🔬

KDIGO AKI Definition

AKI is defined by any one of the following criteria (KDIGO 2012):

Creatinine Rise (48h)

Serum creatinine increase ≥26.5 μmol/L within 48 hours

Creatinine × Baseline (7d)

Serum creatinine rise to ≥1.5× known or presumed baseline within the prior 7 days

Urine Output

Urine output <0.5 mL/kg/h for ≥6 consecutive hours

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KDIGO Staging System

Stage 1 — Mild

Creatinine: ×1.5–1.9 baseline or rise ≥26.5 μmol/L

Urine Output: <0.5 mL/kg/h for 6–12 h

Action: Identify cause, optimise fluids, stop nephrotoxins

Stage 2 — Moderate

Creatinine: ×2.0–2.9 baseline

Urine Output: <0.5 mL/kg/h for ≥12 h

Action: Nephrology review, intensive monitoring

Stage 3 — Severe

Creatinine: ×3.0+ baseline, ≥353.6 μmol/L, or RRT initiation

Urine Output: <0.3 mL/kg/h for ≥24 h or anuria ≥12 h

Action: ICU/HDU, consider RRT

🧠

THINK Mnemonic — AKI Aetiology

Apply THINK prompt to all high-risk admissions to screen for reversible AKI causes

T
Toxins
Contrast, NSAIDs, aminoglycosides, heavy metals
H
Hypovolaemia
Dehydration, haemorrhage, diarrhoea, burns
I
Infection / Inflammation
Sepsis, vasculitis, glomerulonephritis
N
New Medications
ACE-I, ARBs, diuretics, SGLT2-i, metformin
K
Kidney Obstruction
Stones, BPH, malignancy, clots, strictures
🏷️

AKI Classification by Anatomical Location

Pre-Renal (Most Common ~55–70%)
  • Hypovolaemia (haemorrhage, dehydration, GI losses)
  • Cardiac failure (low CO → reduced renal perfusion)
  • Sepsis (vasodilation → relative hypovolaemia)
  • Hepatorenal syndrome
Responds to fluidsIntact tubular function
Intrinsic Renal (~25–40%)
  • ATN (85% of intrinsic) — ischaemia/nephrotoxic
  • Glomerulonephritis (rapidly progressive)
  • Acute interstitial nephritis (drug-induced, infection)
  • Vascular (renal artery/vein thrombosis, TMA)
No fluid responseTubular dysfunction
Post-Renal (~5–10%)
  • Urinary stones (bilateral/solitary kidney)
  • BPH / prostate malignancy
  • Pelvic malignancy (cervical/bladder/rectal)
  • Clot retention, strictures
Relieved by catheter/nephrostomy
🌍
GCC-Specific AKI Risk Factors

The GCC region carries elevated AKI risk: extreme heat climate causing dehydration, high prevalence of NSAID use for musculoskeletal pain, high rates of iodinated contrast procedures, and a high background burden of diabetes mellitus and hypertension — the two leading causes of CKD and AKI susceptibility.

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History Taking in AKI

Fluid Balance History

  • Recent fluid intake (oral/IV) and output volumes
  • Bleeding — GI, surgical, traumatic
  • Diarrhoea, vomiting, excess sweating (heat exposure)
  • Burns history (rhabdomyolysis/fluid loss)

Urological Symptoms

  • Frequency, hesitancy, poor stream (BPH)
  • Acute urinary retention
  • Loin pain / haematuria (stones)
  • Pelvic malignancy history

Medication Review (Critical)

  • NSAIDs — afferent arteriolar vasoconstriction
  • ACE inhibitors / ARBs — efferent arteriolar dilation
  • Diuretics — exacerbate hypovolaemia
  • Aminoglycosides — direct tubular toxicity
  • Iodinated contrast — contrast-induced AKI
  • SGLT2 inhibitors — volume depletion, euglycaemic DKA
  • Metformin — lactic acidosis accumulation in AKI
  • Calcineurin inhibitors (tacrolimus, ciclosporin)
🩺

Clinical Examination

Volume Status Assessment

  • JVP — elevated (fluid overload / RHF), flat (hypovolaemia)
  • Skin turgor and mucous membrane dryness
  • Postural blood pressure drop (≥20 mmHg systolic)
  • Capillary refill time (>2 seconds = poor perfusion)
  • Lung bases — crepitations (fluid overload)
  • Peripheral oedema — can coexist with hypovolaemia

Specific Findings by AKI Type

  • Palpable bladder → post-renal obstruction → catheterise
  • Renal angle tenderness → pyelonephritis / obstruction
  • Purpuric rash → vasculitis, TTP/HUS
  • Maculopapular rash + eosinophilia → allergic interstitial nephritis
  • Signs of liver disease → hepatorenal syndrome
  • Pericardial rub → uraemic pericarditis (Stage 3)
🔭

Bedside & Urine Investigations

TestPre-Renal ResultIntrinsic (ATN) ResultClinical Significance
Urine dipstick blood + proteinNegativePositiveIntrinsic/GN/infection
Urine osmolality : plasma ratio>1.5<1.1>1.5 = concentrating → pre-renal
Urine sodium (mmol/L)<20>40Tubular reabsorption intact in pre-renal
FENa (%)<1%>2%FENa = (urine Na × plasma Cr) / (plasma Na × urine Cr) × 100
Urine: granular castsAbsentPresentATN — hallmark finding
Urine: RBC castsAbsentPresentGlomerulonephritis
Urine: WBC castsAbsentPresentPyelonephritis / interstitial nephritis

Note: FENa unreliable if patient on diuretics — use FEUrea instead (<35% pre-renal)

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Serum Investigations

Priority Bloods

  • Potassium — hyperkalaemia is the most life-threatening acute complication
  • Creatinine trend — serial values to assess trajectory and staging
  • Urea:Creatinine ratio — >100 suggests pre-renal or upper GI bleed
  • Bicarbonate — metabolic acidosis (anion gap ↑ in renal failure)
  • Phosphate, calcium, magnesium — electrolyte disturbances

Additional Investigations

  • FBC — haemolysis (↑LDH, ↓platelets, fragmented RBCs) → TMA/HUS
  • CRP / Procalcitonin — infection/sepsis
  • ANCA, anti-GBM, ANA, complement — glomerulonephritis screen
  • Blood cultures — sepsis
  • CK — rhabdomyolysis (myoglobinuria), especially in GCC heat exposure
  • LFTs — hepatorenal syndrome

Imaging & Biopsy

USS Kidneys (First-line Imaging)

Hydronephrosis → post-renal obstruction (dilated pelvicalyceal system)

Small, bright (echogenic) kidneys → CKD (chronic disease, not AKI)

Normal size (10–12 cm) supports acute process

Duplex Doppler for renal vascular causes

Other Imaging & Biopsy

CT KUB — if urinary stone suspected (no contrast needed)

Kidney biopsy — native kidney biopsy for glomerular disease, unexplained intrinsic AKI, interstitial nephritis confirmation

Requires USS guidance, INR <1.5, platelets >80

⚠️
First Priority: Exclude and Treat Life-Threatening Complications

Hyperkalaemia (K+ >6.0 mmol/L) and severe metabolic acidosis (pH <7.2) require immediate management before addressing the underlying AKI cause.

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Pre-Renal AKI — Fluid Resuscitation

  1. Fluid Challenge Administer 250–500 mL isotonic crystalloid (0.9% NaCl or Hartmann's) IV over 15–30 minutes. Monitor response.
  2. Reassess After Bolus Urine output improving (response confirms pre-renal aetiology). Repeat bolus if still hypovolaemic. Do NOT give further fluid if overloaded or non-responsive.
  3. Goal-Directed Fluid Therapy Target MAP ≥65 mmHg. In sepsis/vasodilatory shock → vasopressors (noradrenaline) after fluid optimisation. Avoid excessive fluid overload.
  4. Ongoing Monitoring Hourly urinary catheter output, 4-hourly fluid balance review, daily weight, creatinine trend every 12–24 hours.
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Nephrotoxin Management — STOP in AKI

WITHHOLD Immediately in AKI
  • ▸ ACE inhibitors (ramipril, lisinopril, perindopril)
  • ▸ ARBs (losartan, valsartan, irbesartan)
  • ▸ ARNi (sacubitril-valsartan / Entresto)
  • ▸ SGLT2 inhibitors (dapagliflozin, empagliflozin)
  • ▸ Diuretics (unless for fluid overload with medical review)
  • ▸ Metformin (lactic acidosis risk)
  • ▸ NSAIDs (all routes — oral, topical, suppository)
USE WITH CAUTION / Dose Adjust
  • ▸ Aminoglycosides — dose reduce per TDM, avoid if possible
  • ▸ IV contrast — use iso-osmolar (IOCM), pre-hydrate
  • ▸ Vancomycin — TDM essential (AUC-guided dosing)
  • ▸ Low molecular weight heparin — dose adjust in severe AKI (use UFH)
  • ▸ Digoxin — toxicity risk, check levels

Resume medications after AKI resolution — nephrology guidance required

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Post-Renal AKI — Obstruction Relief

Bladder Outlet Obstruction

Urethral catheterisation — immediate relief. Clamp catheter for 30 minutes every 500 mL if large bladder to prevent haematuria ex-vacuo.

Post-obstructive diuresis expected — replace urine output 50–75% with IV fluids, monitor electrolytes closely.

Ureteric Obstruction

Percutaneous nephrostomy (urology/interventional radiology) — urgent referral for bilateral ureteric obstruction or obstruction in solitary kidney.

Ureteric stenting (JJ stent) as alternative or subsequent procedure.

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Intrinsic AKI — Treat Underlying Cause

Intrinsic CauseSpecific TreatmentUrgency
Sepsis-AKI (most common)Antibiotics (1h target), source control, IV fluids, vasopressors for MAP ≥65Emergency
Drug-induced interstitial nephritisSTOP causative drug, corticosteroids (prednisolone 1 mg/kg/d) if no improvementUrgent
Rapidly progressive GN (RPGN)Pulsed IV methylprednisolone ± cyclophosphamide, plasma exchange if anti-GBMEmergency
TMA / HUS / TTPPlasma exchange (TTP), eculizumab (aHUS), treat underlying causeEmergency
Rhabdomyolysis-AKIAggressive IV fluids (target UO 200–300 mL/h), consider urine alkalinisation if myoglobinuriaUrgent
Contrast-induced AKIPre/post hydration with 0.9% NaCl, IOCM, withhold metformin 48hPrevention

Hyperkalaemia Emergency Protocol

Most life-threatening complication of AKI — act immediately. Use interactive tool in Tab 6 for individualised guidance.

  1. Calcium Gluconate 10% — Membrane Stabilisation 10 mL IV over 2–5 minutes (or 30 mL over 10 min if less urgent). Repeat if ECG changes persist. Does NOT lower K+ — protects myocardium. Duration: 30–60 minutes.
  2. Insulin-Dextrose — Transcellular Shift 50 mL of 50% dextrose (25 g) + 10 units short-acting insulin (Actrapid) IV. Reduces K+ by 0.6–1.0 mmol/L within 15–30 minutes. Monitor glucose hourly for 6 hours (hypoglycaemia risk).
  3. Salbutamol Nebulised — Transcellular Shift 10–20 mg nebulised salbutamol (2.5–5× standard bronchodilator dose). Reduces K+ by additional 0.5–1.0 mmol/L. Acts within 15–30 min. Caution: tachycardia.
  4. Resonium / Patiromer — GI Excretion Calcium Resonium 15 g PO/PR. Patiromer (Veltassa) 8.4 g PO — newer agent, better tolerated. Removes K+ over 4–6 hours. Not for emergency use alone.
  5. Dialysis — Definitive Removal If K+ >6.5 refractory or ongoing release (rhabdomyolysis/haemolysis). RRT is the only definitive treatment. IHD removes K+ faster than CRRT.
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Dialysis Indications — AEIOU Mnemonic

A
Acidosis
Refractory metabolic acidosis pH <7.1 despite bicarbonate
E
Electrolytes
K+ >6.5 refractory to medical management
I
Intoxications
Dialysable toxins: methanol, ethylene glycol, salicylates, lithium
O
Overload
Refractory pulmonary oedema not responsive to diuretics
U
Uraemia
Uraemic encephalopathy, uraemic pericarditis, bleeding
⚙️

RRT Modalities — Comparison

IHD

Intermittent Haemodialysis

3–4 hour sessions, typically 3×/week. High-efficiency solute clearance. Risk of haemodynamic instability — rapid fluid and solute shifts.

Best for stable patientsFast K+ removal
CRRT

Continuous RRT (24h)

Continuous infusion 24 h/day in ICU. Haemodynamically gentle — slow fluid/solute removal. Preferred for unstable patients and cerebral oedema.

ICU standardHaemodynamically stable
PIRRT / SLEDD

Prolonged Intermittent RRT

Hybrid: 6–12 hour sessions (slow low-efficiency daily dialysis). Combines benefits of IHD efficiency and CRRT haemodynamic tolerance.

Hybrid approachStep-down from CRRT
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CRRT Modalities Explained

ModalityMechanismClearance TypeReplacement Fluid
CVVH
Continuous Veno-Venous Haemofiltration
Convection — hydrostatic pressure drives plasma water + dissolved solutes across membraneConvective (larger molecules)Yes — pre/post dilution
CVVHD
Continuous Veno-Venous Haemodialysis
Diffusion — concentration gradient across membrane with dialysate counter-current flowDiffusive (small molecules)No
CVVHDF
Haemodiafiltration
Combined convection + diffusionBoth small & medium moleculesYes
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RRT Dose

Target effluent dose: 20–25 mL/kg/h (RENAL and RAVE trials — higher doses ≥35 mL/kg/h showed no additional benefit). Prescribe higher to account for circuit downtime.

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Anticoagulation for CRRT Circuit

Systemic Heparin

  • Unfractionated heparin (UFH) infusion into circuit pre-filter
  • Target APTT: 45–60 seconds (circuit) or 1.5–2× normal
  • Systemic anticoagulation risk — bleeding complications
  • Monitor platelet count (HIT risk)
  • Use if no bleeding risk and no HIT

Regional Citrate Anticoagulation (RCA) — Preferred

  • Citrate infused pre-filter → chelates ionised calcium → inhibits coagulation cascade in circuit
  • Calcium-depleted blood returns to patient → systemic calcium infusion via separate line (CVC)
  • Reduces systemic bleeding risk — preferred in high-bleeding-risk patients
  • Ionised calcium monitoring: circuit target 0.25–0.40 mmol/L; systemic target 1.1–1.3 mmol/L
  • Citrate accumulation risk in liver failure — monitor total:ionised calcium ratio (>2.5 = toxicity)
👩‍⚕️

CRRT Nursing Care — Key Responsibilities

Circuit Monitoring

  • Transmembrane pressure (TMP) — rising TMP indicates filter clotting
  • Access and return pressures — alarms indicating line issues
  • Filter/circuit visible inspection for clot formation
  • Document filter life — report premature clotting (<12h)
  • Bag changes: replacement/dialysate fluid, accurately document volumes

Vascular Access

  • Large-bore dialysis catheter (11–14 Fr) — non-tunnelled for acute RRT
  • Preferred sites: right internal jugular vein (IJV) > femoral > left IJV
  • Subclavian avoided (stenosis risk for future AV fistula)
  • Daily line inspection — infection signs, dressing changes per protocol

Fluid Balance Management

  • Hourly fluid balance documentation (inputs + outputs + ultrafiltration)
  • Cumulative net fluid balance — target as prescribed by medical team
  • Pre-dilution vs post-dilution replacement fluid documentation
  • Weight daily if able

Calcium Monitoring (RCA)

  • Ionised calcium from circuit (post-filter) every 4–6 hours
  • Systemic ionised calcium every 4–6 hours from CVC/arterial line
  • Adjust citrate rate if circuit iCa >0.40 (insufficient anticoagulation)
  • Adjust systemic calcium infusion if systemic iCa <1.1 or >1.3
  • Signs of hypocalcaemia: Chvostek's, Trousseau's, paraesthesia
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AKI Recovery & RRT Cessation

Signs of AKI Recovery
  • ▸ Increasing urine output (>500 mL/24h without diuretics)
  • ▸ Falling serum creatinine on serial measurements
  • ▸ Electrolytes manageable without RRT
  • ▸ Acid-base status improving
RRT Cessation Criteria
  • ▸ Urine output >500 mL/day without high-dose diuretics
  • ▸ Creatinine stable or falling
  • ▸ No ongoing AEIOU dialysis indications
  • ▸ Clinical decision by nephrology — furosemide stress test may guide
  • ▸ 25% of AKI on RRT may not recover — early CKD planning
🛡️

AKI Care Bundle

Apply to all patients with AKI (Stage 1+) and high-risk patients on admission

  1. Assess Volume and Fluid BalanceAssess for hypovolaemia and hypervolaemia. Institute accurate hourly fluid balance. Insert urinary catheter if Stage 1+ AKI.
  2. Avoid All NephrotoxinsReview medication chart — stop NSAIDs, ACE-I/ARB, SGLT2-i, metformin, aminoglycosides unless essential with TDM.
  3. Optimise HaemodynamicsEnsure MAP ≥65 mmHg. Treat sepsis. Optimise cardiac output. Avoid vasoconstrictors where possible.
  4. Monitoring PlanFrequency of creatinine/electrolyte monitoring based on stage. Stage 1: 12-hourly bloods. Stage 2–3: 6–8 hourly.
  5. Specialist ReviewNephrology consultation: Stage 2+ AKI, unclear aetiology, suspected glomerulonephritis, AKI on CKD.
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Electronic AKI Alerting

GCC hospitals increasingly deploying electronic AKI alerting systems (based on UK NADIA model) — automated lab-triggered alerts when creatinine meets AKI criteria, prompting care bundle activation.

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Contrast-Induced AKI Prevention

Definition

Rise in serum creatinine ≥26.5 μmol/L OR ≥25% above baseline within 48 hours of IV iodinated contrast administration.

High-Risk Patients

  • eGFR <45 mL/min/1.73m²
  • Diabetes mellitus with nephropathy
  • Dehydration / hypovolaemia at time of procedure
  • Heart failure
  • Large contrast volumes
  • Concurrent nephrotoxic medications

Prevention Protocol

  • IV isotonic saline — 1 mL/kg/h for 12h pre and 12h post procedure
  • Use IOCM — iso-osmolar contrast media (iodixanol) preferred over high/low osmolar
  • Lowest contrast volume — minimise volume used
  • Withhold metformin — 48h pre and post if eGFR <60
  • N-acetylcysteine — evidence weak, may still be used in some protocols
  • Avoid NSAIDs/diuretics peri-procedure
  • Creatinine check 48–72h post-contrast in high-risk patients
🏋️

Rhabdomyolysis-Associated AKI

🌡️
GCC-Specific Risk: Heat-Related Rhabdomyolysis

Construction workers and labourers working outdoors in extreme GCC summer heat (temperatures exceeding 45°C) are at high risk of exertional heat stroke and rhabdomyolysis-AKI — a unique regional occupational health concern.

Pathophysiology

  • Muscle cell breakdown → myoglobin release
  • Myoglobin precipitates in tubules (pH-dependent)
  • Direct tubular toxicity + cast obstruction
  • CK >5,000 U/L significant; >10,000 U/L high risk for AKI
  • Urine: "tea-coloured" / dipstick blood without RBCs on microscopy

Other Causes

  • Crush injury / trauma
  • Seizures, extreme exercise
  • Statins (especially with CYP3A4 interactions)
  • Infections (influenza, Legionella)
  • Alcohol excess

Management

  • Aggressive IV fluids — target urine output 200–300 mL/h until CK falling and urine clears
  • May require 10–20 L/day initially
  • Urine alkalinisation — sodium bicarbonate to target urinary pH >6.5 (prevents myoglobin precipitation)
  • Monitor electrolytes — hyperkalaemia, hyperphosphataemia, hypocalcaemia
  • Serial CK monitoring every 12h
  • Avoid NSAIDs and nephrotoxins
  • RRT if AKI severe or refractory hyperkalaemia
⚕️

High-Risk Clinical Scenarios

Sepsis-AKI (Most Common ICU Cause)
  • ▸ Sepsis accounts for 45–70% of ICU AKI
  • ▸ Early antibiotics within 1 hour and source control
  • ▸ Vasopressors (noradrenaline) to maintain MAP ≥65 mmHg
  • ▸ Avoid hyperglycaemia — target 6–10 mmol/L
  • ▸ Sepsis Surviving Campaign bundles apply
Post-Surgical AKI
  • ▸ Cardiac surgery (CPB) — ischaemia-reperfusion, emboli
  • ▸ Major vascular surgery — suprarenal aortic clamping
  • ▸ Abdominal surgery — raised intra-abdominal pressure
  • ▸ Pre-op optimisation: hydration, stop nephrotoxins
  • ▸ Intra-op: maintain MAP, avoid prolonged hypotension
Burns AKI
  • ▸ Fluid resuscitation: Parkland formula (4 mL × kg × %TBSA, first 24h)
  • ▸ Rhabdomyolysis from electrical burns or crush
  • ▸ Forced alkaline diuresis for myoglobinuria
  • ▸ High infection risk — sepsis AKI common in burns
AKI Long-Term Outcomes
  • ▸ 25% of AKI survivors develop CKD
  • ▸ 7.8× increased risk of ESRD post-AKI
  • ▸ All AKI patients: nephrology follow-up 3 months post-discharge
  • ▸ Recheck creatinine 1–3 months to document recovery
  • ▸ Blood pressure management essential for renal protection
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Aminoglycoside TDM & Monitoring

Aminoglycoside Nephrotoxicity

  • Gentamicin, tobramycin, amikacin — accumulate in proximal tubular cells
  • Risk: prolonged therapy (>5 days), pre-existing CKD, concomitant nephrotoxins
  • Non-oliguric AKI — may present insidiously
  • Once-daily dosing preferred (less nephrotoxic than multiple daily dosing)

Therapeutic Drug Monitoring

  • Gentamicin: trough <1 mg/L (before next dose); peak 5–10 mg/L (1h post-dose)
  • Amikacin: trough <5 mg/L; peak 25–35 mg/L
  • Check renal function daily during therapy
  • If creatinine rises ≥26.5 μmol/L → STOP aminoglycoside and review
  • Alternative: urinary β2-microglobulin (early tubular injury marker)
🌍

GCC-Specific AKI Context

Elevated AKI Risk Factors in GCC

  • Hot climate dehydration — extreme summer heat, high insensible fluid loss
  • High NSAID use — widespread OTC availability for musculoskeletal pain
  • Iodinated contrast — high volume of cardiac catheterisation, CT angiography
  • DM & hypertension prevalence — GCC has one of highest global rates of type 2 DM
  • Exertional rhabdomyolysis — outdoor construction workers in summer heat
  • Hajj and Umrah pilgrims — dehydration + exertion AKI surge

GCC Healthcare System AKI Initiatives

  • AKI care bundles implemented in DHA, DOH, MOH, and NGHA-affiliated hospitals
  • Electronic AKI alerting from laboratory systems in major tertiary centres
  • THINK mnemonic promoted across GCC nursing education curricula
  • SCFHS (Saudi Commission), DHA (Dubai), DOH (Abu Dhabi) include AKI in nursing competency frameworks
  • National CKD prevention programs in KSA, UAE, Qatar, Kuwait

Interactive: Hyperkalaemia Emergency Management Guide

Hyperkalaemia Clinical Decision Tool
Enter patient parameters to generate individualised step-by-step treatment protocol
📝

DHA / DOH / SCFHS Exam Practice — 10 MCQs

Click "Show Answer" to reveal the correct answer and explanation

1. According to KDIGO criteria, AKI is defined as a rise in serum creatinine of at least:
  • A. 10 μmol/L within 24 hours
  • B. 26.5 μmol/L within 48 hours
  • C. 50 μmol/L within 72 hours
  • D. 100 μmol/L within 7 days
Answer: B — KDIGO defines AKI as serum creatinine rise ≥26.5 μmol/L within 48 hours, OR ≥1.5× baseline within 7 days, OR UO <0.5 mL/kg/h for ≥6 hours.
2. A patient with AKI Stage 3 has a urine output criterion of:
  • A. <0.5 mL/kg/h for 6–12 hours
  • B. <0.5 mL/kg/h for ≥12 hours
  • C. <0.3 mL/kg/h for ≥24 hours or anuria ≥12 hours
  • D. <1.0 mL/kg/h for ≥6 hours
Answer: C — KDIGO Stage 3 UO criterion: <0.3 mL/kg/h for ≥24 hours OR anuria (essentially zero) for ≥12 hours. Stage 1 = 6–12h, Stage 2 = ≥12h at <0.5 mL/kg/h.
3. Which urinary finding is characteristic of Acute Tubular Necrosis (ATN)?
  • A. RBC casts
  • B. WBC casts
  • C. Granular (muddy brown) casts
  • D. Hyaline casts
Answer: C — Granular (muddy brown) casts are the hallmark of ATN — formed from sloughed tubular epithelial cells. RBC casts = glomerulonephritis; WBC casts = pyelonephritis/interstitial nephritis.
4. A urine sodium of 15 mmol/L in a patient with oliguria suggests:
  • A. Intrinsic renal failure (ATN)
  • B. Pre-renal AKI with intact tubular reabsorption
  • C. Post-renal obstruction
  • D. Glomerulonephritis
Answer: B — Urine sodium <20 mmol/L indicates intact tubular function avidly reabsorbing sodium (pre-renal). ATN causes tubular dysfunction → urine sodium >40 mmol/L. FENa <1% also supports pre-renal.
5. Which medication should be WITHHELD in all patients with AKI Stage 1 or above?
  • A. Oral prednisolone
  • B. Low-dose aspirin (75 mg)
  • C. ACE inhibitors (e.g. ramipril)
  • D. Proton pump inhibitors
Answer: C — ACE inhibitors (and ARBs, ARNi, SGLT2-i) should be withheld in AKI as they reduce efferent arteriolar resistance, dropping GFR further. Resume only after AKI resolution under nephrology guidance.
6. The FIRST step in emergency management of hyperkalaemia with broad QRS complexes on ECG is:
  • A. Insulin-dextrose infusion
  • B. Sodium bicarbonate IV
  • C. Calcium gluconate 10% IV
  • D. Salbutamol nebuliser
Answer: C — Calcium gluconate is the first-line treatment when ECG changes are present. It stabilises the cardiac membrane (cardiac protection) within minutes. It does NOT lower potassium — insulin-dextrose follows for transcellular shift.
7. The dialysis indication mnemonic AEIOU includes all of the following EXCEPT:
  • A. Refractory metabolic acidosis
  • B. Uraemic pericarditis
  • C. Hypernatraemia refractory to fluids
  • D. Pulmonary oedema refractory to diuretics
Answer: C — AEIOU = Acidosis, Electrolytes (K+), Intoxications, Overload, Uraemia. Hypernatraemia is not a classic standalone dialysis indication.
8. In CRRT with regional citrate anticoagulation (RCA), the systemic ionised calcium target is:
  • A. 0.25–0.40 mmol/L
  • B. 0.5–0.8 mmol/L
  • C. 1.1–1.3 mmol/L
  • D. 2.0–2.5 mmol/L
Answer: C — Systemic iCa target is 1.1–1.3 mmol/L (normal). Circuit (post-filter) target is 0.25–0.40 mmol/L for anticoagulation. Monitored separately — systemic from CVC/arterial line, circuit from post-filter port.
9. A construction worker in Riyadh presents in July with tea-coloured urine, CK 45,000 U/L, and rising creatinine. The priority nursing intervention is:
  • A. Insert urinary catheter and restrict fluids to 500 mL/day
  • B. Administer aggressive IV fluids targeting UO 200–300 mL/h
  • C. Start haemodialysis immediately
  • D. Administer NSAIDs for muscle pain
Answer: B — Rhabdomyolysis-AKI from heat exposure. Aggressive IV fluids (UO target 200–300 mL/h) flush myoglobin from tubules. NSAIDs absolutely contraindicated. RRT only if refractory.
10. Which USS finding suggests CKD rather than acute AKI?
  • A. Normal kidney size (10–12 cm) with good corticomedullary differentiation
  • B. Bilateral hydronephrosis
  • C. Small, hyperechoic (bright) kidneys bilaterally
  • D. Unilateral renal cyst
Answer: C — Small (<9 cm), hyperechoic kidneys indicate chronic fibrosis → CKD. Normal-sized kidneys support acute AKI. Bilateral hydronephrosis → post-renal obstruction.
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Quick Reference Summary — Key Numbers

ParameterValueClinical Relevance
AKI creatinine rise (48h)≥26.5 μmol/LKDIGO definition criterion 1
AKI creatinine baseline (7d)≥1.5×KDIGO definition criterion 2
AKI urine output threshold<0.5 mL/kg/h × 6hKDIGO definition criterion 3
Stage 3 creatinine absolute≥353.6 μmol/LOr ×3.0 baseline or RRT
Pre-renal urine sodium<20 mmol/LIntact tubular reabsorption
ATN urine sodium>40 mmol/LTubular dysfunction
Pre-renal FENa<1%Avid sodium retention
ATN FENa>2%Tubular cell damage
CRRT effluent dose20–25 mL/kg/hRENAL/RAVE trial recommendation
RCA systemic iCa target1.1–1.3 mmol/LMonitor 4–6 hourly
RCA circuit iCa target0.25–0.40 mmol/LPost-filter sample
Dialysis K+ threshold>6.5 mmol/L refractoryAEIOU indication
Dialysis pH threshold<7.1 refractoryAEIOU indication
AKI → CKD risk25%All AKI need 3-month nephrology follow-up