CCS Acute Kidney Injury: Floor Management & Workup

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Acute kidney injury (AKI) is one of the most frequently tested CCS cases, appearing as a primary problem or complicating hospitalization for another condition. Examiners expect you to rapidly classify AKI as pre-renal, intrinsic (renal), or post-renal; calculate and interpret FENa; assess volume status; identify and remove nephrotoxins; adjust medication dosing; and recognize when dialysis is necessary. The clinical pearl separating strong candidates is understanding that pre-renal AKI is reversible with volume repletion, while missed post-renal obstruction leads to permanent renal damage. This comprehensive guide covers the complete AKI workup and floor management algorithm.

AKI Definitions and Classification

KDIGO Staging for AKI

AKI is defined as an abrupt (hours to days) increase in serum creatinine or decrease in urine output:

Three-Category Classification

Pre-renal AKI (55-60% of cases):

• Decreased renal perfusion without parenchymal injury

• Causes: Volume depletion (GI losses, hemorrhage, third-spacing), decreased cardiac output (cardiogenic shock, sepsis), renal vasoconstriction (NSAIDs, ACE-I/ARB)

• Urinalysis: Bland (no protein, no casts)

• FENa: <1% (kidney avidly retaining sodium)

• Prognosis: Reversible with volume/perfusion restoration

Intrinsic renal AKI (35-40% of cases):

• Direct renal parenchymal injury

• Subcategories:

◦ Acute tubular necrosis (ATN): Most common; caused by ischemia (prolonged shock) or nephrotoxins (aminoglycosides, cisplatin, rhabdomyolysis, contrast)

◦ Glomerulonephritis (GN): ANCA-associated, post-infectious, lupus

◦ Acute interstitial nephritis (AIN): Drug allergy (beta-lactams, NSAIDs, PPIs), infection, malignancy

◦ Thrombotic microangiopathy (TMA): HUS, TTP, ADAMTS13 deficiency

• Urinalysis: May show hematuria, proteinuria, casts (muddy-brown casts pathognomonic for ATN; RBC casts for GN)

• FENa: >2% (tubules unable to reabsorb sodium; damaged)

• Prognosis: Variable; depends on cause and duration

Post-renal AKI (5-10% of cases):

• Urinary tract obstruction distal to kidney

• Causes: Obstructing stone, stricture, prostate enlargement, malignancy, bladder outlet obstruction

• Presentation: Often oliguric; elevated BUN/Cr ratio

• Prognosis: Usually reversible if obstruction relieved promptly

> Study Tip: AKI classification and differential diagnosis are tested on virtually every renal CCS case. The StudyCCS question bank includes 16+ AKI cases where you must classify, calculate FENa, order appropriate imaging, and manage fluid/medication dosing with real-time feedback.

Comprehensive Workup Algorithm

Initial Labs and Interpretation

Essential:

• Serum creatinine and BUN: Establish baseline (compare to prior values); elevated BUN/Cr ratio (>20) suggests pre-renal or post-renal; ratio <20 suggests intrinsic renal disease

• Electrolytes (Na, K, Cl, HCO3): Hyperkalemia in AKI (especially if acidosis) requires ECG and urgent treatment

• Calcium, phosphate, magnesium: Hyperphosphatemia, hypocalcemia develop; monitor for seizures (hypocalcemia) and arrhythmias (hyperkalemia)

• Complete blood count (CBC): Anemia common (EPO deficiency); elevated WBC suggests infection; platelet count (low in TMA)

• Liver function tests (LFTs): Screen for hepatorenal syndrome (liver disease + AKI)

• Coagulation studies (PT/INR, aPTT): Assess for DIC (associated with sepsis, rhabdomyolysis)

• Urinalysis (UA): Critical for classification

◦ Bland (few casts, no RBC, no WBC) → Pre-renal or post-renal

◦ Muddy-brown casts → ATN

◦ RBC casts, dysmorphic RBC, proteinuria → GN

◦ WBC casts, eosinophiluria, pyuria → AIN

• Urine osmolality: (If calculating FENa not readily available) Urine Osm >500 mOsm/kg suggests pre-renal; <350 suggests intrinsic renal disease

FENa Calculation and Interpretation

Formula:

FENa (%) = (Urine Na × Serum Cr) / (Serum Na × Urine Cr) × 100

Interpretation:

• FENa <1%: Pre-renal physiology (kidney conserving sodium)

• FENa 1-2%: Gray zone; consider clinical context

• FENa >2%: Intrinsic renal disease (tubular dysfunction; sodium wasting)

Caveats:

• If patient on diuretics: FENa unreliable; calculate Fractional Excretion of Urea (FEUa) instead (same interpretation)

• If patient on ACE-I/ARB: FENa may be misleading (can be <1% even with intrinsic disease due to efferent arteriolar vasodilation)

> Practice Alert: FENa calculation and clinical context integration are frequently tested CCS skills. The StudyCCS question bank includes cases where you must interpret FENa in the setting of diuretics, ACE-I use, and mixed pre-renal/intrinsic disease.

Imaging Studies

Bedside ultrasound (first-line to assess volume status and rule out post-renal AKI):

• IVC diameter: >2 cm (low collapsibility) suggests fluid overload; <1.5 cm suggests hypovolemia

• Renal size: Normal 10-12 cm long; small echogenic kidneys suggest chronic kidney disease (CKD), not AKI

• Hydronephrosis: Enlarged collecting system → post-renal AKI; obtain non-contrast CT abdomen/pelvis for obstructing lesion

CT abdomen/pelvis (non-contrast): Definitive for stone obstruction

Renal ultrasound with Doppler: Assess renal artery/vein patency if thrombosis suspected

Volume Status Assessment: The Clinical Anchor

Accurate volume assessment is the cornerstone of pre-renal AKI management.

Clinical Examination

Signs of hypovolemia:

• Orthostatic vital sign changes (SBP drop >20 mmHg with standing)

• Dry mucous membranes, poor skin turgor

• Flat jugular venous pressure (JVP); <2 cm when upright

• Tachycardia (HR >90), tachypnea (RR >20)

• Hypotension (SBP <100)

Signs of hypervolemia:

• Elevated JVP; >6-8 cm when semi-upright

• Peripheral edema (pitting, bilateral), sacral edema (bedridden patients)

• Pulmonary edema (rales on lung exam, dyspnea, orthopnea)

• Weight gain acutely

Signs of euvolemia:

• JVP 4-6 cm

• No edema, lungs clear

• Stable vital signs

Ancillary Assessment Tools

• Daily weights: Most sensitive; acute gain/loss >0.5 kg/day = fluid gain/loss

• Intake and output (I&Os): Track fluid administration, urine, drains, insensible losses

• Ultrasound IVC: <1.5 cm or >50% collapse → hypovolemia; >2 cm without collapse → hypervolemia

Pre-renal AKI Management: Volume Repletion

Assess Deficit and Repletion Strategy

Estimate volume deficit:

• Mild hypovolemia (5% body weight): Elevated BUN/Cr, FENa <1%, mild elevation in creatinine (Cr <2 mg/dL)

• Moderate hypovolemia (10% body weight): Orthostatic changes, significant creatinine elevation

• Severe hypovolemia (≥15% body weight): Shock, oliguria, severe azotemia

Calculate replacement:

• 1 kg = ~1 L fluid loss

• Example: 80 kg patient with 5% deficit = 4 L loss

Fluid Type and Rate

Pre-renal AKI from volume depletion:

• Isotonic crystalloid (0.9% NaCl or Lactated Ringer's): First-line

• Rate: Rapid repletion (250-500 mL/hr) if hemodynamically compromised; slower if stable

• Monitor: Vital signs, urine output (goal >0.5 mL/kg/hr once fluid repletion initiated), creatinine response

Expected response:

• Urine output increases within 1-2 hours of adequate fluid resuscitation

• Creatinine begins declining by 24-48 hours

• Full recovery in 3-7 days if renal perfusion restored

If minimal response to fluid bolus:

• Reassess volume status: May have missed hypervolemia (requires diuretics, not fluids)

• Consider vasopressor support: If cardiogenic shock; add dobutamine or milrinone

• Check cardiac output: Echocardiography if uncertain

Intrinsic Renal AKI Management: Identify and Remove Insult

Acute Tubular Necrosis (ATN)

Management:

1. Remove offending agent: Stop nephrotoxic drugs (aminoglycosides, NSAIDs, cisplatin, ACE-I/ARB if hypotensive)

2. Ensure adequate perfusion: Volume repletion if hypovolemic; vasopressor support if necessary

3. Avoid fluid overload: Patients with ATN often develop oliguria; balance renal protection with overload prevention

4. Hydration in rhabdomyolysis:

◦ Goal urine output: 200-300 mL/hr (aggressive hydration prevents myoglobin precipitation in renal tubules)

◦ Use aggressive IV fluids (LR preferred; avoid potassium-containing fluids due to hyperkalemia risk)

◦ Consider sodium bicarbonate (alkaline urine reduces myoglobin precipitation) if urine pH <6.5

◦ Dialysis if severe hyperkalemia, hyperphosphatemia, or renal failure not resolving

Acute Interstitial Nephritis (AIN)

Management:

1. Identify and remove drug: Beta-lactams, NSAIDs, PPIs most common culprits

2. Corticosteroids: Prednisone 1 mg/kg/day (max 80 mg) × 1-2 weeks, then taper

◦ Most effective if started within 3 weeks of AKI onset

◦ Consider in severe AKI or delayed diagnosis

3. Monitor renal function: Creatinine typically improves within 1-2 weeks once drug removed

4. Avoid NSAIDs and ACE-I/ARB during recovery

Glomerulonephritis (GN) and Vasculitis

Management:

1. Serologic workup: ANCA (c-ANCA for GPA/Wegener, p-ANCA for microscopic polyangiitis), ANA, Anti-GBM, complement levels

2. Urinalysis: RBC casts are pathognomonic

3. Kidney biopsy: If diagnosis unclear or rapid progression; guides immunosuppression

4. Immunosuppression:

◦ Pulse methylprednisolone (1 g IV daily × 3-5 days) followed by oral prednisone taper

◦ Add cyclophosphamide or rituximab for severe/ANCA-positive disease

5. Plasmapheresis: For anti-GBM disease or ANCA-positive with pulmonary hemorrhage

Post-renal AKI Management: Relief of Obstruction

Management:

1. Imaging confirmation: Ultrasound showing hydronephrosis; CT or IVP to identify obstruction

2. Urgent relief:

◦ Ureteral obstruction: Percutaneous nephrostomy (urgent if bilateral obstruction or solitary kidney)

◦ Bladder outlet obstruction: Foley catheter trial; if spontaneous void adequate, discontinue; if not, may need percutaneous suprapubic catheter

◦ Uric acid nephropathy: Aggressive IV hydration + allopurinol/febuxostat to prevent crystal precipitation

3. Prognosis: Usually excellent if obstruction relieved promptly (within days); delayed relief may result in permanent renal scarring

Medication Dosing Adjustments in AKI

Calculate estimated GFR (eGFR) or use creatinine clearance to guide dosing:

Creatinine Clearance (mL/min):

Male: [(140 - age) × weight (kg)] / [72 × serum Cr]

Female: [(140 - age) × weight (kg) × 0.85] / [72 × serum Cr]

Common adjustments:

• eGFR 30-59 mL/min: Reduce dose by 25-50% for renally cleared drugs

• eGFR 15-29 mL/min: Reduce dose by 50-75%

• eGFR <15 mL/min: Contraindicated or require dialysis adjustment

High-risk drugs requiring dose adjustment:

• Antibiotics: Aminoglycosides (gentamicin, tobramycin), fluoroquinolones, trimethoprim, vancomycin (check levels; target trough 15-20 mcg/mL)

• Antivirals: Acyclovir, valacyclovir, oseltamivir

• Anticoagulation: DOAC (apixaban, rivaroxaban, dabigatran), fondaparinux

• Analgesics: NSAIDs (contraindicated in AKI), morphine metabolites accumulate

Drugs contraindicated in AKI:

• ACE-inhibitors and ARBs (worsen renal function in pre-renal AKI; used cautiously in intrinsic AKI)

• NSAIDs

• Metformin (lactic acidosis risk)

• Thiazide diuretics (ineffective; promote volume depletion)

Hyperkalemia Management in AKI

Hyperkalemia (K+ >5.5 mEq/L) is life-threatening and common in AKI.

Immediate Assessment

ECG findings:

• K+ 5.5-6.5: Peaked T-waves

• K+ 6.5-7.5: Prolonged PR, widened QRS, diminished P-wave amplitude

• K+ >8: Sine-wave pattern, asystole risk

Management (if ECG changes present)

1. Calcium gluconate 1-2 amps IV over 2-5 min: Stabilizes cardiac membrane; repeat Q5-10 min if ECG worsening

2. Insulin 10 units IV + Dextrose 25 g (D50) IV: Shifts K+ into cells; effect within 10-20 min, lasts 4-6 hours

3. Albuterol 10-20 mg nebulized: Alternative K+ shift; effect within 30 min

4. Sodium bicarbonate 50-100 mEq IV (1-2 amps): Useful if concurrent acidosis

5. Diuretics (if euvolemic): Furosemide 20-40 mg IV if urine output maintained

6. Cation exchange resin (Kayexalate): PO or PR; slow effect but removes total body K+ (takes 4-24 hours)

7. Dialysis: If medical management fails or K+ >7 with ECG changes

Dialysis Indications: AEIOU Mnemonic

Initiate dialysis when:

Additional indications:

• Severe hyperphosphatemia (>8-10 mg/dL) if refractory to medical management

• Profound hypocalcemia (<6.5 mg/dL) with symptoms

• Severe metabolic acidosis unresponsive to conservative measures

Modality choice:

• Intermittent hemodialysis (IHD): Stable, non-ICU patients; 3-4 hours QMon/Wed/Fri or daily

• Continuous renal replacement therapy (CRRT): Hemodynamically unstable ICU patients; provides gentle fluid removal and acid-base balance

• Peritoneal dialysis: Rarely used in AKI; available if vascular access impossible

Complete Order Set for AKI Management

Initial AKI Workup

Labs: CBC, CMP (Cr, BUN, K, Na, Ca, Phos), UA with microscopy, urine osmolality, urine Na/Cr

Imaging: Bedside renal ultrasound (assess hydronephrosis, IVC diameter, renal size)

Calculations: FENa, BUN/Cr ratio, eGFR, creatinine clearance

Assessment: Volume status (exam, weight, I&Os, JVP)

Prior labs: Compare current Cr to baseline (if available)

Pre-renal AKI Management

IV fluids: 0.9% NaCl or LR at 250-500 mL/hr (titrate to urine output >0.5 mL/kg/hr)

Medications: STOP NSAIDs, ACE-I/ARB, diuretics

Monitoring: Daily weights, strict I&Os, urine specific gravity, repeat Cr in 24-48 hours

Follow-up labs: Check Cr after 24 hours of fluid repletion; if improving, continue support

Intrinsic AKI (ATN/AIN/GN)

Labs: Send ANCA, ANA, Anti-GBM, complement levels if GN suspected

Imaging: CT abdomen/pelvis if rhabdomyolysis suspected (assess CK, myoglobin)

Medications: STOP offending drug; adjust all renally cleared medications

IV fluids: Careful fluid management; avoid overload while maintaining perfusion

Specific: Aggressive hydration + Na bicarb if rhabdomyolysis; corticosteroids if AIN; immunosuppression if GN

Monitoring: Daily weights, strict I&Os, CMP daily; watch for hyperkalemia

Post-renal AKI (Obstruction)

Imaging: CT non-contrast abdomen/pelvis to confirm obstructing lesion

Urology consult: Urgent if bilateral obstruction or solitary kidney

Intervention: Percutaneous nephrostomy or Foley catheter placement

Monitoring: Daily weights, I&Os, Cr trends; expect improvement in 24-48 hours post-relief

Hyperkalemia Management

ECG: Stat 12-lead ECG (assess for peaked T, prolonged QRS, sine wave)

Treatment (if ECG changes): Calcium gluconate 1-2 amps IV → Insulin 10 units + D50 → Albuterol 10-20 mg neb

Resin: Kayexalate 15-60 g PO/PR (slower acting, removes total body K)

Dialysis: If K >7 with ECG changes or refractory to medical management

Ongoing: Daily K monitoring; restrict K intake; adjust medications

2-Minute Screen

In the hospital floor, prioritize:

1. Is AKI real or artifact? Compare current Cr to baseline (on chart, prior discharge notes)

2. Volume status: Exam (orthostasis, JVP, edema), weight change, I&Os, bedside ultrasound

3. Classify AKI: Calculate FENa, assess UA for casts/hematuria → pre-renal vs intrinsic

4. Remove insult: Identify and STOP nephrotoxic drugs (NSAIDs, ACE-I, aminoglycosides)

5. Check K+ and ECG: Hyperkalemia is life-threatening; treat if present

6. Adjust dosing: All renally cleared medications dosed to eGFR

Don't-Miss Diagnoses

• Post-renal Obstruction: Delayed relief within 24-48 hours → permanent renal scarring; bilateral obstruction is emergency

• Hyperkalemia with ECG Changes: >6.5 mEq/L with peaked T or widened QRS → cardiac dysrhythmia/asystole risk

• Rhabdomyolysis-Induced AKI: CK >5000, myoglobin-positive urine → requires aggressive hydration, sodium bicarbonate, possible dialysis

• Thrombotic Microangiopathy (HUS, TTP): Renal failure + microangiopathic hemolytic anemia + thrombocytopenia → plasma exchange for TTP

• Glomerulonephritis/Vasculitis: RBC casts, hematuria, rapid rise in Cr → kidney biopsy, immunosuppression needed

• Hepatorenal Syndrome: Cirrhosis + AKI refractory to fluids → Terlipressin + albumin, consider transplant

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Ready to practice? The StudyCCS question bank includes 22+ acute kidney injury cases covering classification, FENa calculation, volume status assessment, medication dosing, hyperkalemia management, and dialysis indications with real-time scoring. Test your AKI differential diagnosis and floor management skills today.