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Acute tubular injury and nephrotoxic AKI

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Escalate

Suspected acute tubular injury with severe hyperkalaemia, refractory acidosis, pulmonary oedema, shock, anuria, toxin accumulation or rapidly worsening multi-organ failure needs immediate stabilisation and urgent nephrology or critical-care review; remove the precipitant while emergency complications are treated.

Synopsis

Identify ischaemic, septic and toxic tubular injury, stop avoidable exposure, provide organ support and anticipate delayed or polyuric recovery without promising a drug reversal.

  • Acute tubular injury is the structural syndrome often called acute tubular necrosis; common triggers are prolonged hypoperfusion, sepsis, major surgery, pigment, and dose- or exposure-related nephrotoxins.
  • The transition from reversible haemodynamic fall in filtration to tubular injury is a continuum, so a patient can have both reduced perfusion and established parenchymal damage.
  • A creatinine rise typically lags behind the insult. Determine when hypotension, antimicrobial dosing, surgery, contrast, chemotherapy or another exposure occurred rather than dating injury from the blood result.

Key red flags

Ischaemic tubular injury

AKI follows sustained shock, haemorrhage, cardiac arrest, major surgery or prolonged severe depletion and does not promptly resolve after circulation is restored. Multi-organ hypoperfusion and an oliguric trajectory increase suspicion.

Investigation priorities

01
Dated creatinine, electrolyte and urine-output trajectoryFirst step

Relate onset and severity to the suspected ischaemic, septic or toxic exposure.

Management branches

Exposure controlStop preventable ongoing tubular insult

ATI is suspected after hypotension, infection, surgery or a potentially nephrotoxic medicine.

  1. 1. Build an exposure timeline using observations, operations, cultures, drug administration, levels, contrast and CK rather than relying on the admission diagnosis.
  2. 2. Treat shock, infection, pigment release or another primary cause and remove non-essential nephrotoxins immediately; seek an effective substitute when therapy remains essential.

Key medicines

Loop diuretic for fluid overloadUse an intravenous or oral dose selected from prior diuretic exposure, renal function and the local acute heart-failure or renal protocol, then assess urine and sodium response promptly.
Aminoglycoside under level-guided prescribingWhen clinically indispensable, use the locally approved weight- and indication-based regimen with exact timed concentrations and extend or withhold subsequent dosing as renal clearance changes.
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Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

Authoring stateRapid draftClinical stateAwaiting reviewJurisdictionUnited Kingdom