NUR 315 Module 1 Case Study example

From Muscle Cell to Kidney: A Case Study of Cellular Injury in Exertional Rhabdomyolysis

[Student Name]

Southern New Hampshire University

NUR 315: Pathophysiology for Nurses

Module One Case Study

[Instructor Name]

[Date]

The organization, setting and figures below are a composite written as a model document. No real employer, client, colleague or patient is described.

From Muscle Cell to Kidney: A Case Study of Cellular Injury in Exertional Rhabdomyolysis

Case Presentation

A 23-year-old man attended his first high-intensity group fitness class on a humid August evening after several months without regular exercise. The session included repeated squats, burpees and weighted lunges for 50 minutes. He felt severe thigh pain that night and the next morning could barely climb stairs. On the second day he noticed urine the color of cola and came to the emergency department. His thighs were swollen, firm and tender. Blood pressure was 128/76 mmHg, pulse 102 beats per minute and temperature 37.4 degrees Celsius. He reported drinking little water during or after the class.

Initial laboratory results showed a creatine kinase of 48,600 units per liter (reference below about 200), potassium of 5.6 mmol/L, creatinine of 1.9 mg/dL compared with 0.9 mg/dL at a physical two months earlier, calcium of 8.1 mg/dL, phosphate of 5.9 mg/dL and uric acid of 9.2 mg/dL. Urine dipstick was strongly positive for blood, but microscopy showed only one to two red blood cells per high-power field. He was diagnosed with exertional rhabdomyolysis with acute kidney injury.

The Injured Muscle Cell

Skeletal muscle cells depend on a steady supply of adenosine triphosphate (ATP) to power contraction and, just as importantly, to run the membrane pumps that keep the inside of the cell stable. The sodium-potassium pump keeps sodium out and potassium in, and calcium pumps move calcium out of the cytoplasm and back into storage in the sarcoplasmic reticulum. During intense, unaccustomed exercise, especially in heat and with poor hydration, the demand for ATP outstrips supply. As ATP falls, the pumps slow (Rogers, 2023).

The first changes are reversible. When the sodium pump fails, sodium and water enter the cell and it swells. The cell shifts toward anaerobic metabolism, producing lactate and lowering intracellular pH. If energy supply is restored at this stage, the cell can recover. In this patient, however, repeated eccentric contractions such as lowering into squats also damaged the cell membrane mechanically. Calcium then flooded into the cytoplasm faster than the failing pumps could remove it. Eccentric work, heat, dehydration and a lack of recent training are the risk factors most often described in exercise-related cases, and this patient had all four (Kim et al., 2016).

Uncontrolled intracellular calcium is the step that pushes the cell from reversible to irreversible injury. Calcium activates proteases that break down structural proteins and phospholipases that digest the membrane, and it disrupts mitochondria, further reducing ATP production. The membrane loses integrity and the cell dies by necrosis, spilling its contents into the interstitial fluid and bloodstream (Bosch et al., 2009).

Linking the Laboratory Values to the Mechanism

Each abnormal value in the case reflects a specific consequence of muscle cell death, as summarized below.

Table 1

Laboratory Findings and Their Mechanisms in the Case

From the Muscle to the Kidney and the Heart

Myoglobin, the oxygen-binding protein of muscle, is small enough to be filtered by the glomerulus. In the kidney it causes injury in three ways (Bosch et al., 2009). First, fluid shifts into the swollen muscles reduce circulating volume, which lowers renal blood flow, particularly in a patient who was already dehydrated. Second, in concentrated and acidic urine, myoglobin forms casts that obstruct the tubules. Third, the heme in myoglobin generates oxidative injury to tubular cells. The rise in creatinine from 0.9 to 1.9 mg/dL in this patient reflects all three.

The heart is at risk from potassium. Released potassium raises the extracellular concentration, which reduces the resting membrane potential of cardiac cells and can cause dangerous rhythms. Because the kidney is also the main route for excreting potassium, acute kidney injury removes the body's usual correction. A value of 5.6 mmol/L on arrival may therefore climb over the next day as more muscle breaks down and excretion remains limited.

Nursing Implications

The mechanisms point directly to nursing priorities. Because low renal blood flow and concentrated urine drive kidney injury, early and generous intravenous fluid is the central treatment, and the nurse's role is to deliver it and monitor its effect. Hourly urine output measurement, often targeting a high output ordered by the provider, shows whether the kidneys are being flushed. Urine color gives a quick visual check as myoglobin clears.

Because potassium may keep rising, the nurse monitors serial potassium levels and places the patient on cardiac monitoring, watching for peaked T waves or arrhythmias. Creatine kinase and creatinine are trended rather than read once, since a falling creatine kinase indicates that muscle breakdown is slowing. The swollen thigh muscles also need regular neurovascular checks, because swelling within a closed muscle compartment can compress vessels and nerves. Finally, patient teaching should address why the injury occurred: gradual training, hydration and rest when muscle pain is severe, since exertional rhabdomyolysis can recur, and a return to training should be gradual and planned with his provider (Kim et al., 2016).

Conclusion

This case follows a single chain of events. Intense, unaccustomed exercise in heat depleted the ATP that muscle cells need to control their internal environment. Calcium overload and membrane damage pushed the cells past the point of recovery, and their contents entered the blood. Myoglobin injured the kidney through low blood flow, tubular casts and oxidative damage, while released potassium threatened the heart as kidney excretion fell. Understanding that chain explains every abnormal value in the case and tells the nurse what to watch for in the hours that follow.

References

Bosch, X., Poch, E., & Grau, J. M. (2009). Rhabdomyolysis and acute kidney injury. New England Journal of Medicine, 361(1), 62-72. https://doi.org/10.1056/NEJMra0801327

Kim, J., Lee, J., Kim, S., Ryu, H. Y., Cha, K. S., & Sung, D. J. (2016). Exercise-induced rhabdomyolysis mechanisms and prevention: A literature review. Journal of Sport and Health Science, 5(3), 324-333. https://doi.org/10.1016/j.jshs.2015.01.012

Rogers, J. L. (Ed.). (2023). McCance & Huether's pathophysiology: The biologic basis for disease in adults and children (9th ed.). Elsevier.