Renal: Emergencies

• Acute kidney injury: What is AKI? | Causes of AKI | Assessing AKI | Managing AKI | Medicines and AKI | When to Start Dialysis | Recovery After AKI
• Renal emergencies: Hyperkalaemia | Severe Metabolic Acidosis | Fluid Overload and Pulmonary Oedema | Rapidly Progressive Glomerulonephritis | Acute Interstitial Nephritis | Rhabdomyolysis | Urinary Obstruction | Contrast and AKI | Other Causes to Recognise
• Revision: Drug Reference Table | Spot the Emergency | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🫘 Acute kidney injury (AKI) affects about 1 in 5 emergency admissions and is linked to around 100,000 deaths a year in England. Much of it is preventable — from dehydration, sepsis, drugs and missed urinary obstruction. Most AKI is managed by general teams; the skill is spotting it early, finding the cause, and recognising the few patients who need urgent nephrology input.
Your four questions for every patient: Is this AKI — and how severe? Is the cause pre-renal, renal or post-renal (obstruction)? Are there life-threatening complications (high potassium, acidosis, fluid overload, uraemia)? Which drugs need stopping or dose-adjusting?

What is AKI?

Definition (KDIGO, NICE NG148) — any of:

• A rise in serum creatinine of 26 µmol/L or more within 48 hours.
• A rise of 50% or more from baseline within the past 7 days.
• Urine output under 0.5 mL/kg/hour for more than 6 hours.

Stages:

• NHS AKI warning algorithm — labs flag AKI stages automatically by comparing results with previous values.
• Creatinine lags behind injury, and is lower in people with low muscle mass (older, frail, amputees) — a "normal" creatinine can hide AKI.
• Risk factors:
  • Age 65 or over.
  • CKD.
  • Heart failure; liver disease; diabetes.
  • Sepsis; hypovolaemia.
  • Nephrotoxic drugs.
  • Recent contrast.
  • History of urinary obstruction.
  • Cognitive impairment or dependence on others for fluids.

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Causes of AKI

• Pre-renal (reduced blood flow to the kidneys — the commonest):
  • Hypovolaemia — vomiting, diarrhoea, bleeding, poor intake, diuretics.
  • Sepsis and low BP.
  • Heart failure (cardiorenal syndrome).
  • Liver cirrhosis (hepatorenal syndrome).
  • Drugs that reduce kidney blood flow — NSAIDs, ACE inhibitors and ARBs, especially with diuretics ("triple whammy").
  • Renal artery stenosis.
• Intrinsic renal:
  • Acute tubular injury (ATN) — prolonged low blood flow, sepsis, nephrotoxins (aminoglycosides, contrast, myoglobin in rhabdomyolysis, cisplatin).
  • Acute interstitial nephritis — drugs (PPIs, antibiotics, NSAIDs), infection.
  • Glomerulonephritis — ANCA vasculitis, anti-GBM disease, lupus, post-infectious.
  • Vascular — thrombotic microangiopathy (HUS, TTP), malignant hypertension, scleroderma renal crisis, cholesterol emboli (after angiography), renal vein thrombosis.
  • Myeloma cast nephropathy.
  • Tumour lysis syndrome (uric acid).
• Post-renal (obstruction):
  • Prostatic enlargement or cancer; urinary retention (drugs, constipation).
  • Stones (in a single kidney, or bilateral).
  • Pelvic cancers (cervix, bladder, prostate, colorectal).
  • Blocked catheter.
  • Retroperitoneal fibrosis.

💡 Clinical Pearl: Most hospital AKI is multifactorial — for example, an older person with sepsis, poor intake, and ongoing ACE inhibitor, diuretic and NSAID use.

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Assessing AKI

• History:
  • Fluid losses and intake.
  • Drugs (new, over-the-counter NSAIDs, contrast, antibiotics, PPIs).
  • Urinary symptoms (poor flow, retention, haematuria).
  • Systemic features — rash, joint pains, haemoptysis, nosebleeds, sinus problems (vasculitis), weight loss, back pain (myeloma).
  • Previous creatinine (baseline).
• Examination:
  • Fluid status — BP, pulse, JVP, capillary refill, mucous membranes, oedema, lung crackles.
  • Palpable bladder.
  • Rash (vasculitis, cholesterol emboli, drug reaction).
  • Muscle tenderness (rhabdomyolysis).
• Urine dipstick — before a catheter if possible:
  • Blood and protein without infection suggests glomerulonephritis — urgent nephrology discussion.
  • Blood without red cells on microscopy suggests myoglobin (rhabdomyolysis).
  • Leucocytes without infection — interstitial nephritis.
  • Urine ACR or PCR.
• Blood tests:
  • U&E, potassium.
  • Venous blood gas (pH, bicarbonate).
  • FBC (anaemia, low platelets — TMA), film if platelets low.
  • CRP; CK; LFTs; calcium and phosphate; urate.
  • Glucose.
• If glomerulonephritis or no clear cause:
  • ANCA, anti-GBM, ANA and dsDNA, complement (C3, C4).
  • Immunoglobulins, serum protein electrophoresis and free light chains (myeloma).
  • Hepatitis B and C, HIV.
  • ASOT; blood cultures.
• Renal tract ultrasound (NICE NG148):
  • Within 24 hours if obstruction is suspected or the cause is unclear.
  • Within 6 hours if there is suspected infected obstructed kidney (pyonephrosis).
• Bladder scan — retention.

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Managing AKI

Remember "STOP AKI":

• S — Sepsis: Look for and treat it (cultures, antibiotics at renally adjusted doses).
• T — Toxins: Stop nephrotoxic drugs (NSAIDs, aminoglycosides, contrast if possible); adjust renally cleared drugs.
• O — Optimise blood pressure and fluid status:
  • If hypovolaemic — balanced crystalloid (e.g. 500 mL bolus), then reassess.
  • Avoid fluid overload — it worsens outcomes.
  • Hold antihypertensives if BP is low; consider vasopressors in sepsis (critical care).
• P — Prevent harm:
  • Treat complications (potassium, acidosis, overload).
  • Relieve obstruction (urinary catheter; nephrostomy or stents).
  • Fluid balance chart and daily weights.
  • Monitor U&E daily (more often if potassium is high).
  • Nutrition.

Refer to nephrology if:

• The cause is unclear, or glomerulonephritis or vasculitis is suspected (blood and protein in urine).
• AKI is stage 3 or not improving.
• There are complications not responding to treatment.
• Kidney transplant, or CKD stage 4–5.
• Possible need for dialysis.

Refer to urology for obstruction (and immediately for an infected obstructed kidney).

Catheters: Use for retention or accurate monitoring in the critically ill — not routinely; remove as soon as possible.

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Medicines and AKI

• Temporarily stop (and restart when kidney function recovers):
  • NSAIDs.
  • ACE inhibitors and ARBs (and sacubitril/valsartan).
  • Diuretics (unless overloaded).
  • Metformin (lactic acidosis).
  • SGLT2 inhibitors (and ketoacidosis risk).
  • Spironolactone and other potassium-sparing diuretics.
  • Trimethoprim (raises potassium and creatinine).
• Dose-adjust or review:
  • Gentamicin and vancomycin (levels).
  • DOACs and LMWH (bleeding).
  • Opioids — morphine metabolites accumulate (drowsiness, myoclonus).
  • Gabapentin and pregabalin.
  • Lithium (toxicity) and digoxin.
  • Sulfonylureas and insulin (hypoglycaemia).
  • Methotrexate.
  • Aciclovir, co-trimoxazole, nitrofurantoin.
• Sick day rules — advise patients to pause certain drugs during dehydrating illness (vomiting, diarrhoea, fever) and restart 24–48 hours after eating and drinking normally. A common memory aid is "SADMANS":
  • Sulfonylureas.
  • ACE inhibitors.
  • Diuretics.
  • Metformin.
  • ARBs.
  • NSAIDs.
  • SGLT2 inhibitors.
• Drug dosing — use creatinine clearance (Cockcroft–Gault) for drugs with narrow safety margins; eGFR isn't valid during AKI (it assumes stable function).

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When to Start Dialysis

Indications for urgent renal replacement therapy in AKI, when medical treatment fails ("AEIOU"):

• A — Acidosis — severe metabolic acidosis (e.g. pH under 7.15).
• E — Electrolytes — refractory hyperkalaemia (e.g. 6.5 mmol/L or more despite treatment).
• I — Intoxication — dialysable poisons: lithium, methanol, ethylene glycol, salicylates, metformin-associated lactic acidosis, some others.
• O — Overload — pulmonary oedema not responding to diuretics.
• U — Uraemia — pericarditis, encephalopathy (confusion, seizures), uraemic bleeding.

Types:

• Continuous haemofiltration (CVVH/CVVHDF) in ICU — gentler on the blood pressure.
• Intermittent haemodialysis — on the renal unit; faster removal (poisons, potassium).
• Access via a temporary central venous dialysis catheter.

Decide in the context of the patient's wishes and prognosis — dialysis isn't always appropriate (e.g. advanced frailty, end of life).

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Recovery After AKI

• Polyuric phase — during recovery from ATN or after relieving obstruction, large urine volumes can cause dehydration and low potassium, sodium and magnesium. Match fluids carefully and check electrolytes.
• Post-obstructive diuresis — after catheterising chronic retention: monitor hourly urine output; replace a proportion of losses; watch U&E.
• Restart medicines step by step as creatinine returns towards baseline (ACE inhibitors, diuretics, metformin, SGLT2 inhibitors).
• Long-term risk: AKI increases the risk of CKD, further AKI, cardiovascular events and death.
  • Check U&E at follow-up (e.g. within 3 months).
  • Record the AKI episode in discharge letters (stage, cause, drugs stopped).
  • Give patients information on sick day rules and avoiding NSAIDs.

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Hyperkalaemia

Severity (UK Kidney Association):

• Mild — 5.5–5.9 mmol/L.
• Moderate — 6.0–6.4 mmol/L.
• Severe — 6.5 mmol/L or more.
• Any level with ECG changes is an emergency.

Causes:

• AKI and CKD.
• Drugs — ACE inhibitors, ARBs, spironolactone, amiloride, trimethoprim, NSAIDs, heparin, ciclosporin and tacrolimus, potassium supplements.
• Tissue breakdown — rhabdomyolysis, tumour lysis, haemolysis, burns.
• Acidosis; DKA (insulin deficiency).
• Addison's disease.
• Pseudohyperkalaemia — haemolysed sample, delayed processing, very high white cells or platelets. Repeat, but don't delay treatment if the ECG is abnormal.

ECG changes:

• Tall tented T waves.
• Flattened or absent P waves; long PR.
• Broad QRS.
• Sine wave pattern, then VF or asystole.
• Bradycardia.
• The ECG can be normal even at dangerous levels.

Emergency treatment (potassium 6.5 or more, or ECG changes):

• Cardiac monitoring.
• 1. Protect the heart — IV calcium:
  • Calcium gluconate 10% 30 mL IV over 5–10 minutes (or calcium chloride 10% 10 mL via a large vein).
  • Repeat if ECG changes persist.
  • It doesn't lower potassium.
• 2. Shift potassium into cells:
  • Insulin–glucose — 10 units soluble insulin with 25 g glucose (e.g. 50 mL of 50% or 125 mL of 20%) IV over 15 minutes.
  • Monitor glucose hourly for at least 6 hours (hypoglycaemia is common). Give a 10% glucose infusion if pre-treatment glucose is under 7 mmol/L.
  • Salbutamol 10–20 mg nebulised as an add-on (caution in heart disease).
• 3. Remove potassium:
  • Potassium binders — sodium zirconium cyclosilicate 10 g three times daily (up to 72 hours), or patiromer.
  • Stop potassium-raising drugs.
  • Treat the cause (fluids, relieve obstruction).
  • Dialysis if refractory, especially with oliguric AKI.
• Recheck potassium at 1, 2, 4 and 6 hours, and 24 hours.
• Sodium bicarbonate only if there is significant acidosis (specialist).

⚠️ Safety Pearl: Hypoglycaemia after insulin–glucose treatment is common and dangerous — especially with low starting glucose, kidney failure, low body weight and no diabetes. Check glucose for at least 6 hours.

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Severe Metabolic Acidosis

• Causes in kidney patients:
  • AKI and CKD (retained acids).
  • Lactic acidosis (sepsis, shock, ischaemic bowel, metformin).
  • Ketoacidosis (DKA, alcohol, starvation; euglycaemic DKA on SGLT2 inhibitors).
  • Toxins — methanol, ethylene glycol, salicylates.
  • Diarrhoea; renal tubular acidosis.
• Anion gap = Na − (Cl + HCO3), normal about 8–12:
  • High — lactate, ketones, toxins, uraemia.
  • Normal — diarrhoea, renal tubular acidosis, saline infusion.
• Treatment:
  • Treat the cause (fluids, sepsis, insulin).
  • IV sodium bicarbonate (e.g. isotonic 1.26%) for severe acidosis in AKI, if the patient isn't overloaded — under specialist guidance; it adds sodium and fluid.
  • Dialysis for refractory acidosis or toxic alcohols.
  • Fomepizole for methanol and ethylene glycol poisoning.
• Oral sodium bicarbonate for chronic acidosis in CKD (see the CKD chapter).

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Fluid Overload and Pulmonary Oedema

• Causes:
  • Over-enthusiastic IV fluids in oliguric AKI (common in hospital).
  • Heart failure.
  • Missed dialysis.
  • Nephrotic syndrome.
• Features: Breathlessness, hypoxia, crackles, raised JVP, peripheral oedema, weight gain, high BP.
• Treatment:
  • Stop IV fluids; sit up; oxygen.
  • IV furosemide — higher doses are needed in kidney impairment (e.g. 80–250 mg), or an infusion.
  • IV nitrates if BP allows.
  • CPAP.
  • Dialysis or ultrafiltration if there is no response.
• Prevention: Daily weights, fluid balance charts, and regular review of fluid prescriptions (NICE CG174 — "the 5 Rs": resuscitation, routine maintenance, replacement, redistribution, reassessment).

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Rapidly Progressive Glomerulonephritis

What it is: Kidney failure over days to weeks, with blood and protein in the urine, and crescents on biopsy. It is a nephrology emergency — without treatment, the kidneys can fail permanently within days.

• Causes:
  • ANCA-associated vasculitis (GPA, MPA) — the commonest; older adults.
  • Anti-GBM disease (Goodpasture's) — kidney failure, often with lung haemorrhage (haemoptysis); young men and older women; smokers.
  • Lupus nephritis.
  • IgA nephropathy and IgA vasculitis.
  • Post-infectious glomerulonephritis; endocarditis.
• Clues:
  • Haematuria and proteinuria on dipstick; red cell casts.
  • Hypertension; oedema.
  • Systemic features — rash (vasculitic purpura), joint pains, sinusitis, nosebleeds, haemoptysis, fever, weight loss, eye inflammation, neuropathy.
• Urgent tests: ANCA (PR3 and MPO), anti-GBM, ANA and dsDNA, complement, chest X-ray, and an urgent kidney biopsy.
• Pulmonary–renal syndrome (lung haemorrhage with AKI) — anti-GBM disease or ANCA vasculitis: ICU, urgent treatment.
• Treatment (often started before biopsy):
  • High-dose steroids (IV methylprednisolone).
  • Rituximab or cyclophosphamide.
  • Avacopan (steroid-sparing, ANCA vasculitis).
  • Plasma exchange — anti-GBM disease; selected severe ANCA vasculitis.
• See the Glomerular Disease chapter.

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Acute Interstitial Nephritis

• What it is: Inflammation of the kidney tissue between the tubules — usually an allergic reaction to a drug.
• Causes:
  • Drugs (about 70%):
    • PPIs (a common cause in older people, often weeks to months after starting).
    • Antibiotics — penicillins, cephalosporins, quinolones, rifampicin.
    • NSAIDs (may also cause nephrotic syndrome).
    • Mesalazine.
    • Allopurinol.
    • Checkpoint inhibitors.
  • Infection — pyelonephritis, leptospirosis, legionella.
  • Systemic disease — sarcoidosis, Sjögren's syndrome, TINU syndrome (with uveitis), IgG4 disease.
• Features:
  • AKI, often without symptoms.
  • The "classic" triad of fever, rash and eosinophilia is present in only a minority.
  • White cells in the urine (sterile pyuria), mild proteinuria.
  • Urine eosinophils are unreliable.
• Diagnosis: Kidney biopsy (if the cause is unclear or the AKI is severe).
• Treatment:
  • Stop the culprit drug (record it as an allergy).
  • Steroids (e.g. prednisolone 1 mg/kg, tapering over weeks) if there is no improvement after stopping the drug, or if severe — early treatment improves recovery.

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Rhabdomyolysis

• What it is: Muscle breakdown releases myoglobin (toxic to the tubules), potassium, phosphate and urate.
• Causes:
  • Long lie after a fall (older people).
  • Crush injury; compartment syndrome.
  • Extreme exercise (including sickle cell trait).
  • Seizures; severe agitation.
  • Drugs and toxins — statins (with fibrates or interacting drugs), cocaine, amphetamines, ecstasy, alcohol, neuroleptic malignant syndrome, serotonin syndrome.
  • Hyperthermia (heat stroke, malignant hyperthermia).
  • Infections (influenza, COVID-19).
  • Low potassium or phosphate.
  • Metabolic myopathies (McArdle's).
• Features:
  • Muscle pain, swelling or weakness (may be absent).
  • Dark ("cola") urine.
  • CK very high — usually over 5 times normal, often over 10,000 IU/L.
  • Urine dipstick positive for blood with no red cells on microscopy.
  • High potassium, high phosphate, low calcium (early), high urate.
  • AKI.
• Treatment:
  • Aggressive IV fluids (crystalloid) — aim for a high urine output (e.g. 200–300 mL/hour), watching for overload.
  • Treat hyperkalaemia.
  • Don't treat low calcium unless symptomatic or with severe hyperkalaemia (calcium deposits in muscle and rebounds later).
  • Stop causative drugs (statins).
  • Monitor CK, U&E and fluid balance.
  • Compartment syndrome — severe pain, tense limb: urgent orthopaedic review (fasciotomy).
  • Dialysis if needed.

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Urinary Obstruction

• Acute urinary retention:
  • Painful, palpable bladder; inability to pass urine.
  • Causes:
    • Benign prostatic hyperplasia.
    • Constipation.
    • Drugs — anticholinergics, opioids, antihistamines, decongestants.
    • Infection; after surgery or anaesthesia.
    • Spinal cord compression or cauda equina (check neurology).
    • Clot retention.
  • Catheterise; record the residual volume.
  • Alpha-blocker (tamsulosin) before a trial without catheter.
• Chronic retention — often painless, with a large residual (over 1 L), overflow incontinence and high-pressure retention causing AKI. Catheterise; watch for post-obstructive diuresis.
• Upper tract obstruction (ureters):
  • Stones; pelvic cancers; retroperitoneal fibrosis; strictures.
  • Hydronephrosis on ultrasound.
  • Nephrostomy or ureteric stent.
• Infected obstructed kidney (pyonephrosis) — fever, loin pain, sepsis with hydronephrosis. A urological emergency: IV antibiotics and urgent drainage (nephrostomy or stent) — antibiotics alone aren't enough.
• Bilateral obstruction or obstruction of a single functioning kidney causes AKI; one-sided obstruction with a normal other kidney usually doesn't raise creatinine much.

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Contrast and AKI

• Contrast-associated AKI — creatinine rise within 48–72 hours of iodinated contrast. The risk with modern IV contrast is lower than once thought.
• Higher risk:
  • eGFR under 30 (or under 45 with additional risk factors, or for intra-arterial contrast).
  • Dehydration.
  • Heart failure.
  • Diabetes.
  • Myeloma.
  • Large or repeated doses.
• Prevention:
  • Assess risk before contrast.
  • Hydration (oral or IV — e.g. 0.9% saline or isotonic bicarbonate) for high-risk patients.
  • Temporarily hold nephrotoxic drugs (NSAIDs).
  • Metformin — hold for 48 hours after contrast if eGFR is under 30 or there is AKI (Royal College of Radiologists).
  • Use the lowest contrast dose.
  • Check creatinine at 48–72 hours in high-risk patients.
• Don't withhold or delay a necessary scan (e.g. suspected stroke, PE, aortic dissection, sepsis source) because of kidney function — the benefit usually outweighs the risk.
• Gadolinium (MRI) — risk of nephrogenic systemic fibrosis with older agents in severe kidney failure; modern agents are much safer.
• Cholesterol emboli — AKI days to weeks after angiography or vascular surgery, with livedo reticularis, purple toes and eosinophilia.

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Other Causes to Recognise

• Hepatorenal syndrome — AKI in cirrhosis with ascites: stop diuretics, albumin, terlipressin (see the Gastroenterology Emergencies chapter).
• Cardiorenal syndrome — AKI with heart failure. Often from congestion, so may improve with diuretics rather than fluids.
• Thrombotic microangiopathy (HUS, TTP) — AKI with low platelets and schistocytes (see the Haematological Emergencies chapter).
• Malignant hypertension — very high BP with retinal changes and AKI; controlled BP reduction.
• Scleroderma renal crisis — sudden hypertension and AKI in systemic sclerosis (especially after high-dose steroids). Treat with an ACE inhibitor (an exception to stopping ACE inhibitors in AKI).
• Myeloma cast nephropathy — AKI with high calcium, anaemia and back pain: free light chains, fluids, urgent anti-myeloma treatment.
• Tumour lysis syndrome — see the Oncological Emergencies chapter.
• Lithium toxicity — tremor, confusion, ataxia, AKI; stop lithium, fluids, dialysis if severe.
• Renal artery occlusion or renal vein thrombosis — sudden loin pain, haematuria, raised LDH (artery), or nephrotic syndrome (vein).
• Leptospirosis (Weil's disease) — exposure to rat urine (rivers, farming): fever, jaundice, AKI, conjunctival redness.
• Hantavirus, malaria (blackwater fever) — travel-related AKI.

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Drug Reference Table

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Spot the Emergency

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Exam-style Scenarios

1. An 82-year-old on ramipril, furosemide and metformin has 3 days of diarrhoea. Creatinine is 210 µmol/L (baseline 95). BP 98/60.
Answer: Stage 2 pre-renal AKI with hypovolaemia.

• Fluid bolus (balanced crystalloid 500 mL) and reassess; then maintenance as needed.
• Stop ramipril, furosemide and metformin temporarily.
• Urine dipstick; potassium; venous blood gas; stool cultures.
• Daily U&E; restart drugs as she recovers; give sick day advice at discharge.

2. A 70-year-old has potassium 6.8 mmol/L with peaked T waves. Glucose is 5.5 mmol/L.
Answer: Severe hyperkalaemia with ECG changes.

• Cardiac monitoring; calcium gluconate 10% 30 mL IV.
• Insulin 10 units with 25 g glucose, then a 10% glucose infusion (pre-treatment glucose under 7); glucose checks for 6 hours or more.
• Salbutamol nebuliser; SZC 10 g three times daily.
• Stop potassium-raising drugs; treat the cause; recheck potassium at 1, 2, 4, 6 and 24 hours.

3. A 65-year-old has AKI (creatinine 450), 3+ blood and 2+ protein on dipstick, and haemoptysis.
Answer: Pulmonary–renal syndrome (ANCA vasculitis or anti-GBM disease).

• Urgent nephrology referral; ANCA and anti-GBM; chest imaging; ICU review.
• IV methylprednisolone; rituximab or cyclophosphamide; plasma exchange for anti-GBM.
• Urgent kidney biopsy.

4. An older man has AKI (creatinine 380) and a palpable bladder. Bladder scan shows 1,400 mL.
Answer: Post-renal AKI from chronic urinary retention.

• Catheterise; hourly urine output — watch for post-obstructive diuresis.
• Monitor U&E and electrolytes; replace a proportion of losses.
• Renal ultrasound; urology follow-up.

5. A 75-year-old was found on the floor after 36 hours. CK is 35,000 IU/L and creatinine 260.
Answer: Rhabdomyolysis with AKI.

• Aggressive IV crystalloid with urine output targets; watch for overload.
• Treat hyperkalaemia; don't treat asymptomatic low calcium.
• Look for compartment syndrome and the cause of the fall; stop statins.

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Key Points

• AKI: creatinine rise of 26 µmol/L or more in 48 hours, a 50% rise in 7 days, or urine output under 0.5 mL/kg/h for 6 hours.
• Most AKI is pre-renal and multifactorial (dehydration, sepsis, drugs).
• Always dip the urine — blood and protein without infection suggests glomerulonephritis and needs urgent nephrology input.
• Ultrasound within 24 hours if obstruction is suspected or the cause is unclear (within 6 hours if infected obstruction).
• STOP AKI: Sepsis, Toxins, Optimise volume and BP, Prevent harm.
• Stop NSAIDs, ACE inhibitors and ARBs, diuretics, metformin and SGLT2 inhibitors during AKI; adjust renally cleared drugs.
• Teach sick day rules (SADMANS).
• Dialysis indications: acidosis, electrolytes (potassium), intoxication, overload, uraemia.
• Hyperkalaemia with ECG changes or 6.5 or more: IV calcium, insulin–glucose (check glucose for 6 hours), salbutamol, binders, treat the cause.
• Avoid fluid overload in oliguric AKI — daily weights and fluid balance.
• RPGN (ANCA, anti-GBM, lupus) needs urgent steroids, immunosuppression and sometimes plasma exchange.
• Drug-induced interstitial nephritis (PPIs, antibiotics, NSAIDs): stop the drug; steroids if no recovery.
• Rhabdomyolysis: very high CK, dipstick blood without red cells — aggressive fluids.
• Infected obstructed kidney needs urgent drainage.
• Don't delay essential contrast scans for kidney function.

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Guidelines and Further Reading

• NICE NG148: Acute kidney injury — prevention, detection and management
• KDIGO Clinical Practice Guideline for Acute Kidney Injury
• UK Kidney Association (UKKA) guidelines: treatment of acute hyperkalaemia in adults; AKI
• Think Kidneys (NHS England) — AKI resources and sick day guidance
• NICE CG174: Intravenous fluid therapy in adults in hospital
• Royal College of Radiologists: guidance on contrast and kidney function
• BNF — for current doses and renal dose adjustments

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