Avaliação da atividade eritrocitária da superóxido dismutase 1 como biomarcador precoce do desenvolvimento de lesão renal aguda em pacientes com choque séptico
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Data
2016-12-16
Autores
Costa, Nara Aline [UNESP]
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Universidade Estadual Paulista (Unesp)
Resumo
O estresse oxidativo é reconhecido como característica fundamental da sepse e pode ser uma via comum para o desenvolvimento da lesão renal aguda (LRA). Alguns biomarcadores para a detecção precoce da LRA tem sido estudados, no entanto, apesar da importância no combate ao estresse oxidativo, a atividade da superóxido dismutase 1 (SOD1) ainda não foi avaliada na LRA em pacientes críticos. Nosso objetivo foi avaliar a atividade eritrocitária da SOD1 como preditora de LRA em pacientes com choque séptico. Este é um estudo prospectivo observacional que avaliou 175 pacientes consecutivos, maiores de 18 anos e com choque séptico na admissão na Unidade de Terapia Intensiva (UTI). Foram excluídos 43 pacientes. Assim, 132 pacientes foram incluídos no estudo. Nas primeiras 24 horas da admissão dos pacientes, foram coletados os dados demográficos e amostras de sangue para determinação da atividade eritrocitária da SOD1 e da concentração do malondialdeído (MDA). Todos os pacientes foram acompanhados durante a internação na UTI e o desenvolvimento da LRA foi avaliado. Além disso, também foram avaliados 17 indivíduos controle. A média de idade dos pacientes com choque séptico foi 63,2 ± 15,7 anos, 53% eram homens e a mediana do tempo de internação na UTI foi de 8 (4- 16) dias. Aproximadamente 51% dos pacientes desenvolveram LRA durante a internação na UTI. A mediana da atividade eritrocitária da SOD1 foi 2,92 (2,19- 3,92) U/mgHb. Quando comparado com os indivíduos controle, os pacientes com choque séptico tiveram uma maior concentração sérica de MDA [grupo choque: 1,4 (0,8-2,2) µmol/L vs grupo controle: 0,8 (0,5-1,1) µmol/L; p: 0,003] e menor atividade eritrocitária da SOD1 [grupo choque: 2,9 (2,2-3,9) U/mgHb vs grupo controle: 4,4 (3,3-4,7) U/mgHb; p: 0,001]. Na análise univariada, a atividade eritrocitária da SOD1 foi menor nos pacientes que desenvolveram LRA. A análise da curva ROC revelou que a menor atividade eritrocitária da SOD1 foi associada com o desenvolvimento LRA no ponto de corte < 3,32 U/mg Hb. No modelo de regressão logística, atividade da SOD1 maior que 3,32 U/mg Hb foi associada com proteção do desenvolvimento de LRA quando ajustado pela hemoglobina, fósforo e escore APACHE II (OR: 0,309; IC 95%: 0,137-0,695; p: 0,005) e quando ajustado pela idade, gênero, doença renal crônica, categoria da admissão (clínica ou cirurgica) e escore APACHE II (OR: 0,129; IC 95%: 0,033-0,508; p: 0,003). Em conclusão, a atividade eritrocitária da SOD1 é um biomarcador precoce de LRA em pacientes com choque séptico.
Oxidative stress is recognized as a fundamental characteristic of sepsis and may be a common pathway for the development of acute kidney injury (AKI). Some biomarkers for early detection of AKI have been studied, however, despite the importance in combating oxidative stress, the activity of superoxide dismutase 1 (SOD1) has not been evaluated in AKI in critically ill patients. Our objective was to evaluate erythrocyte SOD1 activity as predictor of AKI in patients with septic shock. This is a prospective observational study that evaluated 175 consecutive patients over the age of 18 years with septic shock upon Intensive Care Unit (ICU) admission. Forty-three patients were excluded. Thus, 132 patients were enrolled in the study. In the first 24 hours of the patients’ enrollment, demographic information was recorded and blood samples were taken to determine the erythrocyte SOD1 activity and the concentration of malondialdehyde (MDA). All patients were followed throughout the ICU stay, and the development of AKI was evaluated. In addition, we also evaluated 17 control subjects. The mean age of patients with septic shock was 63.2 ± 15.7 years; 53% were male, and the median ICU stay was 8 (4-16) days. Approximately 51% of patients developed AKI during the ICU stay. The median erythrocyte SOD1 activity was 2.92 (2.19-3.92) U/mg Hb. When compared to control subjects, septic shock patients had a higher serum MDA concentration [shock group: 1.4 (0.8-2.2) µmol/L vs control group: 0.8 (0.5-1.1) µmol/L; p: 0.003] and lower erythrocyte SOD1 activity [shock group: 2.9 (2.2-3.9) U/mgHb vs control group: 4.4 (3.3-4.7) U/mgHb; p: 0.001]. In univariate analysis, erythrocyte SOD1 activity was lower in patients who developed AKI. The ROC curve analysis revealed that lower erythrocyte SOD1 activity was associated with AKI development at the cutoff of < 3.32 U/mg Hb. In the logistic regression models, SOD1 activity higher than 3.32 U/mg Hb was associated with protection of AKI development when adjusted by hemoglobin, phosphorus and APACHE II score (OR: 0.309; CI95%:0.137-0.695; p=0.005) and when adjusted by age, gender, disease chronic renal, admission category (medical or surgery) and APACHE II score (OR: 0.129; CI95%:0.033-0.508; p= 0.003). In conclusion, erythrocyte SOD1 activity is an early predictor of AKI in patients with septic shock.
Oxidative stress is recognized as a fundamental characteristic of sepsis and may be a common pathway for the development of acute kidney injury (AKI). Some biomarkers for early detection of AKI have been studied, however, despite the importance in combating oxidative stress, the activity of superoxide dismutase 1 (SOD1) has not been evaluated in AKI in critically ill patients. Our objective was to evaluate erythrocyte SOD1 activity as predictor of AKI in patients with septic shock. This is a prospective observational study that evaluated 175 consecutive patients over the age of 18 years with septic shock upon Intensive Care Unit (ICU) admission. Forty-three patients were excluded. Thus, 132 patients were enrolled in the study. In the first 24 hours of the patients’ enrollment, demographic information was recorded and blood samples were taken to determine the erythrocyte SOD1 activity and the concentration of malondialdehyde (MDA). All patients were followed throughout the ICU stay, and the development of AKI was evaluated. In addition, we also evaluated 17 control subjects. The mean age of patients with septic shock was 63.2 ± 15.7 years; 53% were male, and the median ICU stay was 8 (4-16) days. Approximately 51% of patients developed AKI during the ICU stay. The median erythrocyte SOD1 activity was 2.92 (2.19-3.92) U/mg Hb. When compared to control subjects, septic shock patients had a higher serum MDA concentration [shock group: 1.4 (0.8-2.2) µmol/L vs control group: 0.8 (0.5-1.1) µmol/L; p: 0.003] and lower erythrocyte SOD1 activity [shock group: 2.9 (2.2-3.9) U/mgHb vs control group: 4.4 (3.3-4.7) U/mgHb; p: 0.001]. In univariate analysis, erythrocyte SOD1 activity was lower in patients who developed AKI. The ROC curve analysis revealed that lower erythrocyte SOD1 activity was associated with AKI development at the cutoff of < 3.32 U/mg Hb. In the logistic regression models, SOD1 activity higher than 3.32 U/mg Hb was associated with protection of AKI development when adjusted by hemoglobin, phosphorus and APACHE II score (OR: 0.309; CI95%:0.137-0.695; p=0.005) and when adjusted by age, gender, disease chronic renal, admission category (medical or surgery) and APACHE II score (OR: 0.129; CI95%:0.033-0.508; p= 0.003). In conclusion, erythrocyte SOD1 activity is an early predictor of AKI in patients with septic shock.
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Palavras-chave
Superóxido dismutase, Lesão renal aguda, Sepse, Estresse oxidativo, Superoxide dismutase, Acute kidney injury, Sepsis, Oxidative stress