Wayne James*, a 35-year-old experienced long-distance runner, arrives at the ED with severe weakness, diarrhea, nausea, hypotension, and tachycardia, which began after he finished a 100-mile race the previous day. The ED nurse draws blood for culture, CBC, and CMP. Mr. James can’t provide a urine sample, so the pro­vider orders a straight catheterization, which ob­tains a small amount of reddish-brown urine.

The urinalysis indicates the presence of protein, blood, and an elevated specific gravity. An ECG shows sinus tachycardia with an HR of 118 BPM. Mr. James’s SpO2 is 97% on room air, and a chest x-ray is normal. The provider orders a fluid bolus of normal saline, and the ED nurse takes his vital signs every 30 minutes.

Mr. James has a history of depression. His home medications include citalopram, and he’s been taking ibuprofen for a recent knee injury. Mr. James says, “I’ve been taking more ibuprofen than I normally do, and I wish I’d stopped at more drink stations during the race.” He’s transferred to your med–surg unit.

On the scene

When you enter the room to introduce yourself, you note Mr. James’s increased respiratory rate. He expresses how tired he is and that he still can’t urinate. He last urinated yesterday after the race. He’s had two episodes of diarrhea and feels nauseated.

You take his vital signs: HR 122 BPM with a regular rhythm, RR 26 breaths per minute, temperature 99.1° F (37.3°C), and BP 88/54 mmHg. His SpO2 is 98% on room air. You notify the patient’s provider, who increases his I.V. fluid to 120 mL/hr and orders a 4 mg I.V. push of ondansetron to control nausea.

Outcome

Mr. James’s blood tests show low calcium and elevated hemoglobin, hematocrit, creatinine, BUN, potassium, and phosphate. The urine culture shows no microorganisms. The pro­vider diagnoses Mr. James with acute kidney injury (AKI) related to increased use of ibu­pro­fen and poor fluid intake.

The provider prescribes an increase in normal saline to 200 mL/hour, continued I.V. ondansetron every 8 hours as needed for nausea, and loperamide 10 mg orally as needed for diarrhea. The provider also orders strict intake and output records and daily weights.

Over the next few days, Mr. James’s BUN and creatinine levels return to normal and his urine output increases dramatically. He’s producing clear, yellow urine and his intake and output stabilize. His edema resolves, but his potassium remains slightly high and calcium slightly low. Over the next 2 days, the patient’s electrolytes stabilize and he’s discharged home.

Education

AKI is a sudden yet reversible injury to the kidney. At discharge, you advise Mr. James to hydrate well during any future races and avoid NSAIDs like ibuprofen, which are nephrotoxic. Common clinical manifestations of AKI include oliguria or anuria, dark urine, and peripheral edema. Supportive treatment, such as nutritious meals, increased fluids, and electro­lyte management, can help the kidneys heal. Most patients recover without long-term damage to the kidneys.

*Name is fictitious.

Jennifer Holmes is associate director of academics and an assistant professor and Emily Cannon is an associate professor at Indiana State University in Terre Haute.

American Nurse Journal. 2025; 20(4). Doi: 10.51256/ANJ042532

References

Goyal A, Daneshpajouhnejad P, Hashmi MF, Bashir K. Acute kidney injury. StatPearls. November 25, 2023. ncbi.nlm.nih.gov/books/NBK441896

MacMillan C. Marathon running and kidney damage: What runners should know. Yale Medicine. October 10, 2019. yalemedicine.org/news/marathons-and-kidney-damage

Tidmas V, Brazier J, Bottoms L, et al. Ultra-endurance participation and acute kidney injury: A narrative review. Int J Environ Res Public Health. 2022;19(24):16887. doi:10.3390/ijerph192416887

Key words: acute kidney injury, non-steroidal anti-inflammatory drugs