Acute Kidney Injury
Rhabdomyolysis

Skeletal muscle breakdown releasing myoglobin and intracellular contents
CK >5 times the upper limit of normal (typically >1,000 U/L), (intrarenal) AKI, specifically acute tubular necrosis (ATN) from myoglobin‑mediated tubular injury and renal ischemia

SYMPTOMS / ASSOCIATED SX

• Classic triad (only ~10% have all three): myalgias + weakness + dark (tea/cola-colored) urine

• Muscle swelling, tenderness, rigidity; focal compartment firmness

• Oliguria, AKI symptoms (nausea, fatigue, edema)

• Severe: cardiac arrhythmias (hyperkalemia), seizures (hypoNa/hypoCa), DIC

• History: found down, crush injury, seizure, extreme exertion, drug/alcohol use, heat stroke

DENIES

• Recent statin initiation or dose increase (drug-induced)

• Chest pain/ischemic symptoms (MI can cause mild CK elevation — rule out if troponin elevated)

• Seizure activity (seizure-induced rhabdo)

• Extreme heat or prolonged exercise (exertional rhabdo)

SOCIAL HISTORY

• Alcohol (direct myotoxin + falls + prolonged immobility); stimulant use (cocaine, MDMA); statin use

• Recent extreme exercise, military training, heat exposure, prolonged immobilization

MAIN ETIOLOGY

• Traumatic/compressive: crush injury, prolonged immobilization ("found down"), compartment syndrome

• Exertional: extreme exercise, heat stroke, seizures

• Toxic: alcohol (most common), statins (especially with CYP3A4 inhibitors), cocaine, MDMA, colchicine, NMS

• Infectious: viral myositis (influenza, COVID-19), bacterial sepsis

• Metabolic: hypothyroidism, hypokalemia, hypophosphatemia; inflammatory: polymyositis/dermatomyositis

MOST COMMON DDX

• AKI from other causes (pigmented casts = rhabdo; coarse granular = ATN)

• MI (troponin elevated but CK-MB fraction <5% of total CK in rhabdo; ECG)

• NMS (antipsychotic use, fever, rigidity, AMS — CK often >1000)

• Malignant hyperthermia (inhalational anesthetic/succinylcholine — RYR1 mutation)

• Serotonin syndrome (serotonergic drugs, hyperreflexia, clonus, agitation)

• Inflammatory myopathy (subacute, skin changes, autoimmune markers)

DATA

• Baseline BUN/Cr: BUN:Cr 10–15 suggests intrinsic AKI (e.g., ATN from rhabdomyolysis)

• CBC

  • BMP: monitor for HyperK, HyperPhos, HyperCa

  • CK: elevated; trend daily

  • LFTs:AST > ALT with normal ALK Phos supports muscle injury over hepatic source

  • Anion Gap: elevated AGMA common

  Urinalysis (UA):

  • Myoglobinuria: positive blood with <3 RBCs/hpf

  • Hyaline casts → pre-renal AKI

  • Muddy brown casts → ATN

  • RBC casts → glomerulonephritis

  • WBC casts → acute interstitial nephritis

  Urine Studies:

  • FeNa <1% → pre-renal

  • FeNa >2% → ATN

    • Less reliable in CKD

  • FEUrea <35% → pre-renal (especially if on diuretics)

  • Urine Na <20 → pre-renal

  • Urine Na >40 → ATN

  • Urine Creatinine

  Imaging:

  • Renal US if concern for obstruction

  • CT A/P if obstruction not adequately evaluated or alternate intra-abdominal pathology suspected

HOME MEDS

• Statins — HOLD immediately; do not restart until CK normalized and etiology investigated

• Fibrates — hold (potentiate statin myopathy)

• ACE inhibitors/ARBs, NSAIDs — hold if AKI

• K-sparing diuretics — hold (hyperkalemia risk)

PLAN

Fluid Resuscitation (Cornerstone)

• LR 1–2 L IV bolus initially → then LR 200–500 mL/hr continuous

• Adjust fluids to urine output goal 200–300 mL/hr

• Continue until:

  • CK downtrending (<5,000 U/L in most guidelines)

  • Cr stable or improving

  • No ongoing myoglobinuria

  • Electrolytes normalized

Monitor for Volume Overload

• Daily assessment for pulmonary edema

• Daily weights

• Strict I/O

• Stop or reduce fluids if:

  • Pulmonary edema develops

  • 3–5 L positive fluid balance

  • Significant volume overload (regardless of CK)

AKI Workup / Monitoring

• Follow FeNa or FEUrea

• Follow Urine Na (>40 ATN; <20 pre-renal)

• Follow Urine Creatinine

• Trend BMP q12h initially, then daily

• Daily BUN/Cr

• Daily CK

Electrolytes

• Monitor and replete electrolytes as needed

• Closely monitor:

  • Hyperkalemia

  • Hyperphosphatemia

  • Hypercalcemia

  • AGMA

Medication Management

• Hold nephrotoxins

• Hold home ACEi/ARB

• Hold diuretics

Monitoring

• Telemetry

• Strict I/O

• Daily weights

• Nephrology consult early for CK >10,000, AKI, or refractory electrolytes

• DISCHARGE:

  • CK trending down (ideally <1000) and renal function stable before discharge

  • HMGCR antibody if statin myopathy not resolving after stopping statin (IMNM)

  • Nephrology follow-up if AKI occurred; PCP 1–2 weeks

  • Metabolic workup if recurrent exertional rhabdo (McArdle's, carnitine deficiency)

RED FLAGS

• Hyperkalemia >6.0 + ECG changes → calcium gluconate immediately + insulin/dextrose + emergent dialysis

• Oliguria unresponsive to >6–10 L IVF → ATN/oliguric AKI; early dialysis

• Compartment syndrome: 6 P's — Pain, Pressure, Paresthesia, Pallor, Pulselessness, Paralysis (late); pressure >30 mmHg = surgical emergency

• CK >50,000 → extremely high AKI risk; aggressive resuscitation + bedside nephrology

• DIC → hematology; FFP/cryoprecipitate as needed

• MH: temperature >40°C + rigidity after anesthesia → dantrolene 2.5 mg/kg IV; cool aggressively; ICU

SENIOR IM RESIDENT PEARLS

• Classic triad present in only ~10% — diagnose biochemically; always check CK in "found down" patients

• Hypocalcemia in rhabdo: DO NOT treat asymptomatically — calcium deposits in muscle reabsorb during recovery → rebound hypercalcemia

• Statin + CYP3A4 inhibitor (azithromycin, diltiazem, fluconazole, grapefruit) dramatically increases myopathy risk

• FeNa <1% early in rhabdo AKI because still prerenal — start fluids immediately, do not wait

• Common mistake: under-resuscitating rhabdo — patients often need 10+ L in first 24h; track urine output hourly

• HMGCR Ab-positive IMNM: does NOT resolve after stopping statin; requires prednisone + immunosuppression

• Bicarbonate alkalinization: target urine pH >6.5; avoid if HCO3 >30 or pH >7.5; monitor q2–4h