A 28-year-old male presents to the primary care office for evaluation of left calf pain, swelling, and redness. He reports that this started one day ago and worsened today. He ran a 27-mile marathon 2 days ago and traveled for 3 hours in a car today. He reports slight pain on walking and a swollen red calf. He took Ibuprofen 600 mg twice today without relief. Patient reports being an experienced runner, running 3-5 miles daily. He trained for the marathon for 4 months. Patient also reports a history of exercise induced asthma and uses albuterol sulfate HFA as needed.
On physical exam patient appears in good health T 99 P 68 R 18 BP 118/78 wt. 175 lb, height 72 in. BMI 23.1. Heart rate is regular without murmurs, rubs, or gallops. Lungs clear bilaterally. HEENT WNL. Strength lower extremities +5 and DTRs + 2. Left calf erythematous, edematous, warm and tender on palpation. Pulses 3+.
Two possible diagnoses were considered: deep vein thrombosis (DVT) and rhabdomyolysis.
Stat ultrasound of left leg to rule out DVT was ordered and read as normal
CBC WNL
Creatine Kinase (CK) 23,000 U/L (normal 24-170 U/L)
BUN and Creatinine WNL
A diagnosis of rhabdomyolysis was made.
- Discuss the pathophysiology of acute renal failure in rhabdomyolysis.
Pathophysiology of Acute Renal Failure in Rhabdomyolysis
Rhabdomyolysis is a condition characterized by the breakdown of skeletal muscle tissue, leading to the release of intracellular components into the bloodstream. This release includes myoglobin, creatine kinase (CK), electrolytes, and other cell contents. Acute renal failure, also known as acute kidney injury (AKI), can occur as a complication of rhabdomyolysis
The pathophysiology acute renal failure rhabdolysis involves several mechanisms:
Myoglobin-induced renal injury: Myoglobin is a protein found in skeletal muscle cells that binds to oxygen and plays a role in muscle function. In rhabdomyolysis, the breakdown of muscle tissue results in the release of large amounts of myoglobin into the bloodstream. Myoglobin is filtered by the kidneys, but its high concentration can overwhelm the filtration capacity and lead to its deposition in the renal tubules. This can cause tubular obstruction and damage, leading to acute tubular necrosis (ATN) and subsequent renal dysfunction.
Inflammatory response: The release of intracellular components from damaged muscle cells triggers an inflammatory response. Inflammatory mediators, such as cytokines and chemokines, are released and can contribute to renal injury. These mediators can induce vasoconstriction, increase vascular permeability, and promote inflammation within the kidneys. This inflammatory cascade can further worsen renal function.
Hemodynamic changes: Rhabdomyolysis can cause significant fluid loss due to leakage of fluid from damaged muscle cells and increased urinary output. This can lead to hypovolemia and subsequent hypoperfusion of the kidneys. Reduced renal blood flow compromises the delivery of oxygen and nutrients to the kidneys, resulting in ischemic injury. Additionally, the decreased blood flow can lead to the activation of the renin-angiotensin-aldosterone system (RAAS), which promotes vasoconstriction and sodium and water retention, further exacerbating renal dysfunction.
Electrolyte imbalances: The breakdown of muscle cells in rhabomyolysis in the release electrolytes such as potassium, phosphate, and calcium into the bloodstream. Elevated levels of these electrolytes can disrupt the normal balance within the body and have detrimental effects on renal function. Hyperkalemia, in particular, can lead to cardiac arrhythmias and further compromise renal perfusion.
In summary,
the pathophysiology of acute renal failure in rhabdomyolysis involves multiple mechanisms, including myoglobin-induced renal injury, inflammatory response, hemodynamic changes, and electrolyte imbalances. These processes collectively contribute to the development of acute tubular necrosis and impaired renal function. Early recognition and prompt management of rhabdomyolysis are crucial in preventing or minimizing the risk of acute renal failure.