RESUMEN
OBJECTIVE: To assess the prevalence of acute kidney injury in patients with subarachnoid hemorrhage patients. DESIGN: Retrospective analysis of all subarachnoid hemorrhage admissions. SETTINGS: Neurocritical care unit. PATIENTS: All patients with a diagnosis of subarachnoid hemorrhage between 2009 and 2014. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Of 1,267 patients included in this cohort, 16.7% developed acute kidney injury, as defined by Kidney Disease Improving Global Outcome criteria (changes in creatinine only). Compared to patients without acute kidney injury, patients with acute kidney injury had a higher prevalence of diabetes mellitus (21.2% vs 9.8%; p < 0.001) and hypertension (70.3% vs 50.5%; p < 0.001) and presented with higher admission creatinine concentrations (1.21 ± 0.09 vs 0.81 ± 0.01 mg/dL [mean ± SD], respectively; p < 0.001). Patients with acute kidney injury also had higher mean serum chloride and sodium concentrations during their ICU stay (113.4 ± 0.6 vs 107.1 ± 0.2 mmol/L and 143.3 ± 0.4 vs 138.8 ± 0.1 mmol/L, respectively; p < 0.001 for both), but similar chloride exposure. The mortality rate was also significantly higher in patients with acute kidney injury (28.3% vs 6.1% in the non-acute kidney injury group [p < 0.001]). Logistic regression analysis revealed that only male gender (odds ratio, 1.82; 95% CI, 1.28-2.59), hypertension (odds ratio, 1.64; 95% CI, 1.11-2.43), diabetes mellitus (odds ratio, 1.88; 95% CI, 1.19-2.99), abnormal baseline creatinine (odds ratio, 2.48; 95% CI, 1.59-3.88), and increase in mean serum chloride concentration (per 10 mmol/L; odds ratio, 7.39; 95% CI, 3.44-18.23), but not sodium, were associated with development of acute kidney injury. Kidney recovery was noted in 78.8% of the cases. Recovery reduced mortality compared to non-recovering subgroup (18.6% and 64.4%, respectively; p < 0.001). CONCLUSIONS: Critically ill patients with subarachnoid hemorrhage show a strong association between hyperchloremia and acute kidney injury as well as acute kidney injury and mortality.
Asunto(s)
Lesión Renal Aguda/sangre , Lesión Renal Aguda/etiología , Cloro/sangre , Hemorragia Subaracnoidea/sangre , Hemorragia Subaracnoidea/complicaciones , Lesión Renal Aguda/epidemiología , Anciano , Creatinina/sangre , Cuidados Críticos , Enfermedad Crítica , Diabetes Mellitus/epidemiología , Femenino , Humanos , Hipertensión/epidemiología , Modelos Logísticos , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , Factores de Riesgo , Factores Sexuales , Hemorragia Subaracnoidea/epidemiología , Hemorragia Subaracnoidea/mortalidadRESUMEN
OBJECTIVES: To assess the reversibility of acute kidney injury-induced neutrophil dysfunction and to identify involved mechanisms. DESIGN: Controlled laboratory experiment and prospective observational clinical study. SETTING: University laboratory and hospital. SUBJECTS: C57BL/6 wild-type mice. PATIENTS: Patients with septic shock with or without acute kidney injury. INTERVENTIONS: Murine acute kidney injury was induced by intraperitoneal injections of folic acid (nephrotoxic acute kidney injury) or by IM injections of glycerol (rhabdomyolysis-induced acute kidney injury). After 24 hours, we incubated isolated neutrophils for 3 hours in normal mouse serum or minimum essential medium buffer. We further studied the effects of plasma samples from 13 patients with septic shock (with or without severe acute kidney injury) on neutrophilic-differentiated NB4 cells. MEASUREMENTS AND MAIN RESULTS: Experimental acute kidney injury significantly inhibited neutrophil migration and intracellular actin polymerization. Plasma levels of resistin, a proinflammatory cytokine and uremic toxin, were significantly elevated during both forms of acute kidney injury. Incubation in serum or minimum essential medium buffer restored normal neutrophil function. Resistin by itself was able to induce acute kidney injury-like neutrophil dysfunction in vitro. Plasma resistin was significantly higher in patients with septic shock with acute kidney injury compared with patients with septic shock alone. Compared with plasma from patients with septic shock, plasma from patients with septic shock and acute kidney injury inhibited neutrophilic-differentiated NB4 cell migration. Even after 4 days of renal replacement therapy, plasma from patients with septic shock plus acute kidney injury still showed elevated resistin levels and inhibited neutrophilic-differentiated NB4 cell migration. Resistin inhibited neutrophilic-differentiated NB4 cell migration and intracellular actin polymerization at concentrations seen during acute kidney injury, but not at normal physiologic concentrations. CONCLUSIONS: Acute kidney injury-induced neutrophil dysfunction is reversible in vitro. However, standard renal replacement therapy does not correct this defect in patients with septic shock and acute kidney injury. Resistin is greatly elevated during acute kidney injury, even with ongoing renal replacement therapy, and is sufficient to cause acute kidney injury-like neutrophil dysfunction by itself.