Acute kidney injury

Pre-renal (hypoperfusion)

Hypovolaemia, haemorrhage, sepsis, cardiac failure, hepatorenal syndrome, NSAIDs and ACEi/ARB in low-flow states

Intrinsic — tubular

Ischaemic acute tubular injury, aminoglycosides, contrast, cisplatin, rhabdomyolysis, haemolysis

Intrinsic — glomerular

Rapidly progressive glomerulonephritis, vasculitis, lupus nephritis, post-infectious GN

Intrinsic — interstitial

Drug-induced interstitial nephritis (PPIs, beta-lactams, NSAIDs), infection, sarcoidosis

Intrinsic — vascular

Thrombotic microangiopathy, cholesterol emboli, renal artery or vein thrombosis, scleroderma crisis

Post-renal (obstruction)

Prostatic enlargement, stones, pelvic malignancy, blocked catheter, retroperitoneal fibrosis

• Affects 10-15% of hospital admissions and over 50% of ICU patients.
• Community-acquired AKI in low-resource settings is often due to diarrhoeal illness, obstetric causes, envenomation and traditional remedies.
• Around 20-30% of hospital AKI is judged preventable by medication and fluid review.

• Age > 65, pre-existing CKD, diabetes, heart failure, cirrhosis, sepsis, major surgery, contrast exposure, nephrotoxic drug combinations (NSAID + ACEi/ARB + diuretic), single functioning kidney, hypovolaemia.

Normal physiology → mechanism → tissue change → clinical picture

1. 1Normal physiology: autoregulation maintains GFR via afferent dilatation (prostaglandins) and efferent constriction (angiotensin II).
2. 2Mechanism: hypoperfusion, direct tubular toxicity or obstruction breaks that balance.
3. 3Tissue change: proximal tubular epithelial injury, cast formation, tubular back-leak, medullary hypoxia, congestion.
4. 4Functional effect: falling GFR, sodium and water retention, impaired potassium and acid excretion.
5. 5Clinical manifestation: oliguria, oedema, hyperkalaemia, metabolic acidosis and rising urea/creatinine.

Acute tubular injury

Loss of brush border, tubular epithelial flattening and necrosis, granular casts, interstitial oedema

Interstitial nephritis

Interstitial lymphocyte and eosinophil infiltrate with tubulitis

Glomerular disease

Crescents in RPGN; immune complex deposition on immunofluorescence

Obstruction

Dilated tubules, hydronephrosis with parenchymal thinning

• Often silent — detected on biochemistry
• Reduced urine output or complete anuria
• Nausea, vomiting, anorexia, hiccups (uraemia)
• Breathlessness with fluid overload
• Cause-specific: diarrhoea, sepsis symptoms, flank pain, rash, joint pain, haematuria

• Volume state: postural hypotension and dry mucosae, or raised JVP, oedema and crackles
• Palpable bladder or enlarged prostate suggesting obstruction
• Asterixis, pericardial rub, uraemic fetor in advanced uraemia
• Rash, uveitis or purpura pointing to interstitial nephritis or vasculitis

1. 1Confirm AKI and stage it against a baseline creatinine using KDIGO criteria.
2. 2Exclude obstruction: bladder scan and renal ultrasound within 24 hours (immediately if anuric or single kidney).
3. 3Assess volume state clinically — this determines fluids versus diuresis.
4. 4Review every medication and stop or hold nephrotoxins; adjust renally cleared drugs.
5. 5Dipstick urine: blood and protein suggest intrinsic glomerular disease and warrant urgent nephrology input.
6. 6Send an immunology screen when glomerulonephritis or vasculitis is possible.
7. 7Reassess after 12-24 hours: response to volume correction, potassium, acid-base and urine output; consider biopsy or dialysis.

KDIGO

AKI definition

Creatinine rise ≥ 26.5 µmol/L (0.3 mg/dL) in 48 h, OR ≥ 1.5× baseline within 7 days, OR urine output < 0.5 mL/kg/h for 6 h

Stage 1

1.5-1.9× baseline or ≥ 26.5 µmol/L rise; urine < 0.5 mL/kg/h for 6-12 h

Stage 2

2.0-2.9× baseline; urine < 0.5 mL/kg/h for ≥ 12 h

Stage 3

≥ 3× baseline, creatinine ≥ 354 µmol/L, RRT initiation, or urine < 0.3 mL/kg/h for ≥ 24 h / anuria ≥ 12 h

Initial

• Creatinine and urea, electrolytes including potassium and bicarbonate, FBC, CRP, urine dipstick, blood gas, ECG if potassium raised.

Cause identification

• Renal tract ultrasound, bladder scan for residual volume, urine protein-creatinine ratio, urine microscopy.

Intrinsic disease work-up

• CK and myoglobin for rhabdomyolysis, calcium and phosphate, LDH and blood film for haemolysis, ANA/ANCA/anti-GBM, complement, serum free light chains, hepatitis and HIV serology.

Monitoring

• Daily creatinine and electrolytes, hourly urine output with catheter where indicated, weight, fluid balance, drug levels.

Definitive

• Renal biopsy when intrinsic disease is likely and treatment depends on histology.

Chronic kidney disease

Rule in: known prior creatinine elevation, small echogenic kidneys, anaemia, renal bone disease. Rule out: documented normal recent baseline.

Pre-renal vs intrinsic

Pre-renal: rapid response to volume, bland urine, high urine osmolality. Intrinsic: granular casts, no response, sodium not conserved.

Post-renal obstruction

Rule in: hydronephrosis, high residual volume. Rule out: normal ultrasound with empty bladder.

Hepatorenal syndrome

Rule in: cirrhosis with ascites, no response to albumin, bland urine. Rule out: shock or nephrotoxin exposure.

Pseudo-AKI

Rule in: creatinine rise from trimethoprim or cimetidine blocking tubular secretion with stable cystatin C. Rule out: falling urine output and rising urea.

Immediate

• Restore perfusion: isotonic crystalloid in hypovolaemia, guided by repeated reassessment — avoid indiscriminate volume loading
• Treat sepsis and shock; vasopressors to maintain MAP ≥ 65 mmHg
• Relieve obstruction (catheter, nephrostomy, stent)
• Stop nephrotoxins: NSAIDs, ACEi/ARB, aminoglycosides, contrast; hold metformin and SGLT2 inhibitors
• Treat hyperkalaemia: calcium gluconate for ECG changes, insulin-dextrose, salbutamol, potassium binders

Targeted supportive

• Loop diuretics only for fluid overload — they do not treat AKI or improve outcome.
• Correct acidosis with sodium bicarbonate in severe acidaemia; treat hypercalcaemia and tumour lysis specifically.

Cause-specific

• Immunosuppression (steroids, cyclophosphamide, rituximab, plasma exchange) for biopsy-proven or strongly suspected vasculitis or anti-GBM disease.

Renal replacement

• Renal replacement therapy for refractory hyperkalaemia, acidosis, fluid overload, uraemic complications or selected poisonings (AEIOU indications).

Supportive

• Nutrition with adequate calories, avoid hypoglycaemia, VTE prophylaxis with renal dosing, medication reconciliation on every ward round.

Acute

• Hyperkalaemia with arrhythmia, pulmonary oedema, metabolic acidosis, uraemic pericarditis and encephalopathy, drug accumulation and toxicity.

Intermediate

• Prolonged dialysis dependence, infection, malnutrition, bleeding from platelet dysfunction.

Late

• Chronic kidney disease, accelerated cardiovascular risk, end-stage kidney disease, recurrent AKI.

• Hospital mortality rises with stage — from under 10% in stage 1 to over 40-50% in dialysis-requiring AKI within critical illness.
• Most survivors recover function, but 15-30% have persistent reduction in eGFR.
• AKI raises the long-term risk of CKD roughly 8-9 fold and end-stage disease around 3 fold in cohort studies.
• Prognosis depends far more on the precipitating illness than on the creatinine level itself.

• Medication review with sick-day guidance for ACEi/ARB, diuretics, metformin and SGLT2 inhibitors
• Peri-procedural hydration and minimum contrast volume in high-risk patients
• Avoid combining nephrotoxins; use therapeutic drug monitoring
• Early recognition of sepsis and hypovolaemia; electronic AKI alerts with care bundles

• Recheck creatinine within 7-14 days of discharge after any episode
• Document the episode and cause in the discharge summary and primary-care record
• Restart held medicines deliberately with a monitoring plan — do not leave them stopped by accident
• Annual eGFR and urine ACR for patients who had stage 2-3 AKI

Pregnancy

Consider pre-eclampsia, HELLP, acute fatty liver, obstetric haemorrhage, pregnancy-associated thrombotic microangiopathy

Paediatrics

Diarrhoeal dehydration and haemolytic uraemic syndrome are leading causes; use weight-based fluids

Elderly

Creatinine underestimates dysfunction because of low muscle mass; polypharmacy is the dominant modifiable factor

Cirrhosis

Albumin challenge, terlipressin for hepatorenal syndrome, avoid NSAIDs and aminoglycosides

Heart failure

Distinguish congestion (needs decongestion) from hypoperfusion (needs output support) — venous congestion often drives AKI

Transplant

Consider calcineurin toxicity, rejection and BK nephropathy; urgent transplant unit input

• KDIGO Clinical Practice Guideline for Acute Kidney Injury (2012, AKD update 2024)
• National AKI care bundle for your service

• Trials of early versus delayed renal replacement therapy show no benefit from starting before conventional indications appear.
• Balanced crystalloids modestly reduce major adverse kidney events compared with saline in several large trials.
• Contrast-associated AKI risk has been substantially revised downward with modern low-osmolar agents.

• KDIGO AKI guideline 2012 (guideline, global).
• DrZep editorial summary, demo dataset v0.1.