Exercise-induced rhabdomyolysis with acute kidney injury resulting from strenuous activities among military trainees: A case report

Abstract

Rhabdomyolysis is a syndrome marked by rapid skeletal muscle breakdown, leading to the release of intracellular components such as myoglobin and creatine kinase into the bloodstream, which may result in acute kidney injury. We report the case of a 31-year-old female army trainee with no prior medical history who developed generalized malaise, muscle pain, fever, and dark urine following intense physical exercise. Laboratory tests revealed elevated creatinine, urea, and liver enzymes, along with hematuria. The patient was treated successfully with intravenous fluids, resulting in clinical and biochemical improvement. Contributing factors included poor physical fitness, intense and prolonged exercise, dehydration, and a hot environment. As 10%–30% of such cases may lead to acute kidney injury, preventive strategies, such as proper hydration, gradual training, and warming-up, are essential. This case highlights the need for early recognition and timely fluid therapy to prevent severe complications, especially in low-resource settings that lack gold standard biomarkers, such as creatine kinase, and also high-risk groups such as military personnel and athletes.

Introduction

Rhabdomyolysis is a serious medical condition characterized by the rapid breakdown of skeletal muscle tissue.^2,3 This breakdown can result from muscle injury, trauma like crush injuries, extreme physical exertion, infections, and genetic or metabolic disorders.^2,3,4,5 The released substances include myoglobin, creatine kinase (CK), electrolytes, and other intracellular components, which can cause complications such as acute kidney injury (AKI), electrolyte imbalance, and compartment syndrome.^1–3 Rhabdomyolysis can affect anyone, but those such as athletes, military personnel, victims of crush injuries, prolonged immobilization, genetic muscle disorders such as muscular dystrophies, infections, people on medication such as statins, or toxins such as alcohol or snake venom, or heat-related stress, such as construction workers or dehydrated individuals, are more prone.^2,3,4,5 Symptoms of rhabdomyolysis include muscle pain and weakness, dark urine, generalized weakness, nausea, vomiting, and confusion.^2,3,4,5

Complications can be severe and include AKI, electrolyte disturbances, disseminated intravascular coagulation, and compartment syndrome.^1–3 Diagnosis is typically made through blood tests (elevated CK levels) and urine tests (positive for myoglobinuria).^2,3,4,5 Treatment involves intravenous fluids to maintain hydration and help flush out toxins, dialysis, or hemofiltration, and addressing underlying causes by managing the initial injury or condition that led to rhabdomyolysis. Early treatment is crucial to prevent long-term complications and improve outcomes.2,3,4,5

In general, rhabdomyolysis is more commonly associated with traumatic injuries, with some studies indicating that up to 85% of victims of traumatic injuries may develop rhabdomyolysis.^2,3 Given the lack of specific data from Tanzania, it is difficult to provide an exact incidence rate for the country. However, factors such as the prevalence of infectious diseases and trauma could influence the incidence of rhabdomyolysis in Tanzania.

A search through prominent biomedical databases such as PubMed and African Index Medicus revealed no published cases or case series specifically documenting exercise-induced rhabdomyolysis (EIR) in Tanzanian military personnel. This makes the case report both plausible and important in expanding the documented geographic and demographic scope of EIR in military populations.

Case presentation

A 31-year-old female with no significant past medical history was referred to our facility with symptoms of generalized body malaise, muscle aches, severe headache, and subjective fevers. These symptoms developed after intensive exercise. She also reported passing dark-colored urine, which started 48 h after intensive training.

The patient denied any history of recent viral illness, such as flu-like symptoms or gastrointestinal infections, prior to engaging in the physical activity. She was not on any prescribed medications, including statins and explicitly denied the use of herbal or traditional remedies. There was no personal or family history suggestive of metabolic or hereditary myopathies.

• At the previous facility at which she was admitted on day 3 since onset of the symptoms, initial laboratory investigations revealed:

Creatinine (Cr; ref.: 53–106 µmol/L): 544.9 µmol/L (elevated), blood urea nitrogen (BUN; ref.: 2.5–7.1 mmol/L): 13.1 mmol/L (elevated), hemoglobin (Hb; ref.: 12.0–15.5 g/dL): 8.1 g/dL (low), urinalysis: +++ red blood cells, serum total protein: 59.5 g/L (low), alanine aminotransferase (ALT; ref.: 7–56 U/L): 195 U/L (elevated), aspartate aminotransferase (AST; ref.: 10–40 U/L): 238 U/L (elevated), as shown in Table 1.

The patient was initially managed with intravenous hydration and transferred to our facility on day 7 for further evaluation and management.

• On admission to our facility, repeat laboratory tests showed significant improvement:

Cr: 271 µmol/L (decreased from baseline), BUN: 6.08 mmol/L (normalized), Hb: 9.2 g/dL (improved), electrolytes (Na, K, Mg, and Cl): within normal limits, ALT, AST, gamma-GT: normalized, total protein: 71.5 g/L (normal), albumin: 45.5 g/L (normal), hepatitis B and C serology: Negative, as summarized in Table 1.

• The patient was followed up 2 weeks after discharge and remained asymptomatic, with normalized renal and liver function tests.

Table 1.

Showing trend of laboratory results elaborated above.

Tests done	References	Initial test results	Day 7 test results
Creatinine	53–106 µmol/L	544.9 µmol/L	271 µmol/L
BUN	2.5–7.1 mmol/L	13.1 mmol/L	6.08 mmol/L
HB	12.0–15.5 g/dL	8.1 g/dL	9.2 g/dL
Urinalysis	NIL RBCs	+++ RBCs	+ RBCs
Serum total protein	60–83 g/L	59.5 g/L	71.5 g/L
ALT	7–56 U/L	195 U/L	40 U/L
AST	10–40 U/L	238 U/L	20 U/L
Albumin	34–55 g/L	No results from previous facility	45.5 g/L

ALT: alanine aminotransferase; AST: aspartate aminotransferase; BUN: blood urea nitrogen; Hb: hemoglobin; RBCs: red blood cells; Gama GT: Gama-glutamyl transferase.

Discussion

EIR is a well-documented but often under-recognized condition, particularly in individuals engaging in unaccustomed or excessive physical activity. The pathophysiology involves muscle injury leading to the release of intracellular contents, including myoglobin, which can cause AKI due to tubular obstruction and direct toxicity. Primary factors that caused EIR in our case include poor body fitness combined with prolonged-duration, high-intensity, and weight-bearing exercises, together with other predisposing factors, which included dehydration and a hot environment.^5,9

The incidence of AKI in patients with EIR is estimated to be between 10% and 30%. The mortality risk can be as high as 59%, even in an ICU setting. The primary causes of AKI are renal vasoconstriction secondary to myoglobin, hypovolemia, elevated circulating endotoxins and cytokines, and enhanced sympathetic tone and renin–angiotensin–aldosterone system activation. Myoglobin effects contributing to kidney damage include the formation of casts in the distal convoluted tubules and the direct toxicity of myoglobin in the proximal convoluted tubules. ⁵

Although EIR is widely reported in high-income countries, literature from Tanzania and sub-Saharan Africa remains scarce. This case appears to be among the first published reports documenting EIR in a Tanzanian military trainee. Unlike other cases requiring dialysis or ICU-level care, our patient improved with intravenous hydration alone, underscoring the importance of early detection. In addition, our case highlights the urgent need for locally tailored preventive measures, including gradual training programs and hydration awareness in military settings.

In evaluating the etiology of rhabdomyolysis, it is essential to consider a broad differential diagnosis. In this case, the absence of recent viral symptoms or infections reduces the likelihood of infectious causes. The patient had no history of medication use, including statins or over-the-counter herbal preparations, which are commonly implicated. Furthermore, the lack of prior muscle symptoms, normal family history, and sudden onset in response to intense exertion argues against underlying metabolic myopathies. These exclusions support the diagnosis of EIR as the most plausible cause. ⁹

EIR diagnosis is typically supported by elevated CK levels, but in resource-limited settings where CK measurement is unavailable, clinical diagnosis can be made based on a combination of history, physical examination, and suggestive laboratory or urine findings.

Clinical diagnosis without CK can be supported by:

• History: Recent intense or unaccustomed physical exercise, often involving eccentric muscle contractions or prolonged exertion, especially in hot conditions or with possible dehydration. Patients often report muscle pain, weakness, stiffness, and swelling disproportionate to typical post-exercise soreness.

• Physical exam: Tenderness, swelling, decreased range of motion, muscle firmness, or weakness in the affected muscles.

• Urine findings: Dark (tea-colored) urine suggesting myoglobinuria. A urine dipstick test positive for blood but negative for red blood cells on microscopy supports the presence of myoglobin rather than hematuria.

• Additional laboratory clues (if available): Elevated serum phosphate, elevated liver enzymes such as AST, or abnormal muscle enzyme panels can indirectly support muscle injury.

• Absence of other causes: Ruling out trauma, infection, toxins, or other muscle diseases helps strengthen the diagnosis.

The diagnosis in resource-limited settings may rely heavily on a high index of suspicion from clinical history and examination supplemented by urine dipstick testing, as CK measurement is the gold standard but often unavailable. This approach must be combined with awareness of complications, such as AKI, which may be detected clinically or with basic renal function tests.

Studies backing the above statement:

CK still remains as gold standard. A military center cohort analysis showed that AST levels strongly correlate with CK ⩾5000 U/L (AST ⩾110 U/L had 97% sensitivity and 85.7% specificity). Such models support surrogate-based decision-making—but CK was still measured in those patients. ⁶

One case report from a less resource-rich environment pointed out that the diagnosis was made clinically and with urine dipstick positivity before CK and other markers were confirmed, illustrating the practical pathway for diagnosis when CK testing is unavailable or delayed. ⁷

Another report emphasizes the short half-life of myoglobin and the faint clinical signs may lead to missed diagnoses if CK and advanced biomarkers are unavailable, underscoring reliance on clinical vigilance. ⁸

The patient’s recovery without the need for advanced interventions such as dialysis highlights the effectiveness of early and adequate hydration.

Conclusion and recommendation

The absence of a prior medical history in this case underscores the fact that rhabdomyolysis can occur in otherwise healthy individuals under extreme physical stress. Military personnel are at an increased risk due to the physically demanding nature of their training.

This case reveals the need for preventative strategies to reduce the incidence of EIR. The following can be done:

1. Gradual progression of training to enable acclimatization to intense physical activity and avoid sudden muscle stress.

2. Adequate fluid intake, before, during, and after exercise, to avoid dehydration and support renal function.

3. Educate people on the signs and symptoms of rhabdomyolysis to ensure early recognition and intervention.

4. Regular screening to help identify at-risk individuals.

Limitations

One limitation in this case is the absence of serum CK, which is the primary biomarker for confirming and monitoring rhabdomyolysis. CK testing was not available at either the referring or receiving facility at the time. Similarly, additional markers such as serum myoglobin and lactate dehydrogenase (LDH) were not assessed due to resource limitations. While the diagnosis was made based on clinical features and supportive laboratory findings, the absence of these markers limits the diagnostic specificity and underscores challenges in managing such conditions in low-resource settings.

Regarding Tanzanian military personnel specifically, there is no publicly available information or documented policy changes directly linked to individual reported EIR cases. However, by analogy with other military organizations facing similar conditions, it is plausible that lessons from such cases would prompt systemic measures such as hydration guidelines, risk screening, and phased return to activity relevant to Tanzanian military training and public health management of EIR.