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.
- Urinalysis may be bland; renal tubular epithelial cells and coarse granular ‘muddy brown’ casts support tubular injury when skilled microscopy is available, but their absence does not exclude it.
- Aminoglycosides, glycopeptides, amphotericin, cisplatin, antivirals and other agents differ in mechanism and monitoring. Check the exact medicine, route, cumulative exposure, interactions and measured concentrations instead of using a generic nephrotoxin label.
- Supportive care means treating sepsis and shock, stopping avoidable insults, adjusting all renally cleared drugs, controlling fluid and electrolytes, ensuring nutrition and initiating replacement therapy for complications—not forcing urine production.
- Loop diuretics can relieve fluid overload in a responsive patient but do not reverse tubular injury or improve survival simply by converting oliguria to measured urine.
- During recovery, filtration and tubular concentration may recover at different rates. A polyuric phase can produce dehydration, hypokalaemia and hypomagnesaemia even while creatinine is falling.
Key red flags
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.
Kidney dysfunction develops during systemic infection through haemodynamic, inflammatory and microvascular mechanisms. Urine output may fall before creatinine rises, and fluid overload can develop despite ongoing circulatory instability.
Investigation priorities
Relate onset and severity to the suspected ischaemic, septic or toxic exposure.
Management branches
ATI is suspected after hypotension, infection, surgery or a potentially nephrotoxic medicine.
- 1. Build an exposure timeline using observations, operations, cultures, drug administration, levels, contrast and CK rather than relying on the admission diagnosis.
- 2. Treat shock, infection, pigment release or another primary cause and remove non-essential nephrotoxins immediately; seek an effective substitute when therapy remains essential.
- 3. Ask pharmacy, microbiology, oncology or toxicology to adjust dose, interval and monitoring for the exact agent and rapidly changing clearance.
- 4. Record the suspected causal association and prevention plan, but avoid an inaccurate permanent allergy label for a dose-related toxic effect.
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.Avoid prescribing solely to convert oliguria into urine. Monitor pressure, sodium, potassium, magnesium, hearing risk at high exposure and cumulative balance; escalating ineffective doses must not delay renal replacement assessment.
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.Do not invent a dose from eGFR during unstable AKI. Involve microbiology and pharmacy, verify actual sampling time, avoid concurrent nephrotoxins where possible and change therapy if toxicity outweighs microbiological benefit.