Case Report: Urinary Proteomic Analysis of Exercise-Induced Rhabdomyolysis with Acute Kidney Injury

preprint OA: closed
Full text JSON View at publisher

Abstract

Exertional rhabdomyolysis (ER) is a frequently observed consequence following sustained strenuous exercise. The incidence of exercise-induced rhabdomyolysis has risen in the healthy population in recent decades, posing potential systemic, life-threatening complications like acute kidney injury (AKI). Early diagnosis requires prompt identification and management to prevent morbidity. This case report details the presentation of a 24-year-old male military member from the amphibious command specialization course, who attended the hospital emergency room with symptoms of nausea and dark brown urine 24 hours after strenuous military physical training. Laboratory results revealed a significant elevation in serum creatine kinase (CK) and creatinine (Cre) levels, reaching 9300 IU/L and 5.7 mg/dL, respectively. Concurrently, liver enzymes and urea levels were elevated, leading to the diagnosis of both ER and AKI. The individual exhibited a polygenic risk profile for ER, increasing susceptibility to inflammation and muscle damage. Further investigation through urine proteomic analysis unveiled the presence of various proteins associated with muscle damage, including creatine kinase M (CKM), myoglobin (MB), carbonic anhydrase (CA1), titin (TTN), as well as proteins linked to AKI, such as alpha-2-macroglobulin (A2MG), beta-2-microglobulin (B2MG), insulin-like growth factor-binding protein 7 (IBP7), metalloproteinase inhibitor 1 (TIMP1), and uromodulin (UROM), among others. Following a 12-day intensive care unit (ICU) treatment, a notable reduction in CK and MB levels was observed, accompanied by the restoration of renal function to normal levels. Subsequent laboratory tests during outpatient follow-up, two weeks after discharge, confirmed the normalization of relevant markers. The utilization of urinary proteomics emerged as a non-invasive method for monitoring pathophysiological changes, offering valuable insights into the mechanisms underlying ER and associated AKI.
Full text 621 characters · extracted from oa-doi-fallback · click to expand
There is a newer version available for this {{ publicationType }}. View latest version {{ publication.field_name }} {{ publication.subfield_name }} Copyright: © {{ publicationYear }} {{ publication.presentation_authors[0].full_name + (publication.presentation_authors.length > 1 ? ' et al' : '') }}. This is an open access publication distributed under the terms of the CC BY 4.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Check the {{ publicationType | capitalize }} Source for copyright and license information. Listen on

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. This is a recent paper (2024) — citers typically take a year or two to land, and the OpenAlex reference graph may still be filling in.

Source provenance

europepmc
last seen: 2026-05-20T01:45:00.602351+00:00