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Level 2 of 6Must-remember

Acute kidney injury

Assess, manage and stay safe — enough on its own

The card — assess, manage, caution

Assessment— look, ask, measure

  • Make the diagnosis on any one of three KDIGO criteria: a rise in serum creatinine of ≥ 26.5 µmol/L (0.3 mg/dL) within 48 hours; or a rise to ≥ 1.5 times a known or presumed baseline within 7 days; or a urine output < 0.5 mL/kg per hour for more than 6 hours — only one is required, and the urine chart declares it hours before any creatinine result.
  • AKI is a finding, not a diagnosis: it obliges you to make one, so ask in order — is the patient blocked, dry, or is the kidney itself injured?
  • Do not use eGFR to judge severity: estimating equations assume a steady state, so while creatinine is rising eGFR overestimates true function and gives false reassurance; use the measured creatinine, its rate of change, and the urine output. Creatinine itself lags 48–72 hours behind the injury.Not available at your setup — Renal function (creatinine/urea).
  • Most patients have no renal symptoms at all — they present with the illness damaging the kidney (sepsis, vomiting and diarrhoea, haemorrhage, heart failure, envenomation, crush injury, poisoning, an obstructed prostate) and the kidney is found on the blood results or the fluid chart.
  • Volume assessment is the central examination and must precede any prescription: look for tachycardia, a postural fall exceeding 20/10 mmHg, dry mucosae and reduced skin turgor, a jugular venous pressure invisible even lying flat, cool peripheries with delayed capillary refill, and weight loss; against these look for expansion — raised JVP, bibasal crackles, sacral and ankle oedema, weight gain.
  • Distinguish the three haemodynamic patterns: hypovolaemia gives a postural drop then hypotension with cool peripheries and a low JVP; low cardiac output gives hypotension with cool peripheries and a raised JVP; vasodilatation (sepsis, cirrhosis) gives hypotension with warm peripheries and a low JVP. Warm peripheries with hypotension is sepsis, not good perfusion.
  • Read the urine output pattern: oliguria (under 400 mL/24 h; in a child under 1 mL/kg per hour, and 1–2 mL/kg per hour in a neonate) denotes more severe injury; complete anuria early has a short differential — complete obstruction, renal artery occlusion, overwhelming septic shock, severe ischaemia with cortical necrosis, and severe proliferative glomerulonephritis or vasculitis; and a preserved or high urine output excludes neither AKI nor obstruction.
  • Do a urine dipstick and microscopy — the cheapest and most under-used investigations: dysmorphic red cells and red cell casts with proteinuria mean glomerulonephritis or vasculitis; white cells and white cell casts mean interstitial nephritis; muddy-brown granular casts mean acute tubular necrosis; dipstick strongly positive for blood with few or no red cells means myoglobin or haemoglobin — send a creatine kinase at once.
  • Centrifuge red or brown urine: if the colour persists in the supernatant the pigment is myoglobin or haemoglobin, not red cells.
  • Get a 12-lead ECG and read it yourself: the hyperkalaemic sequence is tall peaked narrow-based T waves, loss of the P wave, PR prolongation, QRS widening, sine wave, then ventricular fibrillation or asystole — a broad QRS in AKI is a pre-arrest rhythm.
  • Act within minutes to hours on: hyperkalaemia with ECG change (particularly QRS broadening); pulmonary oedema, especially if unresponsive to a diuretic; Kussmaul respiration or pH below 7.1 (H⁺ above 79 nmol/L); anuria or oliguria unresponsive to a fluid challenge; uraemic pericarditis, encephalopathy or bleeding; haemoptysis with AKI (a pulmonary-renal syndrome until proved otherwise); purpura, livedo reticularis, new rash, arthralgia, sinusitis or epistaxis (vasculitis); creatinine rising faster than about 130 µmol/L per day (rhabdomyolysis or a mislabelled sample); a tense abdomen (abdominal compartment syndrome) or tense, woody-hard muscle compartments (compartment syndrome requiring fasciotomy).
  • Stage it by whichever criterion gives the higher stage — stage 1 is creatinine 1.5–1.9 × baseline or a rise ≥ 26.5 µmol/L, or urine output < 0.5 mL/kg per h for 6–12 h; stage 2 is 2.0–2.9 × baseline, or < 0.5 mL/kg per h for ≥ 12 h; stage 3 is ≥ 3.0 × baseline, or creatinine ≥ 353.6 µmol/L (4.0 mg/dL), or starting renal replacement therapy, or under 18 years an eGFR < 35 mL/min/1.73 m², or urine output < 0.3 mL/kg per h for ≥ 24 h or anuria ≥ 12 h.Not available at your setup — Renal function (creatinine/urea).
  • Seek the two examination findings that are easily missed: a pericardial friction rub at the left sternal edge with the patient leaning forward (uraemic pericarditis, which may bleed and tamponade), and prolonged bleeding from puncture sites, gums or gut (uraemic platelet dysfunction).
  • Take the drug history line by line — NSAIDs including over-the-counter and injected preparations, ACE inhibitors and ARBs, aminoglycosides, contrast in the last 1–2 days, diuretics, trimethoprim, proton pump inhibitors — and remember an NSAID combined with an ACE inhibitor or ARB is a particularly high-risk pairing and a frequent, preventable cause.
  • Ask the usual blood pressure: normotensive ischaemic AKI occurs in the dehydrated, in those on diuretics, NSAIDs or renin-angiotensin blockers, and above all in the chronic hypertensive, for whom 120/70 mmHg may be profound relative hypotension. In children hypotension is a late sign of shock, preceded by tachycardia and prolonged capillary refill.
  • Remember what low muscle mass hides: a frail elderly woman with a creatinine of 130 µmol/L may have lost most of her kidney function, and in pregnancy creatinine falls physiologically so a normal value may represent substantial injury.

Management— do this, in order

  • Catheterise early in unexplained AKI — it is both diagnostic and therapeutic: it excludes and relieves bladder outlet obstruction, yields a residual volume (a large residual is diagnostic), gives an hourly output to trend, and supplies urine for dipstick, microscopy and culture.Doctor / Nurse
  • If hypovolaemic, give a fluid challenge of 250–500 mL of balanced crystalloid intravenously over 15 minutes, then reassess pulse, blood pressure, jugular venous pressure, lung bases and urine output; a 250 mL challenge usually establishes whether hypotension is fluid-responsive. In children give 10–20 mL/kg over 15–30 minutes (10 mL/kg where cardiac dysfunction or malnutrition is suspected).Doctor / Nurse
  • Choose the fluid deliberately: use balanced crystalloid (Ringer's lactate/Hartmann's or Plasma-Lyte) in preference to 0.9% sodium chloride when large volumes are anticipated, because large-volume saline causes hyperchloraemic acidosis — but balanced solutions contain about 5 mmol/L of potassium, so where hyperkalaemia is established or suspected, 0.9% sodium chloride is preferred. If the patient is bleeding, give blood.
  • If pulse and pressure have not improved after 2 litres, stop and reassess: look for occult blood loss — gastrointestinal, retroperitoneal, into the pregnant uterus, or into tissues after crush injury or burns — and consider vasodilated sepsis needing a vasopressor rather than a third litre.
  • If euvolaemic, prescribe the previous day's urine output plus gastrointestinal and drain losses plus about 500 mL for insensible loss. Excessive fluid in AKI causes pulmonary oedema.
  • If overloaded, sit the patient upright, give oxygen, and give furosemide 40–80 mg intravenously, no faster than 4 mg per minute — rapid injection causes deafness; the paediatric dose is 0.5–1 mg/kg intravenously (maximum 2 mg/kg per dose). High doses are often required in AKI and are often ineffective.Doctor / Nurse
  • Treat hyperkalaemia on the ECG, not the number — the trigger is potassium above 6.5 mmol/L, or above 6.0 mmol/L with ECG changes, or any hyperkalaemia with a broad QRS or arrhythmia — and give the first three agents together, not sequentially.Not available at your setup — Serum electrolytes.
  • Calcium gluconate 10%, 10 mL IV over 2–5 minutes, repeated at 5 minutes if the ECG is unchanged, up to 3 doses (children 0.5 mL/kg IV over 5–10 minutes, maximum 20 mL); onset 1–3 minutes, duration 30–60 minutes. It stabilises the myocardium and does not lower potassium at all. Calcium chloride 10% 10 mL is an alternative but far more damaging on extravasation.Doctor / Nurse
  • Soluble insulin with dextrose: 10 units in 50 mL of 50% dextrose IV over 15–30 minutes, or 10 units in 250 mL of 10% dextrose over 30 minutes (children 0.1 unit/kg with 5 mL/kg of 10% dextrose IV over 30 minutes); onset 15–30 minutes, duration 4–6 hours. Check glucose before, at 30 minutes, then hourly for 6 hours.Doctor / Nurse
  • Nebulised salbutamol 10–20 mg over 10 minutes (children 2.5 mg under 5 years; 5 mg at 5 years or older); onset 15–30 minutes, duration 2–4 hours; additive to insulin-dextrose, used cautiously in ischaemic heart disease.
  • Sodium bicarbonate 8.4%, 50 mL (50 mmol) IV over 15–30 minutes into a large vein, or 1.26% 500 mL (children 1 mmol/kg, diluted to 4.2% in infants); onset about 30 minutes — only if acidotic and NOT volume-overloaded.Doctor / Nurse
  • Add a potassium binder, the only measure short of dialysis that removes potassium from the body: calcium or sodium polystyrene sulfonate 15 g orally 3–4 times daily or 30 g rectally, or sodium zirconium cyclosilicate 10 g orally three times daily for 48 h then 5–10 g daily (children 0.5–1 g/kg per day orally or rectally in divided doses).
  • Stop everything that adds potassium — potassium-containing fluids and supplements, potassium-sparing diuretics, ACE inhibitors, ARBs, trimethoprim, NSAIDs, and where an alternative exists stored blood — and recheck potassium and the ECG at 1 hour and at least 2-hourly thereafter, because rebound is the rule.Not available at your setup — Serum electrolytes.
  • Stop or withhold the nephrotoxins — this is a treatment, not an administrative task: NSAIDs including over-the-counter and injected preparations, ACE inhibitors and ARBs, aminoglycosides, amphotericin B, vancomycin, tenofovir, high-dose bolus aciclovir, cisplatin, calcineurin inhibitors, iodinated contrast, diuretics if hypovolaemic, metformin and SGLT-2 inhibitors during acute illness, potassium-sparing diuretics, potassium supplements and trimethoprim. Record that stopping is temporary.
  • Re-dose every remaining drug for the kidney the patient has now, taking particular care with anticoagulants (oral agents and heparins accumulate and bleed), opioids, gabapentinoids, digoxin, methotrexate, sulphonylureas and renally cleared antimicrobials — and do not dose from an eGFR printout while creatinine is moving.
  • Relieve obstruction above the bladder with ureteric stenting or percutaneous nephrostomy as soon as possible — recovery is good when obstruction is relieved within hours to days — then anticipate post-obstructive diuresis, replacing measured losses and monitoring sodium and potassium.Doctor / Nurse
  • In rhabdomyolysis give early, vigorous fluid resuscitation — it is the treatment and it is time-critical: 0.9% sodium chloride in large volume, typically exceeding 4 L in 24 hours in an adult, titrated to a urine output of 1–2 mL/kg per hour, reassessing for overload, while examining limbs repeatedly for tense compartments and expecting severe, rapidly recurring hyperkalaemia.
  • Ask AEIOU at every reassessment and arrange renal replacement therapy when an indication appears: Acidosis refractory to medical therapy (pH < 7.1, H⁺ > 79 nmol/L); Electrolytes (hyperkalaemia generally > 6.5 mmol/L with ECG changes, uncontrolled by conservative measures); Intoxication with a dialysable poison; Overload (pulmonary oedema unresponsive to diuresis); Uraemia (pericarditis with or without tamponade, encephalopathy, seizures, uraemic bleeding diathesis).Not available at your setup — Dialysis / renal replacement.

Caution— what harms

  • Never judge severity by eGFR while creatinine is moving — it overestimates true function and offers false reassurance at the moment real GFR may be near zero.
  • Diuretics treat fluid overload; they do not treat kidney injury. There is no evidence that they prevent AKI, alter its course or improve survival, and converting oliguric to non-oliguric AKI has never been shown to reduce mortality. Renal replacement therapy must never be delayed because a diuretic is being tried.
  • Do not give mannitol or renal-dose dopamine — neither is supported by controlled trials, and low-dose dopamine is specifically ineffective at preventing or reversing renal impairment in sepsis. Fenoldopam and N-acetylcysteine have also failed.
  • Hydroxyethyl starch and other synthetic colloids are contraindicated — they worsen AKI.
  • Calcium gluconate does not lower potassium at all — it buys 30–60 minutes of myocardial stability, so never treat it as definitive; and every measure except a binder or dialysis merely redistributes potassium.
  • Late hypoglycaemia after insulin-dextrose is a recognised cause of death from this treatment: check glucose before, at 30 minutes, then hourly for 6 hours.
  • Do not give sodium bicarbonate to a volume-overloaded patient — the sodium load precipitates pulmonary oedema — and it may precipitate tetany if the patient is hypocalcaemic.
  • Do not give calcium for the hypocalcaemia of rhabdomyolysis unless the patient is symptomatic, since calcium translocates out of tissues during recovery and may precipitate with the high phosphate.
  • Do not request urine eosinophils — they are neither sensitive nor specific for interstitial nephritis; and the classic triad of fever, rash and arthralgia is present in only 10–15%.
  • Absence of muddy-brown granular casts proves nothing — they are absent in more than 20% of cases of acute tubular necrosis.
  • Pre-renal indices are worthless in four situations: within 12–24 hours of a diuretic; in established CKD; in non-oliguric patients (the equation was validated only in oliguric patients); and in obstruction of a few days' duration, where the numbers mimic pre-renal AKI exactly.
  • Do not be reassured by a normal or high urine output — it excludes neither AKI nor obstruction; and in established AKI in critical illness the later appearance of oliguria implies near-complete loss of function, so further fluid will be ineffective and harmful.
  • Do not starve a septic patient to protect a number, and do not treat dilutional hyponatraemia with sodium — an oliguric patient who drinks freely or receives 5% dextrose needs fluid restriction, not sodium. Prophylactic antibiotics and barrier nursing are not recommended.
  • Where the acute-chronic distinction cannot be made, treat as AKI — the harm of treating reversible disease is small; the harm of ignoring it is not. And in the polyuric recovery phase, do not let a recovering patient quietly become hypovolaemic and sustain a second injury.

Refer / escalate

Escalate immediately for any AEIOU indication — pH below 7.1, hyperkalaemia above 6.5 mmol/L or with a broad QRS uncontrolled by conservative measures, a dialysable poison, pulmonary oedema unresponsive to diuresis, or uraemic pericarditis, encephalopathy, seizures or bleeding — and refer urgently for suspected glomerulonephritis or vasculitis (red cell casts, haemoptysis, purpura), HUS/TTP, obstruction needing stenting or nephrostomy, compartment syndrome needing fasciotomy, or anuria, since anuria modifies every indication.

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