An observational study on rhabdomyolysis in the intensive care unit. Exploring its risk factors and main complication: acute kidney injury

El-Abdellati, Esmael; Eyselbergs, Michiel; Sirimsi, Halil; Hoof, Viviane Van; Wouters, Kristien; Verbrugghe, Walter; Jorens, Philippe G.

doi:10.1186/2110-5820-3-8

Cited by 85 publications

(72 citation statements)

References 24 publications

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“…First, rhabdomyolysis is a common complication of combat injury, occurring in up to 31.1% of patients [11]. This is a much higher incidence rate than that seen in earthquake-related injuries [12], civilian trauma intensive care unit patients [1,13], or other intensive care unit populations [14]. Second, injury occurs at a definable point in time, as specified by combat trauma records.…”

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confidence: 99%

Rhabdomyolysis among Critically Ill Combat Casualties: Long-Term Outcomes

Faulk

Walker

Howard³

et al. 2018

Am J Nephrol

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Background: Although rhabdomyolysis has been associated with acute kidney injury and mortality in the short term, the long-term consequences of an episode of rhabdomyolysis remain unknown. We sought to identify the long-term outcomes of rhabdomyolysis, including mortality, renal function, and incidence of hypertension (HTN), among service members initially admitted to the intensive care unit after sustaining a combat injury in Iraq or Afghanistan between February 1, 2002 and February 1, 2011. Methods: Information on age, sex, injury severity score, mechanism of injury, serum creatinine, burn injury, presenting mean arterial pressure, and creatine kinase were retrospectively collected and analyzed for 2,208 patients. Standard descriptive tests were used to compare characteristics of patients with and without rhabdomyolysis. Competing risk Cox proportional hazards models were performed to assess the associated risk of rhabdomyolysis with both HTN and poor renal function. Results: While rhabdomyolysis was associated with HTN on univariate analysis (hazard ratio [HR] 1.30, 95% CI 1.03–1.64; p = 0.029), this difference did not persist on multivariable analysis (HR 1.27, 95% CI 0.99–1.62; p = 0.058). The median estimated glomerular filtration rate (eGFR) was 119 (interquartile range [IQR] 103–128) among those with rhabdomyolysis, compared with 108 (IQR 94–121) in the group without rhabdomyolysis (p < 0.001). Conclusion: After adjustment, patients with rhabdomyolysis were not at an increased risk of HTN compared to patients without rhabdomyolysis. eGFR was paradoxically higher in patients with rhabdomyolysis. There was no association found between rhabdomyolysis and mortality.

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confidence: 99%

Rhabdomyolysis among Critically Ill Combat Casualties: Long-Term Outcomes

Faulk

Walker

Howard³

et al. 2018

Am J Nephrol

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“…acute kidney injury; apoptosis; necroptosis; cardiac injury; tumor necrosis factor-␣; rhabdomyolysis RHABDOMYOLYSIS elicits a systemic inflammatory response that may contribute to distant organ injuries (3,35,42). Acute kidney injury (AKI) is the most well-known distant organ injury frequently observed after severe rhabdomyolysis (2,19). A large amount of evidence supports the role of renal ischemia and myoglobinuria as the main mechanisms involved in the renal injury after rhabdomyolysis (9, 41).…”

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confidence: 99%

TNF-α-mediated cardiorenal injury after rhabdomyolysis in rats

Homsi

Andreazzi

Faria

et al. 2015

American Journal of Physiology-Renal Physiology

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Homsi E, Andreazzi DD, Lopes de Faria JB, Janino P. TNF-␣-mediated cardiorenal injury after rhabdomyolysis in rats. Am J Physiol Renal Physiol 308: F1259 -F1267, 2015. First published November 12, 2014 doi:10.1152/ajprenal.00311.2014.-The TNF-␣ serum level increases after rhabdomyolysis and is involved in the subsequent cardiorenal injury. In the present study, we investigated the TNF-␣-dependent cell signaling pathways implicated in cellular injury in these organs. Rhabdomyolysis was induced by intramuscular glycerol injection in rats. Renal function, cardiac and renal pathology, and activation of caspases were evaluated during the first 24 h after glycerol injection. TNF-␣ blockade with infliximab reduced tubular necrosis and cardiorenal apoptosis. Cellular Fas-associated protein with death domain-like IL-1␤-converting enzyme inhibitory protein (cFLIP), an inhibitor of caspase-8, was overexpressed in the kidney but not in the heart. The inhibitory effect of cFLIP blunted caspase-8 activation in the kidney. In this condition, the cellular response to the TNF-␣ stimulus was driven to receptor-interacting protein-1 (RIP1)-mediated necroptosis. Treatment with RIP1 inhibitor (necrostatin-1) isolated or in combination with infliximab showed a similar reduction in tubular necrosis, underscoring the importance of TNF-␣-mediated tubular necroptosis in this model. TNF-␣ played a positive regulatory role in the transcription of proapoptotic Bax and p53-upregulated modulator of apoptosis (PUMA) proteins. Infliximab treatment reduced caspase-9-mediated apoptosis in both organs. Treatment with a caspase-8 inhibitor showed that caspase-8 participated in the process of apoptosis only in the heart, upstream of caspase-9 activation. TNF-␣-mediated necroptosis is the predominant form of tubular injury observed in the glycerol model. TNF-␣ up regulates Bax and PUMA proapoptotic proteins, resulting in activation of the intrinsic pathway of apoptosis in the kidney and heart. acute kidney injury; apoptosis; necroptosis; cardiac injury; tumor necrosis factor-␣; rhabdomyolysis RHABDOMYOLYSIS elicits a systemic inflammatory response that may contribute to distant organ injuries (3,35,42). Acute kidney injury (AKI) is the most well-known distant organ injury frequently observed after severe rhabdomyolysis (2,19). A large amount of evidence supports the role of renal ischemia and myoglobinuria as the main mechanisms involved in the renal injury after rhabdomyolysis (9, 41). Apart from these mechanisms, Shulman et al. (34) showed many years ago that treatment with anti-TNF-␣-neutralizing antibody conferred renal protection to rats subjected to rhabdomyolysis.More recently, Kelly (12) showed an increased serum level and cardiac expression of TNF-␣ after renal ischemia-reperfusion injury (IRI) in rats. Cardiac function was depressed after renal IRI, and the author detected a significant increase in cardiomyocyte apoptosis 48 h after renal IRI. Treatment with anti-TNF-␣ polyclonal antibody simultaneously with renal IRI significantly atten...

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“…CK level in this case was under 250 IU/L throughout the hospital stay. It was much lower than the reported cases of rhabdomyolysis [4,5]. Thus, we consider that the AKI was not caused by rhabdomyolysis, but by hypovolemia from heat stroke.…”

Section: Discussionmentioning

confidence: 42%

Increased Creatinine Clearance in Acute Kidney Injury due to Heat Stroke

Urabe¹,

Kotani²,

Tsujimoto³

2018

J Med Cases

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Acute kidney injury (AKI) is associated with increased mortality and risk of chronic kidney disease (CKD). Whereas AKI is well known to occur frequently in patients with heat stroke, creatinine clearance levels of these patients have not been evaluated in literature. In this report, we present the case of a patient with increased creatinine clearance who developed AKI due to heat stroke. A 40-year-old male with no past medical history was admitted to the intensive care unit of our hospital due to AKI from heat stroke. Although he was diagnosed with stage 3 AKI at admission, his creatinine clearance, measured by a 12-h urine collection, was highly elevated to 230 mL/min/1.73 m 2 . His serum creatinine was decreased to the baseline level 12 h after admission, with fluid resuscitation. This case can suggest that creatinine clearance might be underestimated, although serum creatinine levels are elevated in AKI due to heat stroke.

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An observational study on rhabdomyolysis in the intensive care unit. Exploring its risk factors and main complication: acute kidney injury

Cited by 85 publications

References 24 publications

Rhabdomyolysis among Critically Ill Combat Casualties: Long-Term Outcomes

Rhabdomyolysis among Critically Ill Combat Casualties: Long-Term Outcomes

TNF-α-mediated cardiorenal injury after rhabdomyolysis in rats

Increased Creatinine Clearance in Acute Kidney Injury due to Heat Stroke

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