FORGE CARD #02 — Acute Kidney Injury (AKI)
Medicine › Renal › Acute Kidney Injury
FORGE CARD #02 — Acute Kidney Injury (AKI)
Medicine › Renal › Acute Kidney Injury Yield: ★★★★★ | Frequency: VERY HIGH (Q1+Q3 repeat) | Syllabus: Renal-AKI/CKD
🔑 ONE-LINE ANSWER
AKI discrimination hinges on FeNa and urine indices: Pre-renal (FeNa <1%, osmolality >500) = hypoperfusion → give fluids; ATN/Intrinsic (FeNa >2%, osmolality <350, muddy brown casts) = tubular damage → stop nephrotoxins, support; Post-renal = obstruction → relieve obstruction. Hyperkalemia with ECG changes → IV calcium gluconate FIRST (membrane stabilization), then shift K+, then remove K+ (dialysis if anuric).
🎯 EXAM ATTACK MAP
How the NRE tests this:
- Pattern 1: Oliguria + dehydration + elevated urea/Cr → “Most likely cause?” → Pre-renal AKI → FeNa <1% confirms
- Pattern 2: Patient on aminoglycosides/contrast → rising Cr → ATN → muddy brown granular casts, FeNa >2%
- Pattern 3: Elderly male + anuria alternating with polyuria + suprapubic mass → Post-renal → hydronephrosis on ultrasound
- Pattern 4: CKD patient + K+ 6.8 + peaked T waves + widened QRS → “Immediate management?” → IV calcium gluconate
- Pattern 5: Transplant patient + rising creatinine → biopsy before blind treatment escalation
Favorite disguise: “Pre-renal” vs “ATN” in a patient with sepsis — both can coexist. The NRE tests whether you can use urine indices to distinguish them. Also: a patient on diuretics (which raise FeNa) — FeNa may be falsely elevated; use FEurea instead.
Classic distractor: “Start dialysis immediately” for hyperkalemia — calcium gluconate must come FIRST to stabilize the cardiac membrane. Dialysis is definitive but takes time to arrange.
What discrimination rewards: The ability to use urine indices (FeNa, osmolality, casts) to classify AKI, AND the emergency sequence for hyperkalemia (calcium → shift → remove).
📋 CORE CONCEPT — MUST KNOW
AKI Classification — The Discriminator Table
| Parameter | Pre-Renal | ATN (Intrinsic) | Post-Renal |
|---|---|---|---|
| Cause | Hypoperfusion (dehydration, shock, CHF) | Ischemia/nephrotoxin (aminoglycosides, contrast, rhabdo, myelo) | Obstruction (BPH, stones, tumour, stricture) |
| FeNa | < 1% | > 2% | Variable |
| Urine osmolality | > 500 mOsm/kg | < 350 mOsm/kg | Variable |
| BUN/Cr ratio | > 20:1 | < 15:1 | Variable |
| Urine sediment | Hyaline casts | Muddy brown granular casts | Normal or RBCs |
| Response to fluids | Improves promptly | No improvement | — |
| Key clue | History of volume loss | Nephrotoxin exposure, prolonged ischemia | Anuria alternating with polyuria, suprapubic fullness |
Hyperkalemia — Emergency Management (ECG Changes Present)
| Step | Action | Mechanism | Key Point |
|---|---|---|---|
| 1. FIRST | IV Calcium Gluconate (or calcium chloride) | Stabilizes cardiac membrane | Does NOT lower K+. Protects heart. Give within minutes. |
| 2. THEN | Shift K+ into cells | Temporary reduction | IV Insulin + Dextrose (10 U regular + 50 mL D50), ± B2-agonist nebulization, ± NaHCO3 (if acidosis) |
| 3. DEFINITIVE | Remove K+ from body | Permanent reduction | Hemodialysis (if anuric/severe) OR Kayexalate (if not anuric) |
Hyperkalemia ECG Progression
Peaked T waves → widened QRS → sine wave → VF/cardiac arrest
- Peaked T waves = earliest sign
- Widened QRS = imminent danger → calcium NOW
- Sine wave = pre-arrest → calcium + emergent dialysis
Dialysis Indications — AEIOU
| Letter | Indication | Example |
|---|---|---|
| A | Acidosis | Refractory metabolic acidosis, pH < 7.1 |
| E | Electrolytes | Severe hyperkalemia refractory to medical therapy |
| I | Intoxication | Lithium, methanol, ethylene glycol, aspirin |
| O | Overload | Pulmonary edema refractory to diuretics |
| U | Uremia | Pericarditis, encephalopathy, bleeding |
CKD-MBD (Renal Osteodystrophy) — The Pathway
↓ 1α-hydroxylase → ↓ Calcitriol → ↓ intestinal Ca absorption → ↓ serum Ca → ↑ PTH (secondary hyperparathyroidism) → osteitis fibrosa cystica
| Parameter | Finding |
|---|---|
| Calcium | LOW |
| Phosphate | LOW (PTH causes phosphaturia in early secondary HPT) |
| PTH | HIGH |
| Calcitriol | LOW |
| Alkaline Phosphatase | HIGH |
Drug Contraindications in CKD
| Drug | Threshold | Risk |
|---|---|---|
| Metformin | Contraindicated if eGFR < 30; reduce dose if eGFR 30-45 | Lactic acidosis |
| NSAIDs | Avoid in all CKD | Nephrotoxicity, Na/water retention |
| Sulfonylureas | Avoid in CKD | Hypoglycemia (accumulation) |
⚠️ TRAP FIELD — ERROR SHIELD
❌ Trap 1: Kayexalate or insulin+dextrose as FIRST step in hyperkalemia with ECG changes
✅ Reality: Calcium gluconate is ALWAYS first if ECG changes present. It stabilizes the cardiac membrane within minutes. Insulin/dextrose and Kayexalate take 15-30 minutes. The heart needs immediate protection before K+ is lowered.
❌ Trap 2: Choosing dialysis before calcium in hyperkalemia
✅ Reality: Dialysis is definitive K+ removal but takes time to arrange. Calcium stabilizes the membrane immediately. Sequence: Calcium → shift → then dialysis. Calcium buys time for dialysis to be arranged.
❌ Trap 3: Treating lab labels as isolated facts instead of syndrome recognition
✅ Reality: AKI is a clinical syndrome. A patient with diarrhea + oliguria + elevated Cr is pre-renal — don’t get lost in the numbers. The history (volume loss, nephrotoxin, obstruction) guides the diagnosis. FeNa confirms what the history suggests.
❌ Trap 4: FeNa is always reliable
✅ Reality: Diuretics (furosemide, thiazides) increase FeNa by blocking Na+ reabsorption — FeNa may be >1% even in true pre-renal AKI. In diuretic-treated patients, use FEurea (fractional excretion of urea) instead — <35% suggests pre-renal.
❌ Trap 5: Renal osteodystrophy = hypercalcemia
✅ Reality: Secondary hyperparathyroidism in CKD causes hypocalcemia (from low calcitriol), NOT hypercalcemia. Hypercalcemia suggests primary hyperparathyroidism or tertiary HPT. CKD = low Ca, high PO4, high PTH, low vit D.
🧠 MEMORY ANCHOR
“C-S-R” for Hyperkalemia Emergency:
- Calcium FIRST (membrane stabilization)
- Shift K+ with insulin/dextrose (temporary)
- Remove K+ with dialysis/Kayexalate (definitive)
“MUD” for ATN diagnosis:
- Muddy brown granular casts
- Urine osmolality < 350 (can’t concentrate)
- Diuretic-confounded? Use FEurea
“AEIOU” for dialysis indications (already a classic — keep it)
“LOW Ca, HIGH PTH” for renal osteodystrophy:
- Low calcium
- Osteitis fibrosa cystica
- Wasted bone
- PTH high
- High ALP
🏥 CLINICAL REASONING TRIGGER
“When you see oliguria + dehydration + elevated urea/Cr, think pre-renal AKI. The discriminator is FeNa <1% and urine osmolality >500. Give fluids — it’s reversible.”
“When you see a patient on aminoglycosides or after contrast with rising Cr + muddy brown granular casts, think ATN. The discriminator is FeNa >2% and response to fluids = none. Stop nephrotoxins, support.”
“When you see hyperkalemia + peaked T waves ± widened QRS, immediately give IV calcium gluconate. The discriminator is ECG changes = membrane instability. Calcium first, always.”
“When you see CKD + bone pain + low Ca + high PO4 + high PTH, think renal osteodystrophy (secondary hyperparathyroidism). The discriminator is the calcitriol deficiency pathway.”
🔗 CROSS-LINKS
→ CKD — AKI can progress to CKD; CKD complications (anemia, bone disease, hypertension) → Electrolytes (Acid-Base) — Metabolic acidosis in AKI/CKD; anion gap calculation → Heart Failure — Cardiorenal syndrome (pre-renal AKI from low cardiac output) → Rhabdomyolysis — Cause of intrinsic AKI (myoglobinuric ATN); CK elevated, dark urine → Diabetic Nephropathy — Microalbuminuria → ACEi; progression to CKD → Transplant Medicine — Rising creatinine post-transplant → biopsy before blind treatment
⚡ RAPID FIRE
Q1. A 27-year-old man with 3 days of diarrhea and vomiting presents oliguric, dehydrated, BP 90/60, urea 110, Cr 5.2. Urine osmolality is 580 mOsm/kg, FeNa is 0.5%. What is the most likely cause of AKI?
- A) Acute tubular necrosis
- B) Pre-renal AKI
- C) Post-renal AKI
- D) Glomerulonephritis
- E) Interstitial nephritis
→ Answer: B | Why: History of volume loss (diarrhea/vomiting) + FeNa <1% + urine osmolality >500 = pre-renal AKI from hypoperfusion. The kidneys are intact but underperfused. Give fluids.
Q2. A 65-year-old man with CKD stage 4 presents with K+ 6.8, peaked T waves, and widened QRS on ECG. What is the most appropriate immediate management?
- A) IV insulin + dextrose
- B) Sodium bicarbonate
- C) IV calcium gluconate
- D) Emergency hemodialysis
- E) Kayexalate (sodium polystyrene sulfonate)
→ Answer: C | Why: Hyperkalemia with ECG changes (peaked T waves + widened QRS) = membrane instability. IV calcium gluconate stabilizes the cardiac membrane FIRST. It does NOT lower K+ but protects the heart while definitive therapy is arranged.
Q3. A 70-year-old man presents with anuria alternating with polyuria, suprapubic fullness, and elevated creatinine. Renal ultrasound shows bilateral hydronephrosis. What is the most appropriate next step?
- A) IV fluid bolus
- B) Furosemide
- C) Relieve obstruction (catheterization)
- D) Hemodialysis
- E) Renal biopsy
→ Answer: C | Why: Anuria alternating with polyuria + suprapubic fullness + bilateral hydronephrosis = post-renal AKI from obstruction (likely BPH). The treatment is to relieve the obstruction (urethral catheter). This is reversible if treated promptly.
Q4. A 55-year-old woman with CKD has bone pain, fractures, low Ca, high PO4, and elevated PTH. What is the underlying mechanism?
- A) Primary hyperparathyroidism
- B) Vitamin D deficiency from malnutrition
- C) Secondary hyperparathyroidism from low calcitriol
- D) Pseudohypoparathyroidism
- E) Hyperthyroidism
→ Answer: C | Why: CKD → ↓ 1α-hydroxylase → ↓ calcitriol → ↓ Ca → ↑ PTH (secondary hyperparathyroidism). The pathway is: low calcitriol → low calcium → high PTH → renal osteodystrophy. Primary HPT (A) would have HIGH calcium.
✓ CONFIDENCE CHECK
“Can I classify AKI using urine indices, manage hyperkalemia in the correct sequence, and explain renal osteodystrophy to a peer in 60 seconds?”
Rate: ☆☆☆☆☆
If you hesitated on any zone, revisit that section before moving on.
Source evidence: NRE Dec 2025 recalled paper, NRE May 2026 Intelligence Report (177 MCQs), NRE50 System (Q1+Q3 repeat), MedCORE Day 33 AKI CKD, MedCORE Premium Renal, QBank Q30/Q34/Q44/Q80/Q188.