K KDIGO Definition of AKI

AKI is defined by ANY ONE of the following criteria (KDIGO 2012, reaffirmed 2023):

Clinical PearlA single creatinine value is insufficient. Trend matters. Always establish the patient's baseline creatinine (prior bloods, CKD history, or estimated from age/sex/race using CKD-EPI).

S KDIGO Staging — Creatinine Criteria

StageSerum Creatinine CriterionUrine Output CriterionSeverity
Stage 1 ×1.5–1.9 baseline or +0.3 mg/dL within 48 h <0.5 ml/kg/h for 6–12 h Mild
Stage 2 ×2.0–2.9 baseline <0.5 ml/kg/h for ≥12 h Moderate
Stage 3 ×3.0 baseline or Cr >4.0 mg/dL or initiation of RRT <0.3 ml/kg/h for ≥24 h or anuria ≥12 h Severe
ImportantStage is determined by the HIGHER of creatinine OR urine output criteria. Never down-stage just because one criterion is better.

P Pre-Renal AKI

Causes

  • Hypovolaemia: haemorrhage, vomiting, diarrhoea, burns
  • Dehydration (especially heat-related in GCC summers)
  • Heart failure / cardiogenic shock
  • Hepatorenal syndrome
  • Sepsis-related vasodilation
  • Excessive diuresis
  • Bilateral renal artery stenosis (ACEi/ARB precipitant)
Typically reversible with volume replacement and haemodynamic optimisation.

I Intrinsic Renal AKI

Causes by Compartment

  • Tubules (ATN): ischaemia (prolonged pre-renal), nephrotoxins (aminoglycosides, contrast, myoglobin)
  • Glomeruli (GN): IgA nephropathy, ANCA vasculitis, lupus nephritis
  • Interstitium (AIN): NSAIDs, penicillins, PPIs, infections
  • Vessels: TTP/HUS, renal vein thrombosis, malignant hypertension
  • Rhabdomyolysis: common in Hajj pilgrims, heat stroke, trauma

O Post-Renal AKI

Causes

  • Benign prostatic hypertrophy (very common in GCC elderly males)
  • Ureteric stones (urolithiasis — high incidence in hot climates)
  • Bladder neck obstruction
  • Pelvic malignancy compressing ureters
  • Retroperitoneal fibrosis
  • Blocked urinary catheter

Nursing Action

  • Always check catheter patency first — flush or replace
  • Bladder scan if no catheter: retention >300 ml requires catheterisation
  • Urgent renal ultrasound to exclude hydronephrosis
  • Urology referral if structural obstruction identified
Post-renal AKI is the most immediately reversible — always exclude obstruction first.

L GFR vs Creatinine — Limitations

Creatinine Limitations

  • Affected by muscle mass — low in elderly, malnourished, amputees
  • Rises late — 50% GFR loss before significant Cr rise
  • Falsely elevated by some drugs (trimethoprim, cimetidine)
  • Not reliable in acute changes — steady state takes 24–72h
  • Ethnicity adjustments required (race-free CKD-EPI now preferred)

Novel Biomarkers

  • Cystatin C: less muscle-dependent, earlier rise in AKI
  • NGAL: rises within 2h of kidney injury
  • KIM-1: tubular injury marker
  • TIMP-2 × IGFBP7: predicts AKI 12h in advance (NephroCheck)
In critically ill patients with low muscle mass (common in GCC ICUs), normal creatinine does NOT exclude significant AKI.

B BMP / Renal Panel Interpretation

TestNormal RangeAKI Significance
Serum Creatinine0.6–1.2 mg/dL (men); 0.5–1.1 (women)Rises with falling GFR; compare to baseline
BUN (Urea)7–20 mg/dLBUN:Cr ratio >20:1 suggests pre-renal
eGFR≥90 ml/min/1.73m²Not reliable in acute AKI — use trend
Potassium3.5–5.0 mmol/LRises in AKI — monitor 4–6 hourly in Stage 2–3
Bicarbonate22–28 mmol/LFalls (metabolic acidosis) in moderate-severe AKI
Phosphate0.8–1.5 mmol/LRises in AKI; can worsen cardiac function
Magnesium0.7–1.0 mmol/LOften low — replete carefully (renal clearance)
Haemoglobin120–160 g/LDilutional or haemolytic anaemia in AKI

U Urine Microscopy Findings

FindingDiagnosis Suggests
Muddy brown granular castsATN (ischaemic or toxic)
RBC castsGlomerulonephritis (GN)
WBC castsPyelonephritis / Interstitial Nephritis (AIN)
Hyaline castsNon-specific, concentrated urine, dehydration
Waxy / broad castsAdvanced CKD or severe AKI
Free fat droplets / oval fat bodiesNephrotic syndrome
EosinophiluriaAIN (drug-induced — NSAIDs, antibiotics)
Myoglobin (dipstick blood, no RBCs)Rhabdomyolysis
Urine dipstick showing blood with no RBCs on microscopy = haemoglobin or myoglobin. Check CK urgently.

O Urine Chemistry

Urine Osmolality

  • >500 mOsm/kg = kidneys concentrating = pre-renal
  • <350 mOsm/kg = fixed dilute urine = intrinsic (ATN)
  • Isosthenuria (~300) = tubular dysfunction

Urine Sodium

  • <20 mmol/L = avid Na reabsorption = pre-renal
  • >40 mmol/L = tubular injury = ATN

Urine Specific Gravity

  • >1.020 = concentrated = pre-renal
  • 1.010 (isosthenuria) = ATN
Diuretics invalidate urine sodium interpretation — use FeNaurea instead.

FeNa Calculator — Fractional Excretion of Sodium

Formula: FeNa = (Urine Na × Plasma Cr) / (Plasma Na × Urine Cr) × 100

R Renal Ultrasound Findings

Normal

  • Kidney length 10–12 cm
  • Cortical thickness ≥7 mm
  • No hydronephrosis
  • Corticomedullary differentiation present

Pre-Renal

  • Usually normal ultrasound; possible small echogenic kidneys in CKD-AKI

Post-Renal (obstruction)

  • Hydronephrosis (dilated renal pelvis)
  • Hydroureter if ureteric obstruction
  • Enlarged prostate on bladder scan
  • Residual bladder volume >300 ml

Intrinsic

  • Increased cortical echogenicity (nephritis/fibrosis)
  • Small kidneys (<9 cm) = CKD
  • Normal or enlarged in acute GN / infiltrative disease

F Fluid Resuscitation in AKI

When to Give Fluid

  • Pre-renal AKI with signs of hypovolaemia
  • Septic AKI — initial 30 ml/kg crystalloid (first 3 hours)
  • Rhabdomyolysis — aggressive hydration (target UO 200–300 ml/h)
  • Contrast-induced nephropathy prevention
  • Haemorrhagic shock

Fluid of Choice

  • Balanced crystalloids preferred (Hartmann's / Plasmalyte)
  • 0.9% NaCl causes hyperchloraemic acidosis — use cautiously
  • Colloids (albumin) for hypoalbuminaemia (<20 g/L)
  • Avoid HES (hydroxyethyl starch) — increases AKI and mortality

Fluid Overload Risk

  • Fluid overload independently worsens AKI prognosis
  • >10% weight gain = significant overload
  • Signs: oedema, raised JVP, pulmonary crackles, SpO2 falling
  • CVP not reliable guide to fluid responsiveness
STOP Fluids If: No response to 2 fluid challenges, rising CVP/worsening oedema, or fluid balance >+3L. Consider early vasopressor or diuretic therapy.

Dynamic Fluid Responsiveness Tests

  • Passive Leg Raise (PLR) + CO measurement
  • Pulse Pressure Variation (PPV) >13% on ventilator
  • Stroke Volume Variation (SVV) >10%

U Urine Output Targets & Monitoring

Clinical StateUO TargetAction if Below Target
General ICU patient≥0.5 ml/kg/hAssess volume status, consider fluid challenge
Rhabdomyolysis200–300 ml/hAggressive IV fluids; consider sodium bicarb to alkalinise urine
Post-contrast procedure≥150 ml/h for 6 h postIV fluid bolus, reassess
Post-cardiac surgery≥1 ml/kg/h for first 4 hFluid challenge, low-dose dopamine not recommended
AKI Stage 3 / anuricMonitor for response to treatmentInitiate RRT discussion early
Hourly urine output charting is mandatory in Stage 2–3 AKI. Ensure catheter is patent. Document catheter flushes.

V Vasopressor Support in AKI

Noradrenaline (Norepinephrine) — First Line

  • Target MAP ≥65 mmHg (or ≥75–80 in CKD patients)
  • Increases renal perfusion pressure
  • Start: 0.05–0.1 mcg/kg/min, titrate to MAP
  • Via central venous catheter only
  • Monitor for digital/mesenteric ischaemia at high doses

Vasopressin — Adjunct

  • 0.03 units/min fixed dose as noradrenaline-sparing
  • May reduce AKI progression in vasodilatory shock

Dopamine

  • Renal-dose dopamine NOT recommended — no benefit in AKI prevention
  • May worsen splanchnic ischaemia

MAP Targets by Condition

  • Septic shock: MAP ≥65 mmHg
  • Chronic hypertension: MAP ≥75–80 mmHg
  • Post-cardiac surgery: MAP ≥70 mmHg
  • TBI with AKI: MAP ≥80 mmHg (ICP consideration)
Hypotension (MAP <60) for even 20 minutes increases AKI risk 3-fold. Time-to-vasopressor matters.

N Nephrotoxin Avoidance

NephrotoxinMechanismPrevention / Alternative
NSAIDs (ibuprofen, diclofenac)Reduce prostaglandin-mediated afferent arteriolar dilationUse paracetamol; STOP NSAIDs in AKI
Aminoglycosides (gentamicin, amikacin)Proximal tubule accumulation, free radical injuryOnce-daily dosing; trough levels; use alternatives if possible
VancomycinTubular toxicity, especially with piperacillin-tazobactamTarget AUC/MIC 400–600; avoid vanco + pip-tazo combo
ACE inhibitors / ARBsReduce efferent arteriole tone → drop GFRHOLD in acute AKI or severe volume depletion
IV Contrast (iodinated)Direct tubular toxicity + vasoconstrictionIso-osmolar contrast + IV fluid pre-load + NAC (see below)
Amphotericin BTubular and vascular toxicityLiposomal formulation; ensure hydration
MetforminLactic acidosis if GFR <30HOLD if eGFR <30 or during contrast/acute illness

C Contrast-Induced Nephropathy (CIN) Prevention

Risk Factors for CIN

  • CKD (eGFR <60 ml/min)
  • Diabetes mellitus with nephropathy
  • Volume depletion / haemodynamic instability
  • High contrast volume (>100 ml)
  • Multiple contrast exposures within 72 h
  • Concomitant nephrotoxins (NSAIDs, diuretics)
  • Myeloma (light chain nephropathy)

Prevention Protocol

  • IV Fluid Pre-load: 0.9% NaCl or sodium bicarbonate 1–1.5 ml/kg/h for 3–12 h pre-procedure
  • Continue IV fluids 1 ml/kg/h for 6–12 h post-procedure
  • N-Acetylcysteine (NAC): 600–1200 mg PO BD day before + day of (evidence modest but safe)
  • Iso-osmolar contrast preferred (iodixanol > iopamidol > ionic high-osmolar)
  • Minimise contrast volume — discuss with radiologist
  • HOLD metformin 48 h pre- and post-contrast if eGFR <45
  • Recheck creatinine 24–48 h post-procedure
GCC Context: High coronary angiography rates in GCC countries (high CAD prevalence) mean CIN prevention is a common nursing responsibility in cardiac units.

K Hyperkalaemia — ECG Changes by K+ Level

ECG changes are not always linear — act on clinical context, not ECG alone.

K+ <5.5
Normal / Baseline — no significant ECG changes expected
K+ 5.5–6.0
Peaked (tall, narrow) T-waves — earliest sign; most prominent in V2–V5 and II
K+ 6.0–6.5
PR interval prolongation (>200 ms); P-wave flattening begins
K+ 6.5–7.0
P-wave disappears; widening of QRS (>120 ms); junctional/idioventricular rhythm
K+ >7.0
Sine-wave pattern — QRS merges with T-wave; precursor to VF/VT. EMERGENCY.
K+ >7.5–8.0
Ventricular fibrillation / Cardiac arrest — immediate defibrillation + calcium + dialysis
GCC Defibrillator Note: In GCC ICUs, biphasic defibrillators are standard. For hyperkalaemic VF: charge to 200J biphasic (360J if monophasic). Ensure AED/defibrillator is at bedside for K+ >7.0. Concurrent calcium and insulin infusion while defibrillating.

T Hyperkalaemia Treatment Algorithm

Step 1: Cardiac Membrane Stabilisation

Does NOT lower K+ — protects the heart NOW

  • Calcium Gluconate 10% — 10 ml (1g) IV over 2–3 min
  • Repeat after 5 min if ECG unchanged
  • Onset: 1–3 minutes; Duration: 30–60 min
  • Monitor ECG continuously during infusion
  • Can also use Calcium Chloride 10% (3× more elemental Ca²⁺) — central line preferred
  • Caution: Digoxin toxicity (use 100 ml 10% over 20–30 min)

Step 2: K+ Redistribution (Into Cells)

Lowers plasma K+ within 15–30 min — buys time

  • Insulin + Dextrose: 10 units Actrapid in 50 ml 50% dextrose IV over 15–30 min (lowers K+ ~1 mmol/L; monitor BGL 30-60 min)
  • Salbutamol Nebuliser: 10–20 mg in 4 ml 0.9% NaCl via nebuliser (lowers K+ ~0.5–1 mmol/L; additive with insulin)
  • Sodium Bicarbonate: 50–100 mmol IV (mainly useful if severe metabolic acidosis — modest K+ lowering effect alone)

Step 3: K+ Elimination (From Body)

Definitively removes K+ — essential for sustained control

  • Calcium Resonium (Resonium-A): 15 g PO or 30 g PR in sorbitol; onset 4–6 h; GI side effects
  • Patiromer (Veltassa): 8.4–25.2 g PO daily — newer, better tolerated, avoid in ileus
  • Sodium Zirconium Cyclosilicate: 10 g PO TDS — rapid onset ~1h
  • Furosemide: 40–80 mg IV if residual renal function present
  • Dialysis (IHD or CRRT): most effective; use in refractory hyperkalaemia or oligo-anuric AKI

M Hyperkalaemia Monitoring Protocol

K+ LevelFrequency of MonitoringEscalation
5.1–5.5 mmol/L (mild)Every 4–6 hours; low K+ dietReview K+-sparing drugs; dietary restriction
5.6–6.0 mmol/L (moderate)Every 2–4 hours; 12-lead ECGStart K+ elimination; notify physician; establish IV access
6.1–6.9 mmol/L (severe)Continuous ECG; repeat K+ every 1–2 hCalcium gluconate STAT; insulin/dextrose; emergency dialysis plan
≥7.0 mmol/L (critical)Continuous cardiac monitoring; ICUImmediate calcium; emergency IHD/CRRT; crash call team
Haemolysed samples give falsely HIGH K+. Repeat immediately in a new sample before treating — but do NOT delay treatment if ECG changes are present.

R Indications for RRT in AKI

Absolute Indications (AEIOU)

  • Acidosis — pH <7.1 refractory to treatment
  • Electrolytes — K+ >6.5 refractory, or severe hyponatraemia
  • Intoxication — dialysable toxins (salicylates, methanol, lithium, ethylene glycol)
  • Overload — fluid overload refractory to diuretics, pulmonary oedema
  • Uraemia — uraemic encephalopathy, pericarditis, platelet dysfunction (BUN >100–120 mg/dL)

Timing of RRT

  • No proven benefit to early vs late RRT in trials (STARRT-AKI, IDEAL-ICU)
  • Initiate when above indications present
  • Do not delay for absolute indications
  • Consider early if AKI not recovering after 48–72 h of conservative management
Nephrology/Intensivist discussion for RRT initiation required in all GCC centres. Document time of referral and decision.

D IHD vs CRRT — Modality Selection

FeatureIHD (Intermittent)CRRT (Continuous)
Duration3–5 h sessions, 3–7×/week24 h/day continuous
Haemodynamic stabilityRequires stable MAP >70Preferred for unstable patients
Solute clearanceEfficient small solutes rapidlySlower but continuous — better for cytokines
Fluid removalRapid (can cause hypotension)Gentle, continuous (better tolerated)
Brain oedema / ICPRisk of dialysis disequilibriumPreferred in TBI, hepatic encephalopathy
AnticoagulationHeparin during sessionSystemic heparin or regional citrate
Nursing requirementRenal/dialysis nurse per sessionContinuous ICU nurse monitoring
CostLowerHigher (consumables, fluids)

C CRRT Modalities

CVVH

Continuous Veno-Venous Haemofiltration

  • Convection only (no dialysate)
  • Replacement fluid pre- or post-filter
  • Good for large molecule clearance
  • Pre-dilution: less filter clotting but lower efficiency
  • Post-dilution: more efficient but filter clots faster

CVVHD

Continuous Veno-Venous Haemodialysis

  • Diffusion only (dialysate, no replacement fluid)
  • Better small solute clearance (urea, creatinine)
  • Used when primarily solute clearance needed

CVVHDF

Continuous Veno-Venous Haemodiafiltration

  • Convection + diffusion combined
  • Most common modality in GCC ICUs
  • Superior clearance across molecular weight spectrum
  • Standard dose: 20–25 ml/kg/h effluent
  • Prescribe 25 ml/kg/h to achieve delivered 20 ml/kg/h
Effluent Dose: Delivered dose of 20–25 ml/kg/h is evidence-based (ATN trial, RENAL trial). Higher doses do NOT improve outcomes and increase nursing workload.

A Vascular Access for RRT

SiteAdvantagesDisadvantagesRecommendation
Right Internal Jugular (IJ)Low infection risk, direct path to RA, good flow ratesNeck movement restrictionPreferred for medium/long-term
FemoralFastest insertion, compressible, no pneumothorax riskHigh infection risk, patient must lie flat, recirculation if short catheterUse ≥24 cm catheter; fastest access in emergency
Left IJAcceptable alternativeLonger curved path, higher malposition riskSecond choice IJ
SubclavianLower infection, more comfortableAVOID — risk of subclavian stenosis, compromises future AVF creationLast resort only
Use ultrasound guidance for all dialysis catheter insertions. Document in nursing notes: catheter length, blood flow rates achieved, side.

H CRRT Anticoagulation

Unfractionated Heparin (UFH)

  • Most common in GCC ICUs
  • Loading: 1000–2000 units IV bolus
  • Maintenance: 5–15 units/kg/h infusion pre-filter
  • Target: aPTT 45–60 s (systemic) or ACT 180–200 s (circuit)
  • Risk: HIT (heparin-induced thrombocytopenia) — monitor platelets daily
  • Reversal: Protamine sulphate

Regional Citrate Anticoagulation (RCA)

  • Preferred when systemic anticoagulation contraindicated (active bleeding, post-surgery, HIT)
  • Citrate infused pre-filter → chelates Ca²⁺ → prevents clotting in circuit
  • Calcium replaced post-filter to restore systemic Ca²⁺
  • Monitor: ionised Ca²⁺ (circuit <0.35 mmol/L; systemic 1.0–1.2 mmol/L)
  • Citrate accumulation risk in liver failure — monitor base excess, iCa²⁺ ratio

T CRRT Circuit Troubleshooting

Alarm / ProblemLikely CauseNursing Action
Access pressure high (very negative)Access lumen kinked, clotted, against vessel wallReposition patient, flush access, reverse lines temporarily, check catheter position
Return pressure highFilter/circuit clotting, venous lumen blockedCheck entire circuit for clots; prime new circuit if filter TMP >300 mmHg
TMP rising rapidlyFilter clotting — pre-clotting before scheduled changeIncrease pre-dilution replacement fluid ratio; optimise anticoagulation; plan early filter change
Air detector alarmAir in circuit, loose connectionsCheck all connections; do NOT restart until air fully cleared; escalate if persistent
Clotted filter (dark, no flow)Inadequate anticoagulation, prolonged pause, low flowChange entire circuit; review anticoagulation; document filter lifespan (target >24 h)
Blood leak alarmFilter membrane ruptureClamp circuit immediately; discard blood in filter; change filter urgently
Effluent bag fullNormal scheduled exchangeSwap bag quickly, document volume, ensure fluid balance calculation updated
Each circuit change means blood loss (~100–200 ml). Frequent clotting = 300–600 ml/day blood loss. Review anticoagulation and haemoglobin if filter lifespan <12 h.

G AKI Epidemiology in the GCC Region

Heat-Related AKI

  • Summer temperatures exceed 45°C across KSA, UAE, Kuwait, Qatar
  • Outdoor workers (construction, agriculture) at extreme risk
  • Heat stroke: core temp >40°C + neurological dysfunction → AKI in 30–50%
  • Mechanism: dehydration + rhabdomyolysis + direct thermal injury to tubules
  • Management: rapid cooling + aggressive IV fluids (2–3 L/h initially) + close UO monitoring

Diabetic Nephropathy

  • GCC has world's highest diabetes prevalence (20–25% in adults)
  • Diabetic CKD → heightened AKI risk from ANY insult
  • AKI on CKD — distinct from de novo AKI; harder to recover baseline
  • HbA1c >9% = 3× AKI risk post-contrast

Urolithiasis

  • Kidney stone incidence 2–3× higher in GCC vs Europe (heat, dehydration)
  • Bilateral or solitary kidney obstruction → obstructive AKI
  • Renal colic common ED presentation — check creatinine in all cases
  • Urgent urological decompression (stenting or nephrostomy) if bilateral stones + AKI

Contrast-Related AKI (CAG)

  • High rate of coronary angiography (CAG) in GCC due to CAD epidemic
  • Post-CAG AKI protocol should be standard in all GCC cardiac units
  • Pre-hydration, post-hydration, creatinine check at 24–48 h mandatory

H Hajj-Associated AKI

Epidemiology

  • 2+ million pilgrims annually in Makkah (peak Dhul Hijja)
  • Outdoor activities in extreme heat (Mina, Arafat, Muzdalifah)
  • AKI affects 5–15% of hospitalised Hajj patients
  • Rhabdomyolysis is a leading cause — extensive walking, heat, muscle necrosis
  • Crush injuries during crowd events → rhabdomyolysis AKI

Rhabdomyolysis Management

  • CK >5000 IU/L = significant rhabdomyolysis; >10,000 = severe
  • Myoglobin clogs tubules → pigment nephropathy
  • IV fluid resuscitation: target UO 200–300 ml/h until CK falling
  • Urinary alkalinisation (sodium bicarb) — controversial; use if urine pH <6.5
  • Avoid calcium (can precipitate with phosphate released from damaged muscle)

GCC Hospital Preparedness

  • MNGHA, King Abdulaziz Medical City: large AKI cohorts during Hajj season
  • Mobile dialysis units deployed near Hajj sites in Saudi Arabia
  • Triage nurses trained to identify AKI signs in mass casualty settings

Nursing Role During Hajj Season

  • Rapid IV access and fluid resuscitation triage
  • Creatinine + CK + dipstick on all heat-related admissions
  • Hourly UO monitoring on all admitted pilgrims
  • Escalation pathway for dialysis when UO <0.3 ml/kg/h despite fluids
  • Cultural sensitivity — Arabic/Urdu/Bengali language translation

R Ramadan Fasting & CKD/AKI Risk

Physiological Risk

  • 12–16 h fasting including fluid restriction during daylight
  • Dehydration risk highest in summer Ramadan (longer, hotter days)
  • Patients with CKD Stage 3–5 at significant AKI risk if they fast
  • Diabetic nephropathy patients: hypoglycaemia risk + volume depletion
  • Evidence: serum creatinine rises in 20–35% of CKD patients who fast

Nursing Guidance & Referrals

  • Pre-Ramadan nephrology review for all CKD Stage 3b+ patients
  • Discuss individualised risk with patient + religious scholar if needed
  • Medications timing adjustment (BD → Suhoor + Iftar)
  • Hydration strategy: front-load fluids at Iftar and Suhoor
  • Instruct to break fast if: severe thirst, dark urine, dizziness
  • Post-Ramadan creatinine check in all CKD patients
Islamic scholars permit breaking the fast when fasting poses genuine medical danger. Nurses can reassure patients that their religion supports this dispensation (Rukhsa).

N GCC Nephrology Referral Pathways

IndicationUrgencyPathway
AKI Stage 3 or oligo-anuric AKIEmergency (same day)Direct ICU nephrology consult; document time
Refractory hyperkalaemia (>6.5)Urgent (within 1–2 h)Nephrology + ICU co-management
AKI Stage 2 not resolving at 48 hUrgent (same day)Nephrology inpatient consult
AKI on CKD, eGFR <30 pre-admissionRoutine-urgent (within 24 h)Nephrology review; plan for possible dialysis
CKD Stage 4–5 outpatientRoutine (weeks)CKD clinic — UAE: Sheikh Khalifa Medical City; KSA: KAUH, KFSH; Qatar: HMC Nephrology

Key GCC Dialysis Centres

UAE
Cleveland Clinic Abu Dhabi
Tawam Hospital Al Ain
Rashid Hospital Dubai
American Hospital Dubai

Saudi Arabia
King Faisal Specialist Hospital (KFSH)
King Abdulaziz University Hospital
Prince Sultan Cardiac Centre (Riyadh)
MNGHA network hospitals

Qatar / Kuwait / Bahrain
HMC Hamad Medical Corporation (Qatar)
Al Amiri Hospital (Kuwait)
Salmaniya Medical Complex (Bahrain)
Al Jahra Hospital (Kuwait)

KDIGO AKI Staging Calculator

Enter values below to determine AKI stage and priority care actions.

Q Practice MCQs — AKI Nursing Assessment

Click an answer to reveal instant feedback. 10 questions covering key concepts.

Q1. A 68-year-old male with CKD (baseline Cr 1.4 mg/dL) presents post-CABG. Repeat creatinine at 24 h is 2.1 mg/dL. His urine output has been 0.4 ml/kg/h for 10 hours. What is his KDIGO AKI stage?
Q2. You observe muddy brown granular casts on urine microscopy of a patient with AKI following a 6-hour hypotensive episode post-aortic surgery. This finding is most consistent with:
Q3. A patient's K+ is 6.8 mmol/L. ECG shows widened QRS complexes (140 ms) and absent P-waves. What is the FIRST priority intervention?
Q4. FeNa calculation: Urine Na 12 mmol/L, Plasma Na 140 mmol/L, Urine Cr 60 mg/dL, Plasma Cr 2.0 mg/dL. What does this FeNa suggest?
Q5. A Hajj pilgrim is admitted with heat stroke (temp 41.5°C) and CK 18,000 IU/L. Urine dipstick shows 3+ blood but no RBCs on microscopy. The diagnosis and target UO are:
Q6. Which vascular access site is AVOIDED for dialysis catheter insertion due to risk of central vein stenosis compromising future AVF creation?
Q7. A haemodynamically unstable septic patient (MAP 55 on noradrenaline 0.25 mcg/kg/min, K+ 6.2, pH 7.15, anuric for 18 hours) requires RRT. Which modality is preferred?
Q8. Which contrast agent type is recommended for contrast-induced nephropathy prevention in high-risk CKD patients?
Q9. A CKD patient's CRRT filter clots after only 8 hours (target >24 h). The anticoagulation used is citrate. Which parameter confirms adequate circuit anticoagulation?
Q10. A diabetic CKD patient (eGFR 28) wishes to fast Ramadan. As his renal nurse, your most appropriate action is: