AKI is identified by a creatinine increase of 26 micromol/L or more within 48 hours, a 50% or greater increase within 7 days, or urine output below 0.5 mL/kg/hour for more than 6 hours in adults.
Search for pre-renal hypoperfusion, intrinsic renal injury and post-renal obstruction while reviewing sepsis, medications, volume status, urinalysis and relevant imaging.
Assess potassium, acid-base status, fluid overload and uraemic complications urgently; life-threatening abnormalities require escalation and possibly renal replacement therapy.
Review potentially nephrotoxic medicines and adjust prescribing to clinical condition; do not assume a single eGFR is reliable during a changing creatinine concentration.

Reference: NICE NG148 (checked 2026-10-30). This is a targeted evidence-linked teaching update; the historic article below still requires full clinical reconciliation. Follow local protocols and the current BNF for prescribing.

🔎 Always investigate for acute kidney injury (AKI) by checking serum creatinine (and comparing with baseline), urine dip for nephritis, and assessing fluid status. Most cases are supportive, but some need urgent intervention (e.g., catheter, stent, dialysis).

🚑 General Management Summary (Hyperkalaemia First!)

Emergency Management of AKI
ABC, O₂ if hypoxic, IV access, ECG monitoring. 📉 Treat hyperkalaemia ≥ 6.0 mmol/L immediately. 🌡️ Treat systemic infection or urosepsis with IV antibiotics. Send bloods: FBC, U&E, Ca/P/ALP, CRP, Lactate. Do ECG, CXR, VBG/ABG. Prerenal: Fluids, sepsis treatment, stop BP-lowering drugs (ACEI, ARB, CCB). Consider inotropes if shocked. Renal: Stop nephrotoxins (ACEI/ARB/NSAID/Gent). Order ANCA/ANA/anti-GBM if nephritis suspected. Renal referral. Postrenal: Catheterize. If oliguria/anuria, urgent renal USS (<12h). Consider dialysis if: – Refractory hyperkalaemia – Pulmonary oedema – Severe uraemia (encephalopathy, pericarditis) – Severe acidosis unresponsive to fluids/bicarb.

Emergency Management of AKI

ABC, O₂ if hypoxic, IV access, ECG monitoring.
📉 Treat hyperkalaemia ≥ 6.0 mmol/L immediately.
🌡️ Treat systemic infection or urosepsis with IV antibiotics.
Send bloods: FBC, U&E, Ca/P/ALP, CRP, Lactate. Do ECG, CXR, VBG/ABG.
Prerenal: Fluids, sepsis treatment, stop BP-lowering drugs (ACEI, ARB, CCB). Consider inotropes if shocked.
Renal: Stop nephrotoxins (ACEI/ARB/NSAID/Gent). Order ANCA/ANA/anti-GBM if nephritis suspected. Renal referral.
Postrenal: Catheterize. If oliguria/anuria, urgent renal USS (<12h).
Consider dialysis if: – Refractory hyperkalaemia – Pulmonary oedema – Severe uraemia (encephalopathy, pericarditis) – Severe acidosis unresponsive to fluids/bicarb.

📖 About AKI

AKI has replaced the older term “acute renal failure.”
Defined as a sudden fall in renal function → ↑ urea/creatinine, ↓ urine output.
Often reversible if identified and treated early.
eGFR is unreliable in acute illness - use creatinine and urine output instead.

📊 KDIGO Definition & Staging

Stage	Criteria
1	Creatinine 1.5–1.9× baseline OR ↑ ≥26 µmol/L in 48h OR urine <0.5 ml/kg/hr for 6–12h
2	Creatinine 2–2.9× baseline OR urine <0.5 ml/kg/hr ≥12h
3	Creatinine 3× baseline OR RRT started OR anuria ≥12h

⚡ Renal Functions Affected

Water/electrolyte control
Excretion of toxins & drugs
Acid–base regulation
BP control (RAAS)
EPO & Vitamin D activation

🧾 Causes of AKI

Site	Examples	Actions
Prerenal	Hypovolaemia (bleeding, burns, sepsis), hypotension, ACEI/ARB/NSAIDs, PPIs	Fluids, sepsis control, stop offending drugs, vasopressors if needed
Renal (Intrinsic)	ATN (45%), RPGN, GN, vasculitis, interstitial nephritis, HUS/TTP	Nephrology input, send ANCA/ANA/anti-GBM, stop nephrotoxins, consider biopsy
Postrenal	Stones, strictures, malignancy, prostate obstruction	Catheterize, USS (<12h), consider stent/nephrostomy, urology input

🔬 Prerenal vs Intrinsic Renal (Urine Features)

Urine SG: Prerenal > 1.020 vs. Renal < 1.010
Urine Osmolality: Prerenal > 500 vs. Renal < 350 mOsm/kg
Urinary Na⁺: Prerenal < 20 vs. Renal > 40 mmol/L

🧍 Clinical Presentation

Malaise, lethargy, anorexia, nausea, vomiting
Oliguria/anuria OR polyuria (if concentrating defect)
Confusion, delirium, seizures, coma in severe cases
Fluid overload → pulmonary oedema, raised JVP
Skin pallor, pruritus; bruising (platelet dysfunction)
Uraemic pericarditis → friction rub, tamponade

🧪 Investigations

Bloods: U&E (↑ urea/creatinine, ↑ K⁺), Ca/P/ALP, CRP, FBC, film
Urine: Dipstick (protein/haematuria), microscopy (casts)
Serology: ANCA, ANA, Anti-GBM, complements
Imaging: Renal USS (exclude obstruction), CXR (pulm oedema), ECG (K⁺)
Special: Myeloma screen (high calcium/ESR), HIV, biopsy if unclear

🧪 Selected Targeted Tests

Nephritis: ANCA, ANA
Acidosis: ABG (HCO₃⁻ <19 mmol/L)
Rhabdomyolysis: CK
SBP <110 + sepsis: Lactate
ENT bleed + renal: Anti-GBM
High Ca²⁺ + ESR: Myeloma screen

💊 Management (With Renal/Urology Input)

NEWS monitoring, fluid balance chart, daily U&E
Prerenal: Hydrate (0.9% saline 1L over 2–4h, reassess). Pressors if shocked
Renal: Stop nephrotoxins, treat vasculitis if confirmed, immunosuppression if needed
Postrenal: Relieve obstruction (catheter/stent/nephrostomy)
Acidosis: Consider IV bicarbonate (1.26%)
Hyperkalaemia: Calcium gluconate + insulin/dextrose + salbutamol neb
Dialysis indications (AEIOU): – Acidosis (pH < 7.2) – Electrolytes (K⁺ refractory) – Ingestions (toxin) – Overload (pulm oedema) – Uraemia (encephalopathy, pericarditis)

🧾 Haemofiltration

Preferred in unstable patients in ITU.
Early discussion with renal + intensive care is essential.

📚 References

NICE NG148: Acute Kidney Injury (2019)

Cases - Acute Kidney Injury (AKI)

Case 1 - Pre-Renal (Hypovolaemia) 🩸: A 72-year-old man admitted with profuse diarrhoea and vomiting presents with hypotension and oliguria. Urea:creatinine ratio raised. Diagnosis: AKI due to volume depletion. Management: IV fluids, electrolyte correction, stop nephrotoxic drugs (e.g., NSAIDs, ACEi).
Case 2 - Pre-Renal (Heart Failure) ❤️: A 68-year-old woman with decompensated LV systolic failure presents with worsening breathlessness and reduced urine output. JVP elevated, bilateral crackles. Diagnosis: Pre-renal AKI due to low cardiac output. Management: Diuretics for pulmonary oedema, optimise heart failure therapy, careful fluid balance.
Case 3 - Intrinsic Renal (ATN from Contrast Nephropathy) ⚡: A 65-year-old man undergoes PCI with IV contrast. Two days later, he develops oliguria and rising creatinine. Urine microscopy: muddy brown casts. Diagnosis: AKI due to acute tubular necrosis from contrast. Management: Stop nephrotoxins, IV hydration, consider renal replacement therapy if severe.
Case 4 - Intrinsic Renal (Acute Interstitial Nephritis) 💊: A 54-year-old woman treated with antibiotics for UTI presents with rash, fever, and AKI. Urine: eosinophils present. Diagnosis: Drug-induced acute interstitial nephritis. Management: Stop offending drug; supportive care ± corticosteroids if severe.
Case 5 - Post-Renal (Obstructive) 🚧: An 80-year-old man with known BPH presents with anuria, lower abdominal pain, and bilateral hydronephrosis on ultrasound. Diagnosis: Post-renal AKI due to bladder outlet obstruction. Management: Immediate bladder catheterisation; urology referral; long-term BPH management.

Teaching Commentary 🧠

AKI is classified into: - Pre-renal (hypoperfusion: dehydration, heart failure, sepsis), - Intrinsic (tubular, glomerular, interstitial, vascular), - Post-renal (obstruction). Always look for reversible causes: hypovolaemia, sepsis, drugs, obstruction. Initial management is ABCDE, stop nephrotoxins, check fluid status, catheterise, and correct potassium. Early nephrology input if severe or prolonged.

Additional related clinical topics

Renal syndromes

💧 Renal syndromes are a group of disorders that impair the kidneys’ ability to regulate fluid balance, electrolyte homeostasis, and waste excretion. They may arise from vascular, inflammatory, autoimmune, metabolic, or genetic causes. Early recognition and appropriate management can prevent irreversible renal damage and improve outcomes. 🩺🧠

🧠 Summary Table of Major Renal Syndromes

🩸 Syndrome	⚙️ Definition & Mechanism	🧪 Key Diagnostic Features	💊 Management
🚨 Acute Kidney Injury (AKI)	Sudden decline in kidney function → accumulation of urea, creatinine, and fluid. 🧩 Classified as: • Pre-renal: ↓ renal perfusion (shock, dehydration) • Intrinsic: tubular/glomerular injury (toxins, ischaemia) • Post-renal: obstruction (stones, prostate, tumour)	• ↑ Serum creatinine, ↓ urine output • Urea:Creatinine ratio helps differentiate pre-renal vs intrinsic • Ultrasound: obstruction or structural cause	• Restore perfusion (fluids, treat shock) • Remove toxins / stop nephrotoxic drugs • Relieve obstruction if post-renal • Dialysis if refractory or severe 🩸
⏳ Chronic Kidney Disease (CKD)	Progressive & irreversible decline in kidney function over months–years. Often due to diabetes, hypertension, or glomerulonephritis. Leads to uraemia, anaemia, and bone–mineral disorders.	• eGFR < 60 mL/min for ≥3 months • Proteinuria or abnormal urine sediment • US: small shrunken kidneys (except diabetic nephropathy)	• Control BP (ACEi/ARB) 💊 • Manage diabetes • Restrict salt/protein intake • Treat anaemia & CKD-MBD • Dialysis or transplant if eGFR < 15 mL/min
💦 Nephrotic Syndrome	Massive protein loss in urine due to glomerular barrier defect → ↓ plasma oncotic pressure → oedema & hyperlipidaemia. Common causes: Minimal change disease, FSGS, diabetes, lupus.	• Proteinuria > 3.5 g/day • Hypoalbuminaemia, oedema, hyperlipidaemia • Fatty casts (“Maltese crosses”) on microscopy	• Salt restriction, diuretics for oedema 💧 • Corticosteroids ± immunosuppressants • Statins for dyslipidaemia • Treat underlying disease
🩸 Nephritic Syndrome	Glomerular inflammation → ↓ GFR, RBC leakage → haematuria & hypertension. Common causes: Post-streptococcal GN, IgA nephropathy, lupus nephritis.	• Haematuria (RBC casts) 🔬 • Proteinuria (usually < 3 g/day) • Oliguria, ↑ creatinine, hypertension • Complement levels may be low (C3↓)	• Treat infection or autoimmune trigger • Corticosteroids / immunosuppressants • Control BP (ACEi/ARB) • Dialysis in severe renal failure
🧬 Polycystic Kidney Disease (PKD)	Genetic disorder (ADPKD or ARPKD) → progressive cyst formation, kidney enlargement, and renal failure. Associated with hepatic cysts & berry aneurysms. 🧠	• Family history of PKD • Imaging (US/CT/MRI): multiple bilateral cysts • Genetic testing (PKD1, PKD2)	• BP control (ACEi/ARB) 💊 • Pain management • Treat infection or stones • Tolvaptan (vasopressin antagonist) slows progression • Dialysis or transplant in ESRD

🧭 Key Teaching Points

💡 AKI = sudden & potentially reversible; CKD = gradual & irreversible.
💦 Nephrotic → heavy protein loss + oedema; Nephritic → blood + hypertension.
🧬 PKD → genetic, cystic enlargement of kidneys; monitor family members.
🧠 Always assess for reversible factors: dehydration, infection, obstruction, or medication toxicity.
🫀 Control blood pressure - the single most important measure to slow renal decline.

💡 Teaching Tip: Think of renal syndromes as points along a spectrum - from acute injury (AKI) to chronic failure (CKD), and from protein leak (nephrotic) to blood leak (nephritic). Recognising patterns early can prevent dialysis dependence and preserve kidney life. 💙🩺🧬

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Acute Kidney Injury ✅

Current UK guidance: Acute kidney injury — recognition and immediate evaluation