyolysis: aggressive isotonic fluid, watch the potassium; alkaline diuresis only in selected protocols.[10]
• Myeloma kidney: hydration, treat the clone, avoid NSAIDs, contrast and dehydration; consider dialysis-based clearance of cast nephropathy in specialist centres.[6]

Contrast exposure

Risk is highest with CKD, diabetes, volume depletion and high contrast volume. Prevent with volume expansion when appropriate; stop nephrotoxins; use the lowest contrast dose; routine N-acetylcysteine has no proven benefit.[4]

The trials that changed practice — AKIKI, STARRT-AKI, PRESERVE

KDIGO 2012 is the international standard for definition, staging and management — it folded the older RIFLE and AKIN schemes into one creatinine-plus-urine-output definition and the three-stage classification above.[6]

Dialysis timing — the two landmark trials:[2][3]

• AKIKI (Gaudry et al, NEJM 2016) — a French multicentre RCT in 620 critically-ill patients with severe AKI (KDIGO Stage 3): early (within 12 hours of eligibility) vs delayed (waiting for AKI progression or an urgent AEIOU indication) RRT. No difference in 60-day mortality; the delayed group had less dialysis and one in three never needed it. This backed a watchful, delayed strategy.[2]
• STARRT-AKI (Bagshaw et al, NEJM 2020) — a multinational RCT in 3019 critically-ill patients with severe AKI: accelerated (within 12 hours of Stage 3) vs standard (an AEIOU indication or persistent AKI) strategy. No mortality benefit from accelerated initiation, and more adverse events (fluid overload, catheter complications).[3]

The synthesis examiners want: current evidence does not support early, prophylactic RRT. Start dialysis for AEIOU, for AKI not recovering, or for persistent Stage 3 AKI with complications. The exception is the patient clearly heading toward RRT, for whom early preparation (vascular access, nephrology referral) is sensible.[6]

Contrast-induced AKI — PRESERVE. The PRESERVE trial (Weisbord et al, NEJM 2018) randomised 5177 high-risk patients undergoing angiography in a 2 by 2 factorial to sodium bicarbonate vs isotonic saline and N-acetylcysteine vs placebo. Neither intervention prevented death, dialysis or persistent renal impairment at 90 days. Prevention is now isotonic saline hydration alone; do not rely on N-acetylcysteine or bicarbonate.[4]

Long-term outcomes. James et al (Nature Reviews Nephrology, 2020) made the case that AKI is a risk factor for incident and progressive CKD, end-stage kidney disease, cardiovascular events and mortality, with risk proportional to AKI severity and recurrence. AKI and CKD are a continuum, which is why AKI survivors need long-term follow-up.[5]

Regional deltas:[6]

• KDIGO 2012 (international) — definition, staging, management; the global standard.
• NICE NG148 (UK) — aligned to KDIGO; adds e-alerts, Sick Day Guidance, and the principle that diuretics do not treat AKI.
• ICMR and Indian practice (resource-limited) — emphasises prevention (avoid NSAIDs, judicious fluid), conservative management, and peritoneal dialysis as a low-cost RRT option where haemodialysis access is limited; malnutrition, infections (malaria, leptospirosis, dengue) and nephrotoxic traditional medicines are additional regional causes.[6]

Hyperkalaemia emergency — doses you must know cold

Hyperkalaemia emergency doses (adult)

ECG changes (peaked T, flattened P, wide QRS, sine wave) — give calcium before or while shifting potassium, and do not wait for a lab reconfirm if the tracing is life-threatening.[8]

Indications for urgent RRT (AEIOU)

• Acidosis (severe refractory metabolic acidosis)
• Electrolytes (refractory hyperkalaemia)
• Intoxications (dialysable toxins: lithium, toxic alcohols, salicylate — selected cases)
• Overload (pulmonary oedema refractory to medical therapy)
• Uraemic complications (encephalopathy, pericarditis, bleeding diathesis)[7]

Exam pearls

• FENa under 1 per cent = pre-renal; over 2 per cent = ATN; misleading after diuretics — use FEurea under 35 per cent for pre-renal.[6]
• BUN/creatinine over 20:1 = pre-renal; 10 to 20:1 = intrinsic.
• Muddy brown granular casts = ATN; RBC casts = glomerulonephritis; WBC casts and eosinophiluria = acute interstitial nephritis.[6]
• Dipstick blood positive with no red cells on microscopy = rhabdomyolysis (myoglobin) or haemolysis (haemoglobin).
• KDIGO creatinine thresholds, verbatim: Stage 1 = 1.5 to 1.9 times baseline or up by 0.3 mg/dL; Stage 2 = 2.0 to 2.9 times baseline; Stage 3 = 3.0 times baseline, or over 4.0 mg/dL, or RRT.
• AEIOU = dialysis indications: Acidosis, Electrolytes (hyperkalaemia), Ingestion (lithium, salicylate, methanol, ethylene glycol, metformin), Overload (pulmonary oedema), Uraemia (pericarditis, encephalopathy).
• Hyperkalaemia ladder: calcium gluconate 10 per cent 10 mL IV (membrane stabilisation), then insulin 10 units plus 50 per cent dextrose, then salbutamol nebs, then K-binders, then dialysis.
• Always exclude obstruction with a bladder scan and ultrasound first; stop nephrotoxins (NSAIDs, ACE inhibitors, aminoglycosides, contrast).
• NSAIDs constrict the afferent arteriole; ACE inhibitors and ARBs dilate the efferent arteriole — both drop glomerular pressure. The 'triple whammy' is NSAID plus ACE inhibitor plus diuretic.
• ATN recovery: oliguric phase, then polyuric (diuretic) phase, then recovery. Pre-renal recovers in hours; ATN in days to weeks.
• AKIKI and STARRT-AKI: no mortality benefit of early over delayed dialysis — start for AEIOU or persistent AKI.[2][3]
• PRESERVE: N-acetylcysteine and bicarbonate do NOT prevent contrast-induced AKI — use isotonic saline.[4]
• Surviving Sepsis hour-1 bundle: oxygen, cultures, antibiotics within 1 hour, lactate, 30 mL/kg crystalloid, noradrenaline for shock.[13]
• Creatinine is a late, lagging marker — a normal value early does not exclude significant AKI.[6]

Ward-round test

Stem 1 — the dry septic patient. A 72-year-old with a urinary tract infection is hypotensive, oliguric, creatinine up from 90 to 180, FENa 1.4 per cent on no diuretics, bland sediment. What bucket, what first, what target?[6]

Stem 1 — the dry septic patient (answer)

This is pre-renal AKI on sepsis (a low-normal FENa with bland sediment in a volume-depleted, septic patient). Run the Surviving Sepsis hour-1 bundle — oxygen, cultures, broad-spectrum antibiotics within 1 hour, lactate, balanced crystalloid 30 mL/kg bolus, noradrenaline to MAP 65 mmHg or more — stop any nephrotoxins, catheterise for hourly urine output, and re-check creatinine and potassium. Most pre-renal AKI recovers in hours once perfusion is restored; if it does not, you have drifted into ischaemic ATN.[13][6]

Stem 2 — the trap on the dipstick. A 30-year-old presents after a prolonged collapse on the floor with cola-coloured urine, CK 12,000, and a dipstick positive for 'blood' with no red cells on microscopy. Diagnosis, and what is the fluid target?[10]

Stem 2 — rhabdomyolysis (answer)

Rhabdomyolysis with pigment nephropathy. The dissociation — dipstick positive for blood, no red cells on microscopy — is myoglobin. Treat with aggressive isotonic saline to keep the urine output high until CK falls, manage hyperkalaemia and treat compartment syndrome. Do not correct the hypocalcaemia unless symptomatic. Mannitol is not routinely recommended and urine alkalinisation is controversial.[10][6]

Stem 3 — the glomerular emergency. A 45-year-old presents with smoky urine, oedema, hypertension, a creatinine that has risen over two weeks, and RBC casts on microscopy. What is this, and what do you do in the next 24 hours?[6]

Stem 3 — rapidly progressive glomerulonephritis (answer)

Rapidly progressive glomerulonephritis — a glomerular cause of intrinsic AKI with active sediment and a subacute creatinine rise. Send ANA, ANCA (MPO and PR3), anti-GBM, complement and hepatitis serology, and arrange an urgent renal biopsy. Do not delay treatment in the sick patient: high-dose IV methylprednisolone pulses then oral prednisolone plus cyclophosphamide (rituximab for ANCA vasculitis), and plasma exchange for anti-GBM disease or severe pulmonary haemorrhage. Delayed treatment causes irreversible scarring.[15][16]

Stem 4 — when to dialyse. An ICU patient with Stage 3 AKI has potassium 6.9 despite insulin-dextrose and salbutamol, pH 7.08, and is developing pulmonary oedema. Two examiners' questions: should you have dialysed earlier to prevent this, and what do you do now?[6]

Stem 4 — dialyse now; early initiation would not have helped (answer)

Dialyse now — this patient meets AEIOU three times over (refractory Electrolytes, Acidosis, Overload). On the timing question: AKIKI and STARRT-AKI showed no mortality benefit and more adverse events from early, prophylactic RRT in severe AKI. Start dialysis for AEIOU, AKI not recovering, or persistent Stage 3 AKI with complications — which is exactly this patient.[2][3]

Rapid viva checklist

1. KDIGO definition and PIN classification
2. Pathophysiology chain (why pre-renal recovers fast, ATN slowly)
3. FENa and FEurea thresholds with the diuretic caveat
4. Sediment one-liners (the poor man's biopsy)
5. Universal bundle and hyperkalaemia ladder with doses
6. AEIOU dialysis indications
7. AKIKI, STARRT-AKI and PRESERVE — name the finding
8. Complications and the leading cause of death (hyperkalaemia and infection)
9. Special populations and the triple whammy
10. Three exam traps (dipstick-blood-no-RBCs; FENa-after-diuretics; missing RPGN)[6]

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 Acute Kidney Injury.[6]

References

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3. [3]Bagshaw SM, Wald R, Adhikari NKJ, et al. Timing of Initiation of Renal-Replacement Therapy in Acute Kidney Injury N Engl J Med, 2020.PMID 32668114
4. [4]Weisbord SD, Gallagher M, Jneid H, et al. Outcomes after Angiography with Sodium Bicarbonate and Acetylcysteine N Engl J Med, 2018.PMID 29130810
5. [5]James MT, Bhatt M, Pannu N, Tonelli M. Long-term outcomes of acute kidney injury and strategies for improved care Nat Rev Nephrol, 2020.PMID 32051567
6. [6]Kellum JA, Lameire N; KDIGO AKI Guideline Work Group. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Crit Care, 2013.PMID 23394211
7. [7]Lameire N, Kellum JA; KDIGO AKI Guideline Work Group. Contrast-induced acute kidney injury and renal support for acute kidney injury: a KDIGO summary (Part 2). Crit Care, 2013.PMID 23394215
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10. [10]Veenstra J, Smit WM, Krediet RT, Arisz L. Relationship between elevated creatine phosphokinase and the clinical spectrum of rhabdomyolysis. Nephrol Dial Transplant, 1994.PMID 7970089
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14. [14]Praga M, Gonzalez E, et al. Changes in the aetiology, clinical presentation and management of acute interstitial nephritis, an increasingly common cause of acute kidney injury. Nephrol Dial Transplant, 2015.PMID 25324356
15. [15]Jayne DR, Gaskin G, Rasmussen N, et al. Randomized trial of plasma exchange or high-dosage methylprednisolone as adjunctive therapy for severe renal vasculitis. J Am Soc Nephrol, 2007.PMID 17582159
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18. [18]Moussavi K, Fitter S, Gabrielson SW. Management of Hyperkalemia With Insulin and Glucose: Pearls for the Emergency Clinician. J Emerg Med, 2019.PMID 31084947
19. [19]Jothimani D, et al. Advances in the management of Hepatorenal syndrome. Curr Opin Nephrol Hypertens, 2026.PMID 42471785
20. [20]Singer P, Reintam Blaser A, Berger MM, et al. ESPEN guideline on clinical nutrition in the intensive care unit. Clin Nutr, 2019.PMID 30348463
21. [21]NICE - National Institute for Health and Care Excellence Acute kidney injury: prevention, detection and management (NG148, published 2019, last updated March 2021) NICE guideline, 2019.Source