Rhabdomyolysis can occur due to many traumatic and nontraumatic causes. Rhabdomyolysis has been reported in new type of coronavirus disease (COVID-19) cases. The aim of our study was to examine the effects of rhabdomyolysis on mortality and renal outcomes in patients hospitalized in our hospital's COVID-19 wards. In our single-center and retrospective study, we included patients who were admitted with a diagnosis of COVID-19 by a thorax-computed tomography finding who were older than 18 years of age and with a measured creatinine kinase (CK) > 1000 U/L on any day of hospitalization. The same number of patients hospitalized in COVID-19 services with CK < 1000 U/L and with similar gender and age were determined as the control group. We analyzed the data of 2065 patients, and compared 154 patients in the rhabdomyolysis group (group 1) and 154 patients in the control group (group 2). Acute kidney injury (AKI) (44.2% vs 21.4%; P < .001), intensive care unit (ICU) admissions (53.2% vs 13.6%; P < .001), intubation (75.6% vs 23.8%; P < .001), mortality (36.4% vs 3.2%; P < .001) and the need for dialysis (3.9% vs 0.6%; P = .005) were seen more in the rhabdomyolysis group. When that group was divided into the early rhabdomyolysis group (group 1a), where the CK value reached its highest value in ≤3 days, and the late rhabdomyolysis group (group 1b), where it was ≥ 4 days, AKI (29.7% vs 65.1%; P < .001), ICU (35.2% vs 79.4%; P < .001), intubation (56.2% vs 88%; P = .001), mortality (18% vs 61.9%; P < .001), and dialysis (1.1% vs 7.9%; P = .031), the results were higher in the group 1b. The available data suggest that rhabdomyolysis seen in COVID-19 patients is not a direct predictor of mortality and poor renal outcomes, but is a secondary outcome to multiple-organ failure caused by worsening clinical status.

Rhabdomyolysis in pediatric patients is a rare but potentially life-threatening condition characterized by the breakdown of skeletal muscle fibers, leading to the release of intracellular components such as myoglobin, potassium, and creatine kinase into the bloodstream. This process can result in severe electrolyte imbalances and acute kidney injury (AKI), sometimes necessitating kidney replacement therapy. While rhabdomyolysis is well studied in adults, pediatric cases present unique diagnostic and therapeutic challenges due to distinct etiologies and clinical manifestations. This review explores the pathophysiology, etiologies, complications, treatment, and outcomes of rhabdomyolysis, with a particular focus on the pediatric population. Emerging evidence regarding the role of hemoadsorption in myoglobin removal is discussed and summarized. Additionally, we propose a systematic framework for the management and monitoring of these patients.

Rhabdomyolysis is a severe condition characterized by the breakdown of muscle tissue leading to the release of intracellular components into the bloodstream. This condition, when associated with acute kidney injury (AKI), can result in significant morbidity and mortality, particularly in the context of coronavirus disease 2019 (COVID-19). This editorial discusses a retrospective study on patients with COVID-19 who developed rhabdomyolysis-related AKI. The study highlights that patients with rhabdomyolysis exhibited higher inflammatory markers, such as C-reactive protein, ferritin, and procalcitonin, and experienced worse clinical outcomes compared to those with other causes of AKI. The findings underscore the importance of early recognition and management of rhabdomyolysis in COVID-19 patients to improve prognosis and reduce mortality rates.

Rhabdomyolysis (RM), particularly heat exhaustion-associated rhabdomyolysis (ehsRM), is a significant clinical issue associated with high mortality and healthcare costs. However, the cellular death mechanisms remain incompletely understood. Oncosis, a form of passive cell death distinct from apoptosis, is characterized by cell swelling and triggered by ATP depletion. Additionally, porimin, a specific biomarker, can uniquely identify oncosis. This study aims to investigate the role and mechanisms of oncosis in both in vitro and in vivo models of ehsRM.

This study aims to investigate the role and mechanisms of oncosis in both in vitro and in vivo models of ehsRM.

In the in vitro study, 6-8-week-old male rats were subjected to treadmill exercise at an ambient temperature of (39.5 ± 0.5)°C and relative humidity of 50%-60%, at a speed of 15 meters per minute until their core body temperature (Tc) reached 43.0°C to establish a heatstroke animal model. Skeletal muscle and blood samples from the gastrocnemius were collected for cytokine, biochemical, and histopathological analyses. Pathological findings revealed decreased muscle fiber density, structural disarray, swelling, degeneration, and hemorrhage. Ultrastructural analysis showed cell swelling, structural disarray, cytoplasmic vacuolation, mitochondrial swelling and degeneration, loss of cristae, and nuclear degeneration, indicating myocyte swelling and necrosis. Porimin, CytC, Bax, and caspase-1 expression increased, while Bcl-2 expression decreased. JC-1 staining indicated a decline in mitochondrial membrane potential and dysfunction. ATP levels decreased, and reactive oxygen species (ROS) production increased. In the in vivo study, HSKMC cells were subjected to 4 hours of heat shock at 43°C to establish a heatstroke-induced rhabdomyolysis cell model. Electron microscopy revealed cell swelling, cytoplasmic vacuolation, mitochondrial swelling and degeneration, and nuclear swelling; late-stage (necrotic-like death) was characterized by nucleolar dissolution, nuclear fragmentation, chromatin condensation, and collapse of cytoplasmic structures. After 24 hours post-modeling, the proportion of double-positive cells (porimin + /PI+) and ROS levels significantly increased, as did porimin expression, while mitochondrial membrane potential and ATP levels significantly decreased. The proportion of Annexin V + /PI + double-positive cells and caspase-3 levels showed no significant changes.

In both in vitro and in vivo studies, oncosis played a crucial role in ehsRM. Pathological and ultrastructural analyses demonstrated cell swelling, structural disarray, mitochondrial damage, and nuclear degeneration. Porimin, CytC, Bax, and caspase-1 expression increased, while Bcl-2 expression decreased. ATP levels decreased, and ROS production increased. In the in vivo study, the proportion of porimin + /PI + double-positive cells and ROS levels significantly increased, while mitochondrial membrane potential and ATP levels significantly decreased. The proportion of Annexin V + /PI + double-positive cells and caspase-3 levels showed no significant changes.

Oncosis is predominant in ehsRM, involving mitochondrial dysfunction, ATP depletion, and oxidative stress.

Rhabdomyolysis refers to the breakdown of skeletal muscle with subsequent release of intracellular contents into blood, causing elevated creatine kinase (CK) and renal damage. The four main etiological categories are traumatic, non-traumatic, non-traumatic exertional, and non-traumatic non-exertional. We report a case of a young female who presented with rhabdomyolysis due to agitation, increased motor activity, and venlafaxine use, resulting in severe organ dysfunction. A 30-year-old female on venlafaxine, pregabalin, and fentanyl patch presented to our hospital with a sudden onset of generalized pain and agitation. Before presentation, the patient was flailing her extremities and thrashing herself against the wall, and the patient became more confused, which prompted the mother to bring her to our emergency department. She had icterus, diffuse ecchymosis over bilateral upper and lower extremities, edematous extremities, and generalized weakness of all extremities with 3/5 strength, normal reflexes without rigidity or clonus or tremors. At presentation, the patient had elevated CK, elevated creatinine, transaminitis, international normalized ratio (INR) of 5.4, and ammonia of 126 umol/L. Given rhabdomyolysis and non-oliguric acute kidney injury, the patient was started on aggressive intravenous hydration at admission. However, her creatinine worsened in the next 24 hours, and the patient developed a worsening of creatinine with high anion gap metabolic acidosis. The patient was given a Lasix challenge and sodium bicarbonate infusion to aid in the excretion of myoglobin and N-acetylcysteine infusion for worsening liver function. She became anuric despite diuretics, developed acute tubular necrosis, and was started on intermittent hemodialysis. Over the next few days, her urine output improved and her creatinine gradually improved. During her hospital course, her mental status returned to baseline, she was started on physical therapy as tolerated, her lower extremity strength gradually improved, and she was discharged to an inpatient rehabilitation facility. Agitation is one of the most common presentations to the emergency department and can cause rhabdomyolysis. Careful monitoring, evaluation of other coexisting causes of rhabdomyolysis, and early aggressive hydration are of paramount importance. Additionally, the use of prediction tools such as the McMahon score can aid in identifying patients who will need renal replacement therapy.

The skeletal muscle interstitial space is the extracellular region around myofibers and mediates cross-talk between resident cell types. We applied a proteomic workflow to characterize the human skeletal muscle interstitial fluid proteome at rest and in response to exercise. Following exhaustive exercise, markers of skeletal muscle damage accumulate in the interstitial space followed by the appearance of immune cell-derived proteins. Among the proteins up-regulated after exercise, we identified cathelicidin-related antimicrobial peptide (CAMP) as a bioactive molecule regulating muscle fiber development. Treatment with the bioactive peptide derivative of CAMP (LL-37) resulted in the growth of larger C2C12 skeletal muscle myotubes. Phosphoproteomics revealed that LL-37 activated pathways central to muscle growth and proliferation, including phosphatidylinositol 3-kinase, AKT serine/threonine kinase 1, mitogen-activated protein kinases, and mammalian target of rapamycin. Our findings provide a proof of concept that the interstitial fluid proteome is quantifiable via microdialysis sampling in vivo. These data highlight the importance of cellular communication in the adaptive response to exercise.

Acute rhabdomyolysis (RM) constitutes a life-threatening emergency resulting from the (acute) breakdown of skeletal myofibers, characterized by a plasma creatine kinase (CK) level exceeding 1000 IU/L in response to a precipitating factor. Genetic predisposition, particularly inherited metabolic diseases, often underlie RM, contributing to recurrent episodes. Both sporadic and congenital forms of RM share common triggers. Considering the skeletal muscle's urgent need to rapidly adjust to environmental cues, sustaining sufficient energy levels and functional autophagy and mitophagy processes are vital for its preservation and response to stressors. Crucially, the composition of membrane lipids, along with lipid and calcium transport, and the availability of adenosine triphosphate (ATP), influence membrane biophysical properties, membrane curvature in skeletal muscle, calcium channel signaling regulation, and determine the characteristics of autophagic organelles. Consequently, a genetic defect involving ATP depletion, aberrant calcium release, abnormal lipid metabolism and/or lipid or calcium transport, and/or impaired anterograde trafficking may disrupt autophagy resulting in RM. The complex composition of lipid membranes also alters Toll-like receptor signaling and viral replication. In response, infections, recognized triggers of RM, stimulate increased levels of inflammatory cytokines, affecting skeletal muscle integrity, energy metabolism, and cellular trafficking, while elevated temperatures can reduce the activity of thermolabile enzymes. Overall, several mechanisms can account for RMs and may be associated in the same disease-causing RM.

This work comments on an article published in the recent issue of the World Journal of Virology. Rhabdomyolysis is a complex condition with symptoms such as myalgia, changes to urination, and weakness. With the potential for substantial kidney impairment, it has also been shown to be a severe complication of coronavirus disease 2019 (COVID-19). To date, various theoretical explanations exist for the development of rhabdomyolysis induced acute kidney injury (RIAKI) in COVID-19 infection, including the accumulation of released striated muscle myoglobin in the urine (myoglobinuria). In their article, they (2024) demonstrate in a retrospective study that RIAKI in COVID-19 patients tended to have elevated levels of C-reactive protein, ferritin, and procalcitonin. These patients also had poorer overall prognoses when compared to COVID-19 patients who have acute kidney injury (AKI) due to other causes. It is clear from these findings that clinicians must closely monitor and assess for the presence of rhabdomyolysis in COVID-19 patients who have developed AKIs. Moreover, additional research is required to further understand the mechanisms behind the development of RIAKI in COVID-19 patients in order to better inform treatment guidelines and protocols.

Postoperative fluid overload is associated with increased mortality and morbidity in infants with congenital heart disease (CHD). Loop diuretics, such as furosemide, are commonly used to prevent fluid overload in the postoperative period. This study aimed to investigate the effect of postoperative albumin levels on the efficacy of furosemide after surgery in infants with CHD. From 1 January 2017 to 31 December 2022, postoperative albumin levels, total furosemide doses, and three-day postoperative diuresis levels were retrospectively analyzed in 186 patients aged 0-1 years who underwent cardiopulmonary bypass at the Pediatric Intensive Care Unit, Diyarbakır Gazi Yaşargil Training and Research Hospital. Demographic and clinical parameters, along with urine output in the first 6 h, first 24 h, 24-48 h, and 48-72 h postoperatively, were recorded. Patients were divided into two groups based on their albumin levels: normal albumin (≥30 g/dL) and hypoalbuminemia (<30 g/dL). A common protein interaction network for albumin and furosemide was constructed using Cytoscape software (version 3.10.2). Of the 186 patients, 79 (42.5%) were male and 107 (57.5%) were female, with a median age of 97.5 days (range 1-360 days). Furosemide doses were higher in hypoalbuminemic patients on postoperative days 1 and 2 compared to normoalbuminemic patients. On postoperative day 1, hypoalbuminemia was more prevalent in patients with oliguria, whereas normoalbuminemia was significantly higher in patients with normouria and polyuria. Furosemide doses were significantly higher in patients with oliguria than in those with normouria in the first 6 h and lower in patients with polyuria compared to those with normouria. A positive correlation was observed between albumin levels and furosemide efficacy on postoperative day 2. Additionally, a positive correlation existed between albumin levels on postoperative day 1 and urine output in the first 6 and 24 h postoperatively. Furosemide efficacy and urine output were positively correlated in the postoperative period. Mortality risk was significantly higher in hypoalbuminemic patients on postoperative days 1 and 2, as well as in patients with oliguria in the first 6 and 24 h postoperatively. Network analysis revealed that albumin was directly involved in furosemide's target network, along with six other proteins within the common interaction network. Diuresis levels were significantly lower in hypoalbuminemic patients. We suggest that the effectiveness of furosemide is reduced because it cannot bind to albumin at sufficient levels. The effective management of albumin levels may enhance furosemide efficacy and improve postoperative outcomes in infants with CHD.

Acute compartment syndrome is a rare but serious complication following gynecological surgery in the lithotomy position, potentially resulting in permanent neuromuscular dysfunction or limb loss, making early recognition and prompt management essential.

A 41-year-old woman underwent a laparoscopic myomectomy for uterine fibroids, during which she was positioned in the high lithotomy and head-down position for 118 min. Six hours post-surgery, she experienced spasmodic pain and swelling in both lower extremities. Thirteen hours after surgery, her symptoms worsened, leading to the diagnosis of acute compartment syndrome in both legs. An emergency bilateral fasciotomy was performed, and the patient fully recovered within two months without any neuromuscular dysfunction.

ACS should be an important differential diagnosis for lower extremity pain after gynecologic surgery, especially with prolonged lithotomy positioning. Gynecologists should be vigilant for ACS signs and symptoms to prevent delayed diagnosis.

Rhabdomyolysis (RML), characterized by the breakdown of skeletal muscle fibers and the release of muscle contents into the bloodstream, has emerged as a notable complication associated with Coronavirus disease 2019 (COVID-19) infection and vaccination. Studies have reported an increased incidence of RML in individuals with severe COVID-19 infection. However, the exact mechanisms remain unclear and are believed to involve the host's immune response to the virus. Furthermore, RML has been documented as a rare adverse event following COVID-19 vaccination, particularly with mRNA vaccines. Proposed mechanisms include immune responses triggered by the vaccine and T-cell activation against viral spike proteins. This study aims to review the current literature on the incidence, pathophysiology, clinical presentation, and outcomes of RML secondary to COVID-19 infection and vaccination. We identify common risk factors and mechanisms underlying this condition by analyzing case reports, clinical studies, and pharmacovigilance data. Our findings suggest that while RML is a relatively rare adverse event, it warrants attention due to its potential severity and the widespread prevalence of COVID-19 and its vaccines. This review underscores the need for heightened clinical awareness and further research to optimize management strategies and improve patient outcomes in this context.

Earthquakes cause devastating effects, resulting in the deaths of thousands of people each year. Understanding the full range of impacts, including fatalities, and the pathophysiological mechanisms underlying these effects is crucial for mitigating the aftermath of earthquakes. Therefore, this review aims to: delineate the critical golden time periods following earthquakes and identify the most effective responses and resilience factors during these periods; accurately define the terminology for injuries sustained post-earthquake; elucidate the basic pathophysiology of CRUSH injury-induced myopathy, one of the most significant pathologies in post-earthquake patient management; explore the role of nitric oxide (NO) mechanisms in crush injuries, which are believed to be fundamental to the "smiling death phenomenon" and represent the unseen part of the iceberg; and highlight the importance of the 3 main phenomena responsible for mortality-acidosis, coagulopathy, and hypothermia-during disasters. This comprehensive review, based on the latest literature, encompasses search and rescue, pre-hospital processes, emergency department procedures, and subsequent internal and surgical management algorithms.

Rhabdomyolysis (RM) is characterised by the breakdown of skeletal muscle tissue, releasing toxic intracellular components into circulation. It presents with dark urine, muscle weakness, myalgia, and elevated creatine phosphokinase levels (CPK). Drug-induced RM is aetiologically significant. This case report describes a 25-year-old male who developed severe RM and Acute Kidney Injury (AKI) after intramuscular (IM) heroin administration as a first time user. IM heroin use can induce higher CPK levels due to direct myocyte toxicity and mechanical trauma. The highly vascularised gluteal muscles with type 1 fibres at the injection site likely exacerbated the severity. Additional factors included lower mitochondrial density in males and alcohol exposure. Despite aggressive fluid resuscitation, renal replacement therapy (RRT) was required, and the patient responded well to haemodialysis. This case highlights AKI as a severe complication of IM heroin use, underscoring the need for further research into drug-induced RM.

A 14-year-old African American female patient presented to the emergency department with moderate right calf pain of unknown origin. The pain was present for a couple of days without radiation and progressed with an inability to bear weight. Physical examination revealed tenderness to palpation over the right calf. The patient had no history of overweight, trauma, infection, or extreme physical exertion. She took no medications, supplements, herbals, or used any illegal drugs. Of note, the patient was sedentary. Her blood work revealed elevated creatine kinase and liver enzymes, diagnostic of rhabdomyolysis. All other diagnostic evaluations, including EKG, chest X-ray, leg ultrasound, creatine kinase-MB, urinalysis, thyroid levels, and CBC were unremarkable. No other inherited conditions were identified in lab work. The patient was given dextrose 5% in water with sodium bicarbonate and switched to aggressive hydration via normal saline until discharge.

Rhabdomyolysis is a relatively rare condition caused by the damage and release of myocyte contents. It occurs most commonly secondary to strenuous exercise. Rhabdomyolysis carries the risk of life-threatening negative sequelae such as acute kidney injury or death. This case report describes a middle-aged male patient who has presented with rhabdomyolysis five times over the past nine years, each following a viral illness. No inborn errors of metabolism, neuromuscular junction conditions, or myopathies were found to explain the patient's recurrent rhabdomyolysis except for two variants of unknown significance in the SYNE2 gene that has been linked with Emery-Dreifuss muscular dystrophy.

Viral and bacterial infections may be complicated by rhabdomyolysis, which has a spectrum of clinical presentations ranging from asymptomatic laboratory abnormalities to life-threatening conditions such as renal failure. Direct viral injury as well as inflammatory responses may cause rhabdomyolysis in the course of coronavirus disease 2019 (COVID-19). When presented with acute kidney injury (AKI), rhabdomyolysis may be related to higher morbidity and mortality.

To compare rhabdomyolysis-related AKI with other AKIs during COVID-19.

A total of 115 patients with COVID-19 who had AKI were evaluated retrospectively. Fifteen patients had a definite diagnosis of rhabdomyolysis (i.e., creatine kinase levels increased to > 5 times the upper normal range with a concomitant increase in transaminases and lactate dehydrogenase). These patients were aged 61.0 ± 19.1 years and their baseline creatinine levels were 0.87 ± 0.13 mg/dL. Patients were treated according to national COVID-19 treatment guidelines. They were compared with patients with COVID-19 who had AKI due to other reasons.

For patients with rhabdomyolysis, creatinine reached 2.47 ± 1.17 mg/dL during follow-up in hospital. Of these patients, 13.3% had AKI upon hospital admission, and 86.4% developed AKI during hospital follow-up. Their peak C-reactive protein reached as high as 253.2 ± 80.6 mg/L and was higher than in patients with AKI due to other reasons (P < 0.01). Peak ferritin and procalcitonin levels were also higher for patients with rhabdomyolysis (P = 0.02 and P = 0.002, respectively). The mortality of patients with rhabdomyolysis was calculated as 73.3%, which was higher than in other patients with AKI (18.1%) (P = 0.001).

Rhabdomyolysis was present in 13.0% of the patients who had AKI during COVID-19 infection. Rhabdomyolysis-related AKI is more proinflammatory and has a more mortal clinical course.

Skin conditions are common in patients on maintenance hemodialysis and those with pancreatitis. However, there is a lack of research on dermatological issues in patients who have both hemodialysis and pancreatitis concurrently.

A 62-year-old male patient with a 4-year history of maintenance hemodialysis (MHD) presented with pain and was diagnosed with acute pancreatitis and gallbladder stones. Markedly elevated blood amylase, creatine kinase, and myoglobin were noted, alongside a purplish-red skin discoloration. Treatment included inhibition of digestive fluid secretion, anti-infection measures, blood purification, fasting, rehydration, and symptomatic care. Notably, continuous renal replacement therapy (CRRT) combined with hemoperfusion (HP) was employed. The patient's dialysis effluent initially appeared red. Upon examination of the patient's peripheral blood smear, red blood cell debris was not observed. The dialysis effluent (on Day 0) was analyzed, revealing no hemoglobin (0 g/L) but an elevated myoglobin concentration of 80.4 U/L. After the therapeutic intervention, the indicators, including the blood amylase, C-reactive protein, total bilirubin, creatine kinase, and myoglobin were improved. The patient experienced resolution of sternal and upper abdominal pain within two days. After four consecutive days of CRRT and HP treatment, the skin color returned to normal, alongside improved clarity of the dialysis effluent. Subsequently, the patient's method of blood purification was reverted to conventional hemodialysis. On the eighth day of hospitalization, the patient resumed normal diet and was discharged.

In the case of the current patient with acute pancreatitis undergoing MHD, it is noteworthy to report the observation of a unique purplish-red skin discoloration. This phenomenon may be attributable to inflammation resulting from acute pancreatitis, and the retention of myoglobin within the body.

McArdle's disease, also known as glycogen storage disease type V or McArdle syndrome, is a pure muscle myopathy with an autosomal recessive inheritance pattern. It is caused by mutations in the gene that encodes muscle phosphorylase. Symptoms typically begin in late adolescence or early adulthood, presenting as exercise intolerance. This review focuses on the diagnosis of McArdle's disease, initially manifesting as a clinical picture of rhabdomyolysis in an 18-year-old male patient with a history of minor thalassemia who had been followed in pediatric consultation since age three for failure to thrive. After excluding common causes such as alcohol consumption, drug use, traumatic muscle compression, and other conditions, the diagnosis of McArdle's disease was considered. The diagnosis was supported by laboratory tests showing myoglobinuria and elevated creatine kinase levels, as well as the absence of increased serum lactate following ischemic exercise. Genetic testing confirmed the presence of mutations in the PYGM gene, corroborating the diagnosis. Treatment includes administering a diet rich in slow-absorbing carbohydrates, regular low-intensity physical exercise, and, in some cases, supplementation with vitamin B6 and creatine. The prognosis is generally favorable with proper disease management, although vigorous exercise should be avoided to prevent complications such as severe muscle injury and rhabdomyolysis. Although McArdle's disease is a rare condition, it is likely underdiagnosed. Ideally, it should be considered in the differential diagnosis of rhabdomyolysis in all patients with symptoms of exercise intolerance and/or recurrent myoglobinuria.

This case report presents a 22-year-old male who exhibited critically high levels of creatine kinase (CK) (3,600 U/L), elevated liver transaminases (alanine aminotransferase (ALT) 90 U/L; aspartate aminotransferase (AST) 54 U/L), and elevated total bilirubin (30 µmol/L) following vigorous physical activity. The patient's blood work parameters normalized after a short period of exercise abstinence, highlighting the impact of acute exercise on blood work parameters and the importance of considering recent physical activity when interpreting laboratory results.

Rhabdomyolysis is a skeletal muscle injury that can cause myoglobinuria and acute kidney injury (AKI). Risk factors for AKI in children are not clearly understood with no standardized treatment guidelines for rhabdomyolysis. Our study explores factors associated with AKI and management of pediatric patients with rhabdomyolysis. Medical records from a children's hospital network over a 5-year period were retrospectively reviewed. The results are described with respect to the presence or absence of AKI. Of the 112 patients who met the inclusion criteria, AKI incidence was 7.1% (n = 8), with all affected patients having exertional etiology. The overall mean age was 13.5 years; patients without AKI were younger than patients with AKI (13.3 versus 17; p < 0.001). Using regression models for hypothesis generation, we found that patients with AKI were more likely to be older (OR = 1.44, 95%CI [1.11-2.19]; p = 0.03), have myoglobinuria (OR = 22.98, 95%CI [2.05-432.48]; p = 0.02), and have received intravenous bicarbonate (OR = 16.02, 95%CI [1.44-228.69]; p = 0.03). In our study, AKI was uncommon and associated with older age, myoglobinuria and bicarbonate treatment. Larger, prospective studies are needed to further understand AKI risk factors and optimal management of pediatric rhabdomyolysis.

Rhabdomyolysis involves skeletal muscle breakdown leading to high serum creatine kinase (CK) levels and myoglobinuria. Here, we report the case of a middle-aged man who developed rhabdomyolysis, resulting in acute kidney injury (AKI) over pre-existing chronic kidney disease (stage 3a) secondary to focal segmental glomerulosclerosis (primary FSGS), during an asymptomatic COVID-19 infection. The patient had been on treatment with cyclosporine and statin, among other drugs, for his comorbidities. He had initially presented to the hospital after a fall due to difficulty walking in the setting of increasing edema. Lab workup revealed elevated CK and AKI. Urinalysis showed "large" blood on a dipstick with only two RBCs per high-power field on microscopy, suggesting myoglobinuria. A standard respiratory pathogen polymerase chain reaction panel revealed positive SARS-CoV-2. The chest X-ray and oxygenation were normal, and he had no respiratory symptoms. He was treated with intravenous fluids and albumin, with a steady improvement in renal function. Our case underlines that rhabdomyolysis can occur in asymptomatic COVID-19 infection. Therefore, it may be worth monitoring CK levels in COVID-19-positive patients with risk factors for rhabdomyolysis, such as the concurrent usage of statins and cyclosporine, even if they are otherwise asymptomatic.

Rhabdomyolysis can lead to acute kidney injury (AKI), primarily due to myoglobin-induced tubular damage. We present a case of slowly progressive rhabdomyolysis following SARS-CoV-2 infection in a 28-year-old male who was monitored through serial serum creatine kinase (CK) and myoglobin levels. Despite prominent CK elevations, the patient did not develop AKI, probably due to disproportionately mild serum myoglobin elevation with distinctive cyclic spikes. This case underscores the informative value of frequent monitoring of both CK and myoglobin to assess muscle damage severity and AKI risk in rhabdomyolysis, particularly with viral infections like COVID-19 that can cause delayed-onset muscle injury.

Rhabdomyolysis describes a syndrome characterized by muscle necrosis and the subsequent release of creatine kinase and myoglobin into the circulation. Myoglobin elimination with extracorporeal hemoadsorption has been shown to effectively remove myoglobin from the circulation. Our aim was to provide best practice consensus statements developed by the Hemoadsorption in Rhabdomyolysis Task Force (HRTF) regarding the use of hemadsorption for myoglobin elimination.

A systematic literature search was performed until 11th of January 2023, after which the Rhabdomyolysis RTF was assembled comprising international experts from 6 European countries. Online conferences were held between 18th April - 4th September 2023, during which 37 consensus questions were formulated and using the Delphi process, HRTF members voted online on an anonymised platform. In cases of 75 to 90% agreement a second round of voting was performed.

Using the Delphi process on the 37 questions, strong consensus (> 90% agreement) was achieved in 12, consensus (75 to 90% agreement) in 10, majority (50 to 74%) agreement in 13 and no consensus (< 50% agreement) in 2 cases. The HRTF formulated the following recommendations: (1) Myoglobin contributes to the development of acute kidney injury; (2) Patients with myoglobin levels of > 10,000 ng/ml should be considered for extracorporeal myoglobin removal by hemoadsorption; (3) Hemoadsorption should ideally be started within 24 h of admission; (4) If myoglobin cannot be measured then hemoadsorption may be indicated based on clinical picture and creatinine kinase levels; (5) Cartridges should be replaced every 8-12 h until myoglobin levels < 10,000 ng/ml; (6) In patients with acute kidney injury, hemoadsorption can be discontinued before dialysis is terminated and should be maintained until the myoglobin concentration values are consistently < 5000 ng/ml.

The current consensus of the HRTF support that adjuvant hemoadsorption therapy in severe rhabdomyolysis is both feasible and safe and may be an effective method to reduce elevated circulating levels of myoglobin.

This study examined the magnitude of physiological strain imposed by repeated maximal static and dynamic apneas through assessing a panel of stress-related biomarkers.

Eleven healthy men performed on three separate occasions (≥72-h apart): a series of five repeated maximal (i) static (STA) or (ii) dynamic apneas (DYN) or (iii) a static eupneic protocol (CTL). Venous blood samples were drawn at 30, 90, and 180-min after each protocol to determine ischaemia modified albumin (IMA), neuron-specific enolase (NSE), myoglobin, and high sensitivity cardiac troponin T (hscTnT) concentrations.

IMA was elevated after the apnoeic interventions (STA,+86%;DYN,+332%,p ≤ 0.047) but not CTL (p = 0.385). Myoglobin was higher than baseline (23.6 ± 3.9 ng/mL) 30-min post DYN (+70%,38.8 ± 13.3 ng/mL,p = 0.030). A greater myoglobin release was recorded in DYN compared with STA and CTL (p ≤ 0.035). No changes were observed in NSE (p = 0.207) or hscTnT (p = 0.274).

Five repeated maximal DYN led to a greater muscle injury compared with STA but neither elicited myocardial injury or neuronal-parenchymal damage.

Myoglobinuric acute renal failure (MARF) is a structural and functional disorder that occurs in the kidney following the release of muscle cell contents into the circulation. In this present study, possible protective and curative effects of Ferula elaeochytris extract against kidney and liver damage in experimentally induced MARF in a rat model were investigated. 3-4 Month-old, 200-250 g Sprague Dawley rats were divided into 8 equal groups with 7 rats per group. Group I was a no-intervention Control group. All groups except for the Group I were dehydrated for 16 hours. Following this dehydration, 50% v/v aqueous glycerol solution was injected into both hind leg muscles of the animals, at a dose of 8 ml/kg. The rats were given physiological saline (SF) once orally before the model was administered (Group II) and after the model was administered (Group V). Similarly, two different doses of Ferula elaeochytris root extract (40 mg/kg and 80 mg/kg) were dissolved in 2 ml of SF and administered orally before (Groups III and IV) and after (Group VI, VII) the model was created. Following the experimental period, kidney and liver tissues were removed from all groups, and fixed in 10% neutral formaldehyde solution for light microscopic examinations. Intracellular vacuolization, enlargement in the Bowman's space, widespread atrophy in the tubular structures, luminal enlargement, and desquamation were detected in the kidney tissue sections of all the experimental model groups. In the liver tissue sections, was detected hepatocyte degeneration, intracellular vacuolization, irregularity in cell membrane borders, and apoptotic bodies. These histopathological consequences of MARF were evaluated for all groups, and whereas a curative effect of Ferula elaeochytris could be seen, its protective effect was higher than its curative effect.

The use of steroids and protein-based dietary supplements for muscle enhancement is prevalent in contemporary society. While these products promise increased muscle mass and strength, they carry significant risks, including severe medical complications. The consumption of these supplements has been linked to adverse symptoms, including dehydration, gastrointestinal distress, dizziness, and alterations in heart rate and blood pressure, primarily due to ingredients like creatine, arginine, and caffeine. Following the proper dosage, ensuring adequate hydration, and consulting a healthcare provider to verify if the supplement's components could affect any pre-existing conditions is recommended. Indiscriminate use of these products, including taurine, can lead to serious side effects. We present a 36-year-old patient with severe rhabdomyolysis, life-threatening acid-base imbalance, renal and liver injury, and peripheral neuropathy associated with the use of performance-enhanced unregulated supplements and exercise. This case highlights the importance of recognizing and managing complications related to exercise-aid supplements, emphasizing early identification and management. Increasing social awareness and research on those products is highly needed to avoid supplement-associated complications and potential long-term disabilities.

Several urate-lowering drugs have been linked to muscle injury. This study investigated the association of oral urate-lowering drugs with the risk of muscle injury by performing a network meta-analysis of randomized and non-randomized controlled trials. A systematic search of MEDLINE, via PubMed, the ClinicalTrials.gov website, and the Cochrane Central Register of Controlled Trials was conducted to identify relevant studies with a primary outcome of "all muscle injuries." A random-effects model was used to perform a frequentist network meta-analysis to estimate whether there was significant heterogeneity among the studies. In total, 32 studies including 28,327 participants with 2694 (9.5%) "all muscle injuries" were assessed, and the overall risk of bias was judged to be low to moderate. No statistically significant differences were found between placebo and 6 urate-lowering therapies: allopurinol (risk ratio, RR, 1.05; 95% confidence interval, 95%CI, 0.63-1.73), febuxostat (RR 1.10, 95%CI 0.71-1.70), lesinurad (RR 7.00, 95%CI 0.31-160.36), lesinurad concomitant with allopurinol (RR 0.85, 95%CI 0.34-2.11), lesinurad concomitant with febuxostat (RR 1.97, 95%CI 0.55-7.03), and topiroxostat (RR 0.99, 95%CI 0.37-2.65). The findings suggest that there is little need to consider the risk of muscle injury when using urate-lowering drugs in the clinical setting.

Equine atypical myopathy (AM) is a severe environmental intoxication linked to the ingestion of protoxins contained in seeds and seedlings of the sycamore maple (Acer pseudoplatanus) in Europe. The toxic metabolites cause a frequently fatal rhabdomyolysis syndrome in grazing horses. Since these toxic metabolites can also be present in cograzing horses, it is still unclear as to why, in a similar environmental context, some horses show signs of AM, whereas others remain clinically healthy. Label-free proteomic analyses on the serum of 26 diseased AM, 23 cograzers, and 11 control horses were performed to provide insights into biological processes and pathways. A total of 43 and 44 differentially abundant proteins between "AM vs cograzing horses" and "AM vs control horses" were found. Disease-linked changes in the proteome of different groups were found to correlate with detected amounts of toxins, and principal component analyses were performed to identify the 29 proteins representing a robust AM signature. Among the pathway-specific changes, the glycolysis/gluconeogenesis pathway, the coagulation/complement cascade, and the biosynthesis of amino acids were affected. Sycamore maple poisoning results in a combination of inflammation, oxidative stress, and impaired lipid metabolism, which is trying to be counteracted by enhanced glycolysis.

This review illustrates the imaging features of rhabdomyolysis across multiple modalities and in a variety of clinical scenarios. Rhabdomyolysis is the rapid breakdown of striated muscle following severe or prolonged insult resulting in the release of myocyte constituents into circulation. In turn, patients develop characteristically elevated serum creatine kinase, positive urine myoglobin, and other serum and urine laboratory derangements. While there is a spectrum of clinical symptoms, the classic presentation has been described as muscular pain, weakness, and dark urine. This triad, however, is only seen in about 10% of patients. Thus, when there is a high clinical suspicion, imaging can be valuable in evaluating the extent of muscular involvement, subsequent complications such as myonecrosis and muscular atrophy, and other etiologies or concurrent injuries causing musculoskeletal swelling and pain, especially in the setting of trauma. Sequela of rhabdomyolysis can be limb or life-threatening including compartment syndrome, renal failure, and disseminated intravascular coagulation. MRI, CT, ultrasound, and 18-FDG PET/CT are useful modalities in the evaluation of rhabdomyolysis.

Dinitrosyl iron complexes (DNICs) are important physiological derivatives of nitric oxide. These complexes have a wide range of biological activities, with antioxidant and antiradical ones being of particular interest and importance. We studied the interaction between DNICs associated with the dipeptide L-carnosine or serum albumin and prooxidants under conditions mimicking oxidative stress. The ligands of these DNICs were histidine residues of carnosine or His39 and Cys34 in bovine serum albumin. Carnosine-bound DNICs reduced the level of piperazine free radicals in the reaction system containing tert-butyl hydroperoxide (t-BOOH), bivalent iron ions, a nitroxyl anion donor (Angeli's salt), and HEPES buffer. The ability of carnosine DNICs to intercept organic free radicals produced from t-BOOH decay could lead to this effect. In addition, carnosine DNICs reacted with the superoxide anion radical (O2•-) formed in the xanthine/xanthine oxidase enzymatic system. They also reduced the oxoferryl form of the heme group formed in the reaction of myoglobin with t-BOOH. DNICs associated with serum albumin were found to be rapidly destroyed in a model system containing metmyoglobin and t-BOOH. At the same time, these protein DNICs inhibited the t-BOOH-induced oxidative degradation of coenzymes Q9 and Q10 in rat myocardial homogenate. The possible mechanisms of the antioxidant and antiradical action of the DNICs studied and their role in the metabolism of reactive oxygen and nitrogen species are discussed.

Herein, we describe a case of acute rhabdomyolysis in a man in his early 50s undergoing haemodialysis and receiving the antiviral drug, telbivudine, for chronic hepatitis B virus (HBV) infection. Following diagnosis by electromyography (EMG), magnetic resonance image (MRI) scans and laboratory data (i.e., elevated serum creatinine kinase (CK) and myoglobin) telbivudine was discontinued and the patient was treated with methylprednisolone. While his CK and myoglobin levels decreased rapidly, his muscle weakness and pain improved slowly. Learning points include: patients undergoing haemodialysis and concomitantly receiving antiviral treatment for HBV, should have their serum levels of CK and myoglobin monitored regularly; treatment with corticosteroids maybe required; relief from rhabdomyolysis-induced muscle weakness and pain may be slow due to nerve fibre damage.

This report describes the case of a 47-year-old woman with myalgias, weakness, and elevated creatine kinase associated with semaglutide therapy prescribed for weight loss. Her symptoms and laboratory markers were consistent with rhabdomyolysis and resolved after discontinuation of semaglutide. Upon rechallenge at a lower dose, symptoms recurred, and urinalysis was consistent with myoglobinuria. Symptoms again rapidly resolved upon discontinuation of the medication. It is imperative for physicians to recognize semaglutide as a possible cause of myalgias and rhabdomyolysis in clinically suspected patients. To the best of our knowledge, this is the first reported case in the literature and may be specific to semaglutide rather than a class effect of glucagon-like peptide 1 (GLP-1) agonists.

Intensive care unit acquired weakness (ICU-AW) affects both coronavirus disease 19 (COVID-19) and non-COVID-19 patients. ICU-AW can result in a variety of consequences, including increased patient mortality.

The current study aimed to compare muscle strength and ICU-AW in COVID-19 and non-COVID-19 patients.

This was a cross-sectional, descriptive-analytical pilot study.

Fifteen conscious COVID-19 patients and 15 conscious non-COVID-19 patients admitted to the ICUs of a public hospital were selected by convenience sampling. Muscle strength in arms and legs was assessed by a hand-held dynamometer (HHD), and ICU-AW was measured with the medical research council sum score (MRC-SS) scale on the first, fourth, and seventh days of admission to ICUs.

The results showed that muscle strength in the arms and legs of the COVID-19 patients assessed by a HHD and MRC was significantly lower than that of non-COVID-19 patients. On the fourth day of ICU admission, 80% of the COVID-19 patients and 40% of the non-COVID-19 patients had ICU-AW. All COVID-19 patients and 86.8% of the non-COVID-19 patients had ICU-AW on the seventh day of ICU admission.

Decreased muscle strength and ICU-AW are more likely in COVID-19 patients who must stay in the ICU compared with non-COVID-19 patients.

Health systems should plan to provide rehabilitation facilities for COVID-19 patients and prevent prolonged complications of COVID-19.

Recent studies showed that Codonopsis lanceolata (CL) has antihypertensive effects. However, to date, no study has examined the effects of CL on vascular tone under a high extracellular K+ concentration ([K+]o). Thus, the present study examined the effect of an extract of Codonopsis lanceolata (ECL) on the vascular tension of rat carotid arteries exposed to high [K+]o. We used myography to investigate the effect of an ECL on the vascular tension of rat carotid arteries exposed to high [K+]o and the underlying mechanism of action. In arteries with intact endothelia, the ECL (250 μg/mL) had no effect on vascular tension in arteries exposed to normal or high [K+]o. In contrast, the ECL significantly increased vasorelaxation in endothelium-impaired arteries exposed to a physiologically normal or high [K+]o compared with control arteries exposed to the same [K+]o conditions in the absence of ECL. This vasorelaxing action was unaffected by a broad-spectrum K+ channel blocker and an ATP-sensitive K+ channel blocker. The ECL significantly inhibited the vasoconstriction induced by Ca2+ influx through voltage-dependent Ca2+ channels (VDCCs) but not Ca2+ influx induced via receptor-operated Ca2+ channels or the release of Ca2+ from the sarcoplasmic reticulum in the vascular smooth muscle. In summary, our study reveals that the ECL acts through VDCCs in vascular smooth muscle to promote the recovery of vasorelaxation even in arteries exposed to high [K+]o in the context of endothelial dysfunction and provides further evidence of the vascular-protective effects of ECL.

Rhabdomyolysis is a syndrome potentially fatal and has been associated with selective serotonin reuptake inhibitors (SSRIs) treatment in a few case reports. Herein, we purpose to establish the correlation between SSRIs use and rhabdomyolysis using the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS) database. We conducted an analysis on reports that were submitted to the FAERS database during the period between January 1, 2004, and December 31, 2022. Four algorithms, including reporting odds ratio (ROR), proportional reporting ratio (PRR), Bayesian confidence propagation neural network (BCPNN), and empirical Bayes geometric mean (EBGM), were employed to quantify the signals of rhabdomyolysis associated with SSRIs. In total, 16,011,277 non-duplicated reports were obtained and analyzed. Among 33,574 reports related to rhabdomyolysis, SSRIs were classified as primary suspected drug in 889 cases. Disproportionality analysis identified a positive signal between rhabdomyolysis and SSRIs (ROR: 2.86, 95% CI 2.67-3.05; PRR: 2.84, χ²: 1037.16; IC_0.25 = 1.39; EBGM_0.5 = 2.64). Among six SSRIs, fluvoxamine had the strongest signal (ROR: 11.64, 95% CI 8.00-16.93; PRR: 11.38, χ²: 265.51; IC_0.25 = 2.41; EBGM_0.5 = 8.31), whereas no significant signal of rhabdomyolysis was detected for paroxetine (ROR: 1.83, 95% CI 1.55-2.15; PRR: 1.82, χ²: 53.82; IC_0.25 = 0.73; EBGM_0.5 = 1.59). After excluding cases co-administered with statins, the signal of rhabdomyolysis associated with SSRIs remains significant. Our analysis reveals that there are differences in safety signals among six SSRIs in respect to the risk of rhabdomyolysis, with fluvoxamine displaying the highest risk signal, while paroxetine did not show a significant signal. Given the potentially lethal nature of rhabdomyolysis, healthcare professionals should inform patients of the potential risk of rhabdomyolysis associated with SSRIs prior to initiating treatment.

Infections have been recognized as an uncommon cause of rhabdomyolysis, with evidence indicating a worse prognosis when compared to rhabdomyolysis caused by other etiologies. Diseases caused by Legionella pneumophila can present variably, ranging from mild to severe illness, as is sometimes the case with pneumonia. In particular, the triad of Legionnaire's disease, rhabdomyolysis, and acute kidney injury is associated with a significant increase in the morbidity and mortality, with most patients requiring initiation of renal replacement therapy such as hemodialysis. While the exact mechanism of both the muscle and kidney injury in this setting remains unknown, several hypotheses exist, with some research suggesting multiple yet distinct processes occurring in both target organs.

In this case report, we describe a 53-year-old African American man who presented with Legionella pneumophila pneumonia complicated by rhabdomyolysis and acute kidney injury. He was treated with aggressive fluid resuscitation and a 2-week course of azithromycin. His clinical status improved without necessitating renal replacement therapy or mechanical ventilation. We postulate that early recognition and treatment were key to his recovery. He was discharged 10 days later without recurrence of rhabdomyolysis at the time of this report.

While there are several well-established and more common causes of rhabdomyolysis, clinicians should recognize Legionella sp. as an etiology, given its association with significant morbidity and mortality.

Exertional heat stroke (EHS) is a medical emergency, occurring when the body generates more heat than it can dissipate, and frequently associated with exertional rhabdomyolysis (ERM). In the present study we aimed to (I) identify clinical features and risk factors, (II) describe current prehospital management, (III) investigate long-term outcomes including the impact on mental health, and review the guidance received during restarting activities. We hope that our approach will improve individual and organizational heat illness preparedness, and improve follow-up care.

We performed a prospective online survey and retrospective medical record review among athletes and military personnel with an episode of EHS/ERM in the Netherlands between 2010 and 2020. We evaluated prehospital management, risk factors, clinical features and long-term outcomes at 6 and 12 months after the event, including mental health symptoms. Furthermore, we investigated what guidance participants received during follow-up, and assessed the patients' perspective on these outcomes.

Sixty participants were included, 42 male (70%) and 18 female (30%), of which 47 presented with EHS (78%) and 13 with ERM (22%). Prehospital management was inconsistent and in the majority of participants not conducted according to available guidelines. Self-reported risk factors included not feeling well-acclimatized to environmental heat (55%) and peer pressure (28%). Self-reported long-term symptoms included muscle symptoms at rest (26%) or during exercise (28%), and neurological sequelae (11%). Validated questionnaires (CIS, HADS and SF-36) were indicative of severe fatigue (30%) or mood/anxiety disorders (11%). Moreover, 90% expressed a lack of follow-up care and that a more frequent and intensive follow-up would have been beneficial for their recovery process.

Our findings indicate major inconsistencies in the management of patients with EHS/ERM, emphasizing the compelling need for implementing standardized protocols. Based on the results of long-term outcome measures, we recommend to counsel and evaluate every patient not only immediately after the event, but also in the long-term.

Rhabdomyolysis can occur secondary to infections, trauma, or myotoxic substances. Rhabdomyolysis secondary to autoimmune myositis occurs rarely. Distinguishing autoimmune rhabdomyolysis from rhabdomyolysis secondary to other causes is paramount in considering the long-term management of autoimmune rhabdomyolysis. It is further important to continue close follow-up and further testing to completely understand the extent of this disease as diagnoses may be ever-changing.

A previously healthy female presented to the hospital with myalgias and myoglobinuria following a respiratory infection treated with azithromycin and promethazine. Labs demonstrating elevated creatine kinase (CK) prompted treatment for rhabdomyolysis and rheumatology consultation. The patient was given 3 l of intravenous (IV) 0.9% sodium chloride in the Emergency Department. Upon admission, the patient was placed on a continuous IV drip of 0.9% sodium chloride running at 300 cc/hour for all 8 days of her hospital admission. The rheumatology autoantibody panel pointed towards autoimmune myositis as a potential cause of her rhabdomyolysis. The patient was discharged to follow up with rheumatology for further testing.

Autoimmune myositis, although less common than other etiologies of rhabdomyolysis, is important to consider as the long-term management of autoimmune myositis includes the use of immunosuppressants, antimalarials, or IV immunoglobulins, which may be inappropriate for other etiologies of rhabdomyolysis.

Rhabdomyolysis is a well-documented side effect of daptomycin and is associated with hyperuricemia. However, the occurrence of acute gouty arthritis secondary to rhabdomyolysis-induced hyperuricemia has not been reported. We report a case of a patient who presented with daptomycin-induced rhabdomyolysis prior to the usual 7-10-day administration period. This case was complicated with acute gouty arthritis after 7 days from the onset of rhabdomyolysis symptoms. Treatment consisted of fluid management with the addition of prednisone for gouty arthritis treatment given his poor kidney function. This report indicates the importance of early monitoring of creatine kinase levels in patients on daptomycin to prevent complications from rhabdomyolysis.

The identification of rhabdomyolysis as a potential fatal adverse reaction to recent COVID-19 vaccines is essential. As the symptoms of rhabdomyolysis are not specific, the threshold to actively search for this complication should be low.

Panic attacks have been associated with hypophosphatemia, which can lead to numerous complications if unrecognised. Here, we present the case of an otherwise-healthy man in his 20s who experienced a panic attack accompanied by hypophosphatemia and hypokalaemia and subsequently developed rhabdomyolysis. This trajectory highlights the clinical significance of panic attack-associated metabolic derangements and their potential for medical complications such as rhabdomyolysis.

The overriding goal of the treatment of patients is its effectiveness and safety. However, all medications currently being used also exert some adverse pharmaceutical reactions, which may be regarded as an unintended but inevitable cost of pharmacotherapy. The kidney, as the main organ that eliminates xenobiotics, is an organ especially predisposed and vulnerable to the toxic effects of drugs and their metabolites during their excretion from the body. Moreover, some drugs (e.g., aminoglycosides, cyclosporin A, cisplatin, amphotericin B, and others) have a "preferential" nephrotoxicity potential, and their use is associated with an increased risk of kidney damage. Drug nephrotoxicity is, therefore, both a significant problem and a complication of pharmacotherapy. It should be noted that, currently, there is no generally recognized definition of drug-induced nephrotoxicity and no clear criteria for its diagnosis. This review briefly describes the epidemiology and diagnosis of drug-induced nephrotoxicity and characterizes its pathomechanisms, including immunological and inflammatory disturbances, altered kidney blood flow, tubulointerstitial injury, increased lithogenesis-crystal nephropathy, rhabdomyolysis, and thrombotic microangiopathy. The study also lists the basic drugs with nephrotoxicity potential and provides a short overview of the preventive methods for reducing the risk of drug-related kidney damage developing.

Severe liver injury is an uncommon condition caused by non-traumatic rhabdomyolysis. This rare correlation is more commonly seen in the aspartate aminotransferase (AST) than in the alanine transaminase (ALT) level elevation. We report a case of a 27-year-old male with a history of McArdle disease who presented with generalized muscle aches associated with dark urine. His workup showed SARS-CoV-2 positive, severe rhabdomyolysis (creatinine kinase [CK] > 40000 U/L) and acute kidney injury (AKI) followed by severe liver injury (AST/ALT: 2122/383 U/L). He was started on aggressive intravenous hydration. After multiple boluses, he became overloaded, fluids were re-adjusted and continued, his renal function, CK, and liver enzymes improved, and the patient was discharged; during his visit at the post-discharge, the patient was asymptomatic and no clinical or laboratory abnormalities were found. The glycogen storage diseases are challenging, but prompt and accurate assessment is determinant in recognizing potential life-threatening complications of SARS-CoV-2. The failure to identify complicated rhabdomyolysis could lead to the patient's rapid deterioration, ending in multiorgan failure.

There have been numerous case series of exertional rhabdomyolysis (ER) but no comprehensive studies investigating the incidence of ER in the civilian athletic population in the United States (US).

A retrospective review of patients with ER presenting to emergency departments in the US over a 20-year period between 2000 and 2019 was performed using the National Electronic Injury Surveillance System (NEISS) database.

The national estimate of hospital visits in the US for ER during the 20-year period was 40,654 (0.66 per 100,000 population). There was a 10-fold increase in the incidence of ER from the first to the second decade. The odds of ER were 3.77 (95% CI 3.67-3.86, P < .0001) times higher for males (31,921, 78.5%, 1.06 per 100,000) than females (8,733, 21.5%, 0.28 per 100,000) and 3.82 (95% CI 3.71-3.93, P < .0001) higher in African Americans (33.6, 0.93 per 100,000) than white patients (53%, 0.24 per 100,000). American football (3,064, 7.5%) was responsible for 43.9% of the sports-induced ER cases. The majority (67.3%) of ER cases occurred between the ages of 16 and 35 years old. The majority of patients required hospitalization (26,550, 65.3%).

The number of ER cases presenting to emergency departments in the US increased from 2000-2009 to 2010-2019. Young males and African Americans are at highest risk of ER. There was a high rate of hospitalization.

Objective: To investigate the role and mechanisms of action of nafamostat mesylate (NM) in rhabdomyolysis-induced acute kidney injury (RIAKI). Methods: RIAKI rats were assigned into control group (CN), RIAKI group (RM), and NM intervention group (NM). Inflammatory cytokines and proenkephalin a 119-159 (PENKID) were assessed. Cell apoptosis and glutathione peroxidase-4 (GPX4) were detected using TUNEL assay and immunohistochemical staining. Mitochondrial membrane potential (MMP) was detected by JC-1 dye. The expression of genes and metabolites after NM intervention was profiled using transcriptomic and metabolomic analysis. The differentially expressed genes (DEGs) were validated using qPCR. The KEGG and conjoint analysis of transcriptome and metabolome were used to analyze the enriched pathways and differential metabolites. The transcription factors were identified based on the animal TFDB 3.0 database. Results: Serum creatinine, blood urea nitrogen, and PENKID were remarkably higher in the RM group and lower in the NM group compared to the CN group. Pro-inflammatory cytokines increased in the RM group and notably decreased following NM treatment compared to the CN group. Tubular pathological damages were markedly attenuated and renal cell apoptosis was reduced significantly in the NM group compared to the RM group. The expression of GPX4 was lower in the RM group compared to the CN group, and it increased significantly after NM treatment. A total of 294 DEGs were identified in the RM group compared with the NM group, of which 192 signaling pathways were enriched, and glutathione metabolism, IL-17 signaling, and ferroptosis-related pathways were the top-ranking pathways. The transcriptional levels of Anpep, Gclc, Ggt1, Mgst2, Cxcl13, Rgn, and Akr1c1 were significantly different between the NM and RM group. Gclc was the key gene contributing to NM-mediated renal protection in RIAKI. Five hundred and five DEGs were annotated. Compared with the RM group, most of the upregulated DEGs in the NM group belonged to Glutathione metabolism, whereas most of the downregulated DEGs were related to the transcription factor Cytokine-cytokine receptor interaction. Conclusion: NM protects the kidneys against RIAKI, which is mainly associated with NM mediated regulation of glutathione metabolism, inflammatory response, ferroptosis-related pathways, and the related key DEGs. Targeting these DEGs might emerge as a potential molecular therapy for RIAKI.

We investigated the nephroprotective effect of D-panthenol in rhabdomyolysis-induced acute kidney injury (AKI). Adult male Wistar rats were injected with 50% glycerol solution to induce rhabdomyolysis. Animals with rhabdomyolysis were injected with D-panthenol (200 mg/kg) for 7 days. On day 8, we examined AKI markers, renal histology, antioxidant capacity, and protein glutathionylation in kidneys to uncover mechanisms of D-panthenol effects. Rhabdomyolysis kidneys were shown to have pathomorphological alterations (mononuclear infiltration, dilatation of tubules, and hyaline casts in Henle's loops and collecting ducts). Activities of skeletal muscle damage markers (creatine kinase and lactate dehydrogenase) increased, myoglobinuria was observed, and creatinine, BUN, and pantetheinase activity in serum and urine rose. Signs of oxidative stress in the kidney tissue of rhabdomyolysis rats, increased levels of lipid peroxidation products, and activities of antioxidant enzymes (SOD, catalase, and glutathione peroxidase) were all alleviated by administration of D-panthenol. Its application improved kidney morphology and decreased AKI markers. Mechanisms of D-panthenol's beneficial effects were associated with an increase in total coenzyme A levels, activity of Krebs cycle enzymes, and attenuation of protein glutathionylation. D-Panthenol protects kidneys from rhabdomyolysis-induced AKI through antioxidant effects, normalization of mitochondrial metabolism, and modulation of glutathione-dependent signaling.

Cross-discipline fitness, or CrossFit, has exploded in popularity during the last two decades. During this time, there have been a high volume of patients presenting to clinicians with a wide range of associated injuries. Given the high intensity, high repetition, and competitive nature of CrossFit training and competition, athletes are vulnerable to injury, particularly upper extremity injury. The rate of injury to the shoulder, elbow, and wrist in CrossFit is higher when compared to traditional weight-training and more comparable to elite-level gymnastics and Olympic-style lifting. Due to the growing popularity of CrossFit-style exercise and the relatively high rate of injury among its participants, clinicians are likely to encounter these athletes. The purpose of this review is to familiarize clinicians with CrossFit and the associated injuries they will likely encounter.

The medical literature focusing on CrossFit has demonstrated exponential growth, with the first article published in 2012 and 59 articles published in 2020. Although the body of literature is growing, there are no high-level studies focusing on CrossFit. The literature mainly consists of level IV and V studies, primarily consisting of case reports and case series. Recent studies have proven that CrossFit athletes are vulnerable to high rates of upper extremity injury and a few studies have identified risk factors for injury. Future high-level research is required to study modifiable risk factors, diagnostic criteria, and treatment options for these high-risk athletes in order to improve the safety of their sport. The CrossFit body of research is limited to level IV and V studies; however, the literature is clear, CrossFit athletes face a high rate of upper extremity injury. For this reason, clinicians must be familiar with CrossFit and its associated pathology. The goal of this review is to familiarize clinicians with CrossFit and the associated pathologies they will likely encounter.

We investigated the factors associated with serum muscle enzyme elevation in patients with Sheehan's syndrome. A total of 48 patients who were newly diagnosed with Sheehan's syndrome were included and divided into 3 groups: Group 1, creatine kinase (CK) ≥ 1000 U/L; Group 2, 140 < CK < 1000 U/L; and Group 3, CK ≤ 140 U/L. Differences in serum muscle enzymes, serum electrolytes, blood glucose and hormones were compared among the 3 groups. A Spearman correlation analysis and multiple linear regression analysis were performed on serum muscle enzymes and the other variables. Four patients in Group 1 underwent electromyography. Fourteen, 26 and 8 patients were divided into Group 1, Group 2, and Group 3, respectively. The levels of plasma osmolality, serum sodium, free triiodothyronine (FT3) and free thyroxine (FT4) in Group 1 were lower than those in Group 3 at admission (P < .05). There were significant differences in CK, CK-MB, aspartate aminotransferase, lactate dehydrogenase, and alpha-hydroxybutyrate dehydrogenase among the three groups (P < .05). CK was correlated with serum sodium (r = -0.642, P < .001), serum potassium (r = -0.29, P = .046), plasma osmolality (r = -0.65, P < .001), FT3 (r = -0.363, P = .012), and FT4 (r = -0.450, P = .002). Moreover, creatine kinase isoenzyme-MB (CK-MB) was correlated with serum sodium (r = -0.464, P = .001) and plasma osmolality (r = -0.483, P < .001). The multiple linear regression showed that serum sodium was independently and negatively correlated with CK (r = -0.352, P = .021). The electromyogram results supported the existence of myogenic injury. Sheehan's syndrome is prone to be complicated by nontraumatic rhabdomyolysis, with both a chronic course and acute exacerbation. Serum muscle enzymes should be routinely measured. For patients with CK levels > 1000 U/L, a CK-MB/CK ratio < 6% can be a simple indicator to differentiate rhabdomyolysis from acute myocardial infarction. Abnormal serum muscle enzymes observed in Sheehan's syndrome may be associated with hypothyroidism and with hyponatremia in particular.