Acute Kidney Injury (AKI) & Nephrotoxic Drug Stewardship
Recognising triggers, interpreting trends, and safeguarding patients — an evidence-based guide for UK student nurses.
Acute Kidney Injury (AKI) is one of the most common, insidious, and life-threatening complications across acute hospital trusts. It develops silently — often in patients admitted for unrelated conditions — characterised by a sudden, rapid decline in renal filtration function over hours to days. Left unchecked, it leads to fluid overload, electrolyte imbalance, metabolic acidosis, and multi-organ failure.
As a student or newly qualified nurse, mastering AKI recognition and nephrotoxic drug stewardship is central to safe practice. AKI is frequently identified only after substantial damage has occurred — because early warning signs were missed. This guide breaks down what you need to know, aligned with national standards.
1. National Guidance
All content aligned with: NICE Guideline NG148 — Acute Kidney Injury: Prevention, Detection and Management (updated October 2024). This replaces the older CG169.
📎 Source: NICE NG148 — Full Guideline
⚠️ Local AKI detection systems may vary. Some trusts use automated electronic alerts; others rely on manual review. Always follow your trust’s specific pathway.
2. The Three Categories of AKI
Understanding where the block lies changes how you respond:
| Type | What’s Happening | Common Ward Causes |
|---|---|---|
| Pre‑Renal | Reduced blood flow to kidneys — no permanent damage yet if corrected quickly. | Dehydration, sepsis, hypotension, blood loss, excessive vomiting/diarrhoea, over-diuresis. |
| Intrinsic | Actual tissue damage to tubules, glomeruli, or cells. | Prolonged pre‑renal insult, nephrotoxic drugs, IV contrast, rhabdomyolysis, infection. |
| Post‑Renal | Obstruction blocks urine outflow — back‑pressure damages function. | Blocked catheter, enlarged prostate, stones, pelvic masses, urinary retention. |
📎 Source: NICE NG148 — Identifying Causes & Risk Factors
⚠️ Local investigation protocols differ. Your trust’s AKI care bundle may specify which blood tests, imaging, or referrals are required — always check the ward pathway.
3. Staging AKI — What the Numbers Mean
Staging uses KDIGO criteria adopted by NICE — based on creatinine rise from baseline and urine output:
| Stage | Serum Creatinine | Urine Output |
|---|---|---|
| Stage 1 | 1.5–1.9 × baseline OR rise ≥ 26.5 µmol/L within 48 hours | < 0.5 mL/kg/h for 6–12 consecutive hours |
| Stage 2 | 2.0–2.9 × baseline | < 0.5 mL/kg/h for ≥ 12 hours |
| Stage 3 | ≥ 3.0 × baseline OR ≥ 353.6 µmol/L OR renal replacement therapy initiated | < 0.3 mL/kg/h for ≥ 24 hours OR anuria for ≥ 12 hours |
📎 Source: NICE NG148 — Staging & Definition
Important: Creatinine is a Lagging Indicator
Creatinine often does not rise until 50% or more of kidney function is already lost — by the time you see the spike, injury has been developing for 24–48 hours. Trend beats single reading — compare to the patient’s known baseline, not just a generic reference range.
⚠️ Baseline values may be recorded differently locally. Some trusts use the most recent pre‑admission result; others use admission day values. Confirm your trust’s definition of ‘baseline creatinine’.
4. Spotting It Before the Bloods Change
Don’t wait for the lab report. Watch the patient and the fluid balance chart — these signs often appear before creatinine rises:
- Falling urine output: < 0.5 mL/kg/h sustained. For a 70 kg patient, that’s roughly 35 mL/hour. Two consecutive hours of dropping output — speak up.
- Haemodynamic changes: Rising pulse, falling BP, fever, tachypnoea — the body diverts blood away from kidneys to protect vital organs.
- Confusion or drowsiness: Especially in older adults — accumulating waste products impair cognition early.
- Fluid loss history: Vomiting, diarrhoea, high stoma output, recent surgery, diuretic use, poor oral intake.
- Weight change: Sudden loss = dehydration; sudden gain = retention/overload — daily weighing is your most reliable guide.
📎 Source: NICE NG148 — Early Detection & Monitoring
⚠️ Observation frequency policies vary. Follow your trust’s NEWS2 escalation and monitoring protocol — increased frequency may be required for at‑risk patients.
5. Nephrotoxic Drug Stewardship — What You Can Question
This is where you directly protect renal function. When AKI is suspected — or creatinine is rising — review these agents before administration:
- A — ACE Inhibitors & ARBs (Ramipril, Lisinopril, Losartan): Dilate efferent arterioles. If patient is dehydrated or hypotensive, filtration pressure drops sharply — hold and seek review.
- I — NSAIDs (Ibuprofen, Naproxen, Diclofenac): Reduce renal perfusion via prostaglandin inhibition. Stop immediately in suspected AKI — no exceptions.
- N — Nephrotoxic Antibiotics (Gentamicin, Vancomycin, Amikacin): Require therapeutic drug monitoring and extended intervals in AKI — check latest levels before dosing.
- E — Extras & Contrast Media: IV contrast can induce AKI — ensure adequate hydration before and after. Check eGFR pre‑procedure.
- S — Diuretics (Furosemide): Can worsen pre‑renal dehydration — hold if patient is dry, hypotensive, or output is falling.
Do not just give it because it’s written. Document your rationale for holding and escalate to the prescriber — this is safe, accountable practice.
📎 Sources: NICE NG148 — Prevention & Drug Safety | Contrast‑Associated AKI
⚠️ Local drug formularies and withholding protocols differ. Always check your trust’s approved guidance and BNF before withholding or administering medication — and document clearly.
6. Fluid Balance — Restoration vs. Overload
Fluid management in AKI is a delicate balance — too little maintains injury; too much causes harm:
- Pre‑renal AKI: Patient is dry/hypoperfused — carefully titrated IV crystalloids restore perfusion. Reassess output and BP after each bolus.
- Established AKI with low output: Stop — further fluid risks pulmonary oedema. Restrict intake. Seek renal/HDU review.
- Measure precisely: Urine output to the nearest mL. Daily weights at the same time, same scales, same clothes.
- Check the catheter: Kinked tubing or blockage can mimic AKI — check before escalating.
- Watch for overload: Raised JVP, basal crackles, pitting oedema, breathlessness — stop fluids and inform medics immediately.
📎 Source: NICE NG148 — Fluid Management & Monitoring
⚠️ Fluid resuscitation protocols vary. Follow your ward’s AKI care bundle or medical team’s prescribed plan.
7. Red Flags — When to Escalate Urgently
Hyperkalaemia is the most immediately life‑threatening complication. These are your act‑now triggers:
| Clinical Trigger | Risk | Immediate Nursing Action |
|---|---|---|
| Potassium 5.5–6.4 mmol/L Severe: ≥ 6.5 mmol/L |
Cardiac arrhythmia → arrest — can happen without warning | Obtain/perform 12‑lead ECG — watch for tall tented T‑waves, widened QRS. Escalate immediately. Prepare treatment as directed. |
| Fluid overload compromising respiration | Pulmonary oedema → respiratory failure | Sit upright, give oxygen if prescribed. Escalate — may need restriction, diuretics, or HDU review. |
| Oliguria unresponsive to fluids | Intrinsic damage established — recovery uncertain | Escalate to medical team. Review fluid plan. |
| Stage 3 AKI or rapid deterioration | May require renal replacement therapy | Urgent referral to renal team. Monitor NEWS2. Do not delay. |
📎 Source: NICE NG148 — Hyperkalaemia & Urgent Referral
⚠️ Emergency hyperkalaemia protocols vary by trust. Know where your ward’s kit is kept and which team to bleep.