Introduction: Rhabdomyolysis, which resulted from the rapid breakdown of damaged skeletal muscle, potentially leads to acute kidney injury.
Aim: To determine the incidence and associated risk of kidney injury following rhabdomyolysis in critically ill patients.
Methods: All critically ill patients admitted from January 2016 to December 2017 were screened. A creatinine kinase level of > 5 times the upper limit of normal (> 1000 U/L) was defined as rhabdomyolysis, and kidney injury was determined based on the Kidney Disease Improving Global Outcome (KDIGO) score. In addition, trauma, prolonged surgery, sepsis, antipsychotic drugs, hyperthermia were included as risk factors for kidney injury.
Results: Out of 1620 admissions, 149 (9.2%) were identified as having rhabdomyolysis and 54 (36.2%) developed kidney injury. Acute kidney injury, by and large, was related to rhabdomyolysis followed a prolonged surgery (18.7%), sepsis (50.0%) or trauma (31.5%). The reduction in the creatinine kinase levels following hydration treatment was statistically significant in the non- kidney injury group (Z= -3.948, p<0.05) compared to the kidney injury group (Z= -0.623, p=0.534). Significantly, odds of developing acute kidney injury were 1.040 (p<0.001) for mean BW >50kg, 1.372(p<0.001) for SOFA Score >2, 5.333 (p<0.001) for sepsis and the multivariate regression analysis showed that SOFA scores >2 (p<0.001), BW >50kg (p=0.016) and sepsis (p<0.05) were independent risk factors. The overall mortality due to rhabdomyolysis was 15.4% (23/149), with significantly higher incidences of mortality in the kidney injury group (35.2%) vs the non- kidney injury (3.5%) [ p<0.001].
Conclusions: One-third of rhabdomyolysis patients developed acute kidney injury with a significantly high mortality rate. Sepsis was a prominent cause of acute kidney injury. Both sepsis and a SOFA score >2 were significant independent risk factors.
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Rhabdomyolysis-Induced Acute Renal Injury in a Schizophrenic Patient
Nowadays, schizophrenia is treated with atypical antipsychotics that can determine neuroleptic malignant syndrome or rhabdomyolysis appearance. In addition to trauma and muscular hypoxia, there are some drugs and toxins associated with rhabdomyolysis development, among which olanzapine. A case of severe rhabdomyolysis syndrome, with extremely high levels of serum creatine kinase (CK), followed by acute kidney failure, secondary to olanzapine overdose and prolonged immobilization is outlined. Continuous renal replacement therapy was performed, with a slow clearance of serum CK levels. Under supportive therapy, systemic alkalinisation with volume resuscitation and corticotherapy, patient’s general condition was improved, as well as his lower limb paresis. He followed frequent psychiatric evaluations and psychotherapies, before and after being transferred to a medical service. Rhabdomyolysis diagnosis is difficult in mild cases due to non-specific signs and symptoms, but it also has some typical manifestation, generically called “the rhabdomyolysis syndrome triad”. The treatment is usually supportive; renal replacement therapy is required in the presence of acute kidney injury unresponsive to aggressive volume resuscitation. The systemic myoglobin release is responsible for renal injury. Olanzapine muscle toxicity can lead to severe rhabdomyolysis syndrome complicated with acute kidney injury and multiple organ dysfunction syndrome. Rapid identification and aggressive therapeutic management are essential for improving patients’ outcome and prevent the occurrence of irreversible injuries.