The Clinical Study Of The Risk Factors And Prognosis Of Contrast-induced Acute Kidney Injury After Cerebrovascular Intervention

BACKGROUNDAcute kidney injury (AKI) refers to the various causes of glomerular filtration rate (GFR) has fell sharply, leading to the accumulation of metabolites in the body of a kind of clinical syndrome, is for acute renal insufficiency or acute renal failure (ARF) substitution and extension. Contrast- induced nephropathy, also known as contrast-induced acute kidney injury, CI-AKI). Acute kidney injury is a common clinical type, both inpatient and community patients all can happen. Several studies have pointed out that 12-20% of the hospital is the use of contrast agents in patients with acute kidney injury.Contrast nephropathy diagnostic criteria, is refers to the use of contrast agents within 48-72 hours after, serum creatinine increased by more than 0.5 mg/dl (44.2 umol/L), or serum creatinine than the baseline value rose more than 25%, or eGFR fell by more than 25%, and rule out other factors lead to acute kidney injury.Contrast induced acute kidney injury is usually characterized by non oliguria acute kidney injury, often in the contrast of 48-72 hours to a significant rise in serum creatinine,3 to 5 days rise to peak, in most cases in 7 to 10 days fall to a baseline level of serum creatinine.Pathogenesis of contrast nephropathy:mainly contrast resulting in abnormal renal hemodynamics and microcirculation, induced renal medullary ischemia, hypoxia and oxidative stress, caused the damage or necrosis of the renal tubular epithelial cells, severe cases can lead to clinical renal abnormalities.Contrast agent direct toxic effect of renal tubular epithelial cells was also involved in the pathophysiological process of the occurrence and development contrast nephropathy.Cerebro vascular angiography and intervention in China has more than 30 years of history. In the neurological department, cerebrovascular disease diagnosis and treatment have been widely used. And now is the lack of separate for contrast nephropathy in cerebral vascular interventional diagnosis and treatment, epidemiological data and clinical research, only a small sample size of data and case reports, cerebral angiography in the prognosis of postoperative contrast nephropathy research is in a state of blank. Cerebral vascular interventional diagnosis and treatment of clinical practice at present stage and relevant guidelines for many of them are in contrast nephropathy in cardioangiography research results and experience. Cerebral angiography interventional surgery compared with angiography intervention, in the contrast agent into the systemic circulation way, into the proportion of the kidney, drug concentration, the use of contrast agent dose and the patient’s own risk factors is not the same, has its own characteristics. Especially the choice of the contrast agents, dosage, the incidence of CI-AKI, prevention, treatment and prognosis are need to be further studied and discussed.OBJECTIVEThe objective of the present study was to explore risk factors of the patients undergoing cerebrovascular angiography and intervention with postoperative contrast-induced nephropathy. Exploring short-term and long-term prognosis of the patients undergoing cerebrovascular angiography with contrast-induced nephropathy.METHODSWe analyzed retrospectively data from the patients who underwent cerebrovascular angiography and intervention in the department of neurology and neurosurgery in Guangdong General Hospital between January 2009 and December 2013.We evaluated and screened baseline characteristics of patients undergoing cerebrovascular angiography and intervention. We sorted clinical history data to establish database. Inclusion criteria: ① aged≥18 years; ② stroke patients undergoing cerebrovascular angiography and intervetion. Exclusion criteria:1) age<18 years; 2) lack of serum creatinine measurements before angiography or intervention; 3) lack of serum creatinine measurements within 48 hours after angiography or intervention 4) loss to 1-year follow-up; 5) history of end-stage renal disease, dialysis or kidney transplantation; 6) acute kidney injury before the procedure; history of; 7) administration of nephrotoxic drugs (nonsteroidal anti-inflammatory drugs, glycopeptide or aminoglycoside antibiotics, mannitol) 72 hours before and after the procedure; 8) iodic contrast administration in the 72 hours preceding the procedure; 9) pregnancy; and 10) severe hepatic insufficiency, heart failure, acute myocardial infarction, shock, urinary tract obstruction, sepsis, hypotension, or hypovolemia at the time of hospitalization.Collection of indicators and their definitions are as follows: ① preoperative information:gender, age, weight, height, blood pressure, heart rate, respiration, body temperature, baseline eGFR (using the CKD-EPI equation to estimate), cerebrovascular disease types, Glasgow coma score, combined disease, medical history, surgical history, concomitant use of drugs, abnormal signs, hemoglobin platelets, urine, preoperative serum creatinine, liver function, blood cholesterol, blood triglycerides, electrolytes, whether hydration therapy. ② intraoperative data: Intraoperative Glasgow coma score, angiographic intervention treatment, emergency or elective surgery, duration of surgery, the use of contrast agent dose and so on. ③ postoperative data:With the use of drugs, blood pressure, heart rate, respiration postoperative serum creatinine values within 48 hours, after 48 hours after the change of serum creatinine, whether mechanical ventilation, whether the stay ICU, ICU stay, whether postoperative intervention and type of surgery, whether the line blood purification treatment, the total number of days of hospitalization, whether in-hospital death. ④1-yearmortality and time of death.The diagnosis of CI-AKI was guided by the diagnostic criteria from the 2011 European Society of Urogenital Radiology Contrast Media Safety Committee guidelines [8]. CI-AKI was defined as an increase in serum creatinine by 44 μmol/L or≥25% of the baseline value following the intravascular administration of a contrast medium in the absence of an alternative etiology. The last serum creatinine measurement before angiography was considered the baseline measurement in this study. In the prognosis section of this study, we selected in-hospital death and 1-year death as endpoint. Univariate and multivariate logistic regression analyses were used to identify the risk factors for CI-AKI and in-hospital death. One-year mortality curves were generated using the Kaplan-Meier method, and curves were compared with the log-rank test. Univariate and multivariate Cox proportional regression analyses were performed to explore risk factor of 1-year mortality.RESULTSA total of 2015 patients with cerebrovascular angiography and intervention were finally enrolled in the study. Patients’mean age was 51.9 years, with a prevalence of males(50.6%).Overall, CI-AKI was observed in 85 patients (4.2%).Patients with CI-AKI tended to be older and have a worse neurological deficit score, relatively lower eGFR, higher incidence of proteinuria, and higher prevalence of anemia than patients without CI-AKI. Patients with CI-AKI had a higher in-hospital mortality compared with patients without CI-AKI (11.8% vs. 6.1%, P=0.034). Even adjusting confounding factors, CI-AKI also was an independent risk factor for in-hospital death(odds ratio [OR]=2.13;95% confidence interval[CI],1.03-4.39;P=0.042). In addition, CI-AKI increased 1-year mortality in stroke patients undergoing cerebral angiography independently (hazard ratio [HR]=1.79,95%CI,1.10-2.89, P=0.018).Multivariate logistic regression analyses were used to identify the risk factors for CI-AKI. The multivariate logistic regression analysis showed that eGFR<60 ml/min/1.73 m2, anemia, a high NIHSS score and proteinuria were independently associated with CI-AKI.The CI-AKI incidence in patients with proteinuria was higher than that in patients without proteinuria (18.5% vs.3.7%, P<0.001;Fig 1).Subgroup analysis showed that patients with proteinuria have a higher incidence of CI-AKI among both ischemic stroke(16.7% vs 4.0%,P<0.001)and hemorrhagic stroke (40.0% vs. 1.1%,P<0.001)patients.Proteinuria did not increase in-hospital mortality (OR=1.25;95%CI,0.49-3.17; P= 0.639).The Kaplan-Meier curve showed that the 1-year mortality of patients with proteinuria was significantly higher than that of patients without proteinuria (36.7% vs. 13.3%,P<0.001;Figure 2).The Kaplan-Meier curve showed that the 1-year mortality of patients with proteinuria was significantly higher than that of patients without proteinuria (41.5% vs.18.7%, P<0.001;). In the multivariate Cox stepwise regression model, proteinuria was independent risk factor for 1-year mortality among the baseline characteristics (hazard ratio [HR]=2.41,95%CI,1.63-3.56,P<0.001).CONCLUSIONSIn this retrospective observation study, the incidence of CI-AKI was 4.2% among stroke patients undergoing cerebral angiography.CI-AKI was an independent risk factor for in-hospital mortality and 1-year mortality in stroke patients undergoing cerebral angiography. eGFR<60 ml/min/1.73 m2, anemia, a high NIHSS score and proteinuria were independent risk factors for CI-AKI. Especially proteinuria was not only associated with CI-AKI, but also independently associated with 1-year mortality.