✅ Model Answer:
• Diagnosis: Prerenal acute kidney injury (AKI) due to dehydration — elevated serum creatinine (1.2 mg/dL), elevated BUN (45 mg/dL), BUN/Cr ratio >20 (37), concentrated urine (osmolality 560 mOsm/kg). History of vomiting, diarrhea, decreased urine output, and clinical signs of dehydration (dry mucous membranes, sunken eyes).
• Any other test: Serum electrolytes (Na, K, Cl, CO2), blood gas (if acidosis), urine sodium (should be <20 mEq/L in prerenal), FENa (<1% in prerenal), urine culture (if UTI suspected).
• What to do next: IV normal saline bolus (20 mL/kg) over 1-2 hours. Reassess volume status and urine output. If no response, repeat bolus. Monitor urine output, electrolytes, and creatinine.
• Follow-up plan: Daily creatinine until baseline. Rehydrate slowly over 24-48h. Monitor for hyperkalemia if oliguria persists. Treat underlying gastroenteritis. Ensure adequate oral intake once able.

✅ Model Answer:
• Prerenal AKI is caused by decreased renal perfusion without intrinsic kidney damage.
• Common causes:
- Dehydration: Gastroenteritis (vomiting, diarrhea), inadequate fluid intake, excessive sweating.
- Hemorrhage: Trauma, GI bleeding, surgery.
- Sepsis: Systemic vasodilation → decreased effective circulating volume.
- Cardiac causes: Congestive heart failure, pericarditis, cardiomyopathy (decreased cardiac output).
- Nephrotic syndrome: Hypovolemia due to fluid shifts.
- Burns: Fluid loss from skin.
- Third spacing: Ascites, pancreatitis, peritonitis.
- Drugs: NSAIDs, ACE inhibitors (affect renal perfusion).
- Hepatic failure: Hepatorenal syndrome.

✅ Model Answer:
• Key differentiating features:
- Prerenal AKI:
• BUN/Cr ratio: >20
• Urine sodium: <20 mEq/L
• FENa: <1%
• Urine osmolality: >500 mOsm/kg
• Urinalysis: Normal (no casts, no proteinuria)
• Response to fluids: Rapid improvement
• Intrinsic renal AKI (ATN):
• BUN/Cr ratio: 10-20
• Urine sodium: >40 mEq/L
• FENa: >2%
• Urine osmolality: <350 mOsm/kg
• Urinalysis: Muddy brown casts, proteinuria
• Response to fluids: No improvement
• Clinical pearl: FENa (fractional excretion of sodium) is the most reliable test to differentiate prerenal from intrinsic AKI.

✅ Model Answer:
• FENa (Fractional Excretion of Sodium): A measure of kidney sodium handling, calculated as:
- FENa = (Urine Na / Plasma Na) / (Urine Cr / Plasma Cr) × 100%
• Interpretation:
- FENa <1%: Prerenal AKI (kidneys are conserving sodium).
- FENa >2%: Intrinsic renal AKI (acute tubular necrosis, glomerulonephritis).
- FENa 1-2%: May be seen in prerenal AKI with diuretic use, or early intrinsic AKI.
• Limitations:
- May be unreliable in patients on diuretics (increase FENa).
- May be unreliable in neonates (FENa can be >1% normally).
- In acute GN, FENa is typically <1%.
- In contrast-induced nephropathy, FENa is low.
• Alternative: FEurea (fractional excretion of urea) can be used if FENa is unreliable.

✅ Model Answer:
• Fluid resuscitation:
- IV normal saline (0.9% NS): 20 mL/kg bolus over 1-2 hours (repeat if needed).
- Maintenance fluids: Calculate deficit and replace over 24-48 hours.
- Monitor: Urine output (target >1 mL/kg/h), vital signs, weight.
• Electrolyte monitoring:
- Hyperkalemia: If oliguria persists, monitor K+ (ECG if elevated).
- Hyponatremia: Correct slowly to avoid osmotic demyelination.
- Acidosis: May require bicarbonate if pH <7.2.
• Avoid:
- Nephrotoxic drugs (NSAIDs, aminoglycosides).
- Contrast agents (if possible).
• Indications for dialysis: Severe hyperkalemia, refractory acidosis, pulmonary edema, uremic symptoms.

✅ Model Answer:
• Complications:
- Progression to intrinsic AKI: Prolonged renal hypoperfusion → acute tubular necrosis (ATN).
- Hyperkalemia: Can cause cardiac arrhythmias (peaked T waves, widened QRS).
- Metabolic acidosis: Due to decreased acid excretion.
- Pulmonary edema: If fluid overload develops (iatrogenic).
- Hyponatremia: If free water is given.
- Uremia: Accumulation of nitrogenous wastes → nausea, vomiting, confusion.
- Hypocalcemia: Due to decreased vitamin D activation.
- Hyperphosphatemia: Due to decreased excretion.
- Death: Rare in children, but possible if untreated (severe dehydration, shock).

✅ Model Answer:
• Urine output: A key parameter in the diagnosis and monitoring of AKI.
• KDIGO criteria for AKI:
- Stage 1: Oliguria <0.5 mL/kg/h for 6-12 hours.
- Stage 2: Oliguria <0.5 mL/kg/h for >12 hours.
- Stage 3: Oliguria <0.3 mL/kg/h for >24 hours, or anuria for >12 hours.
• Monitoring:
- Hourly: In critically ill patients (Foley catheter).
- Daily: In less severe cases (24-hour urine collection).
- Goal: Maintain urine output >1 mL/kg/h.
• Non-oliguric AKI: Some patients have normal urine output despite renal dysfunction (better prognosis).
• Anuria: Complete absence of urine output — suggests severe injury or obstruction.

✅ Model Answer:
• Prognosis:
- Excellent: With prompt volume repletion, renal function returns to baseline within 48-72 hours.
- Complete recovery: No long-term renal impairment (if treated early).
- If untreated: May progress to intrinsic AKI (ATN) with delayed recovery.
- Mortality: Very low in children (usually from underlying cause, not AKI).
• Long-term follow-up:
- Monitor creatinine: Until baseline is achieved.
- Monitor for recurrence: If underlying cause persists (e.g., ongoing gastroenteritis).
- Avoid nephrotoxins: NSAIDs, aminoglycosides, contrast agents.
- Education: Teach parents to recognize early signs of dehydration.
- No long-term monitoring is usually needed if full recovery occurs.