During a prolonged Roux-en-Y gastric bypass surgery, a patient develops dark urine with low urine output, edema, hyperkalemia, elevated creatinine, and very high CK. What is the most likely explanation for this patient’s acute renal failure?

During a prolonged Roux-en-Y gastric bypass surgery, a patient develops dark urine with low urine output, edema, hyperkalemia, elevated creatinine, and very high CK. What is the most likely explanation for this patient’s acute renal failure?

• A. Rhabdomyolysis
• B. Hypovolemia
• C. Acute myocardial infarction
• D. Abdominal compartment syndrome

Answer: (A)

Rhabdomyolysis from muscle injury during a long operation is the key idea. When muscle tissue is damaged, it leaks contents like myoglobin, potassium, and creatine kinase into the bloodstream. Myoglobin travels to the kidneys and can form casts and cause direct tubular toxicity, especially in settings of reduced kidney perfusion, leading to acute kidney injury. The hallmark signs here are dark urine due to myoglobinuria, very high CK from widespread muscle breakdown, and hyperkalemia from intracellular potassium release, all paired with reduced urine output and rising creatinine. Think through the other possibilities: hypovolemia can cause kidney injury by poor perfusion, but it wouldn’t produce such a dramatic and selective rise in CK or dark urine from myoglobin. Abdominal compartment syndrome can impair renal perfusion as well, yet it wouldn’t typically explain a massively elevated CK or dark urine due to myoglobin. Acute myocardial infarction could raise creatinine via reduced cardiac output but wouldn’t account for the muscle-specific injury markers and myoglobinuria seen here. Thus, the most likely explanation is rhabdomyolysis causing acute renal failure.

Rhabdomyolysis from muscle injury during a long operation is the key idea. When muscle tissue is damaged, it leaks contents like myoglobin, potassium, and creatine kinase into the bloodstream. Myoglobin travels to the kidneys and can form casts and cause direct tubular toxicity, especially in settings of reduced kidney perfusion, leading to acute kidney injury. The hallmark signs here are dark urine due to myoglobinuria, very high CK from widespread muscle breakdown, and hyperkalemia from intracellular potassium release, all paired with reduced urine output and rising creatinine.

Think through the other possibilities: hypovolemia can cause kidney injury by poor perfusion, but it wouldn’t produce such a dramatic and selective rise in CK or dark urine from myoglobin. Abdominal compartment syndrome can impair renal perfusion as well, yet it wouldn’t typically explain a massively elevated CK or dark urine due to myoglobin. Acute myocardial infarction could raise creatinine via reduced cardiac output but wouldn’t account for the muscle-specific injury markers and myoglobinuria seen here.

Thus, the most likely explanation is rhabdomyolysis causing acute renal failure.