Dataset Information

SLPI - a Biomarker of Acute Kidney Injury after Open and Endovascular Thoracoabdominal Aortic Aneurysm (TAAA) Repair.

ABSTRACT: Acute kidney injury (AKI) is a relevant complication following thoracoabdominal aortic aneurysm repair (TAAA). Biomarkers, such as secretory leucocyte peptidase inhibitor (SLPI), may enable a more accurate diagnosis. In this study, we tested if SLPI measured in serum is an appropriate biomarker of AKI after TAAA repair. In a prospective observational single-center study including 33 patients (51.5% women, mean age 63.0 ± 16.2 years) undergoing open and endovascular aortic aneurysm repair in 2017, SLPI was measured peri-operatively (until 72?h after surgery). After surgery, the postoperative complications AKI, as defined according to the KDIGO diagnostic criteria, sepsis, death, MACE (major cardiovascular events) and, pneumonia were assessed. In a subgroup analysis, patients with preexisting kidney disease were excluded. Of 33 patients, 51.5% (n = 17) of patients developed AKI. Twelve hours after admission to the intensive care unit (ICU), SLPI serum levels were significantly increased in patients who developed AKI. Multivariable logistic regression revealed a significant association between SLPI 12?hours after admission to ICU and AKI (P = 0.0181, OR = 1.055, 95% CI = 1.009-1.103). The sensitivity of SLPI for AKI prediction was 76.47% (95% CI = 50.1-93.2) and the specificity was 87.5% (95% CI = 61.7-98.4) with an AUC = 0.838 (95% CI = 0.7-0.976) for an optimal cut-off 70.03?ng/ml 12?hours after surgery. In patients without pre-existing impaired renal function, an improved diagnostic quality of SLPI for AKI was observed (Sensitivities of 45.45-91.67%, Specificities of 77.7-100%, AUC = 0.716-0.932). There was no association between perioperative SLPI and the incidence of sepsis, death, MACE (major cardiovascular events), pneumonia. This study suggests that SLPI might be a post-operative biomarker of AKI after TAAA repair, with a superior diagnostic accuracy for patients without preexisting impaired renal function.

SUBMITTER: Averdunk L

PROVIDER: S-EPMC7044192 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature

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SLPI - a Biomarker of Acute Kidney Injury after Open and Endovascular Thoracoabdominal Aortic Aneurysm (TAAA) Repair.

Averdunk Luisa L Rückbeil Marcia V MV Zarbock Alexander A Martin Lukas L Marx Gernot G Jalaie Houman H Jacobs Michael J MJ Stoppe Christian C Gombert Alexander A

Scientific reports 20200226 1

Acute kidney injury (AKI) is a relevant complication following thoracoabdominal aortic aneurysm repair (TAAA). Biomarkers, such as secretory leucocyte peptidase inhibitor (SLPI), may enable a more accurate diagnosis. In this study, we tested if SLPI measured in serum is an appropriate biomarker of AKI after TAAA repair. In a prospective observational single-center study including 33 patients (51.5% women, mean age 63.0 ± 16.2 years) undergoing open and endovascular aortic aneurysm repair in 2017 ...[more]

PMID: 32103084

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Project description:To characterize the inflammatory and coagulopathic response after endovascular thoracoabdominal aortic aneurysm (TAAA) repair and to evaluate the effect of the response on postoperative renal function.From July 2005 to June 2008, 42 patients underwent elective endovascular repair of a TAAA using custom designed multi-branched stent-grafts at a single academic institution. Four patients were excluded from the analysis. White blood cell count (WBC), platelet count, prothrombin time (PT), and creatinine were measured in all patients. In the last nine patients, interleukin-6 (IL-6), protein C, Factor V, d-dimers, cystatin C, and neutrophil gelatinase-associated lipocalin (NGAL) levels were also measured. Change in lab values were expressed as a percentage of baseline values.The 30-day mortality rate was 5% (2/38). All patients (n = 38) had a higher WBC (mean +/- SD: 139 +/- 80%, P < .0001), lower platelet count (56 +/- 15%, P < .0001), and higher PT (median: 17%, Interquartile range (IQR) 12%-22%, P < .0001) after stent-graft insertion. Twelve of 38 patients (32%) developed postoperative acute renal insufficiency (>50% rise in creatinine). Patients with renal insufficiency had significantly larger changes in WBC (178 +/- 100% vs 121 +/- 64%, P = .04) and platelet count (64 +/- 17% vs 52 +/- 12%, P = .02) compared with those without renal insufficiency. All patients (n = 9) had significant increases in NGAL (182 +/- 115%, P = .008) after stent-graft insertion. Six of nine patients (67%) had increased cystatin C (35 +/- 43%, P = .04) after stent-graft insertion, with a greater rise in those with postoperative renal insufficiency (87 +/- 32% vs 8 +/- 13%, P = .02). IL-6 levels were markedly increased in all patients (n = 9) after repair (9840 +/- 6160%, P = .008). Protein C (35 +/- 10%, P = .008) and Factor V levels (28 +/- 20%, P = .008) were uniformly decreased, while d-dimers were elevated after repair in all patients (310 +/- 213%, P = .008).Leukocytosis and thrombocytopenia were uniform following endovascular TAAA repair, and the severity of the response correlated with post-operative renal dysfunction. Elevation of a sensitive marker of renal injury (NGAL) suggests that renal injury may occur in all patients after stent-graft insertion.

Project description:BACKGROUND:Open surgical repair (OSR) for thoracoabdominal aortic aneurysms (TAA) is associated with a high pulmonary and renal morbidity rate. Ischemic preconditioning (IPC) is a mechanism of protection against the deleterious effects of ischemia-reperfusion. To our knowledge IPC has never been tested during OSR for TAA. METHODS:The primary objective of the study is to evaluate the efficacy of IPC during OSR for TAA with respect to acute kidney injury (AKI) according to KDIGO and pneumonia/prolonged ventilation-time during the first 8 postoperative days. The secondary objectives are to compare both arms with respect to cardiac complications within 48?h, renal and pulmonary complications within 21?days and mortality at 60?days. To assess the efficacy of IPC with respect to pulmonary and renal morbidity, a cox model for competing risks will be used. Assuming that the event occurs among 36% of the patients when no IPC is performed, the allocation of 55 patients to each arm should allow detecting a hazard ratio of at least 2.75 with a power of 80% when admitting 5% for an error of first kind. This means that 110 patients, enrolled in this multicenter study, may be randomised within 36?months of the first randomization. Randomization will be performed to allocate patients either to surgery with preconditioning before aortic cross clamping (Arm 1) or to surgery without preconditioning before aortic cross clamping (Arm 2). Randomization takes place during the intervention after intravenous injection of heparin, or after the start of femoral assistance. The procedure for IPC will be a supra-visceral thoracic aortic cross clamping for 5?min followed by an unclamping period of 5?min. This procedure will be repeated twice before starting thoracic aortic cross clamping needed to perform surgery. CONCLUSIONS:Our hypothesis is that ischemic preconditioning could reduce clinical morbidity and the incidence of lung damage associated with supra-visceral aortic clamping. TRIAL REGISTRATION:EPICATAStudy registered in ClinicalTrial.gov / number: NCT03718312 on Oct.24.2018 URL number.

Project description:Risk of open conversion after endovascular aortic aneurysm repair (EVAR-c) is poorly defined. The purpose of this analysis was to determine outcomes of elective EVAR-c compared with elective primary open abdominal aortic aneurysm repair (PAR) in the Vascular Quality Initiative.Vascular Quality Initiative patients who underwent elective EVAR-c and PAR (2002-2014) were reviewed. Candidate predictors of major adverse cardiac event (MACE) and/or 30-day mortality were entered into a multivariable model, and stepwise elimination was used to reduce the number of covariates to a best subset of predictors. To estimate the additive risk of EVAR-c for MACE or 30-day mortality over PAR, this variable was added along with the best subset of predictors into generalized estimating equations logistic regression models.We identified 159 EVAR-c and 3741 PAR patients. EVAR-c patients were older (73.5 ± 8.1 vs 69.5 ± 8.4 years; P < .0001), more likely to have diabetes (21% vs 15%; P = .03), and history of lower extremity bypass (9% vs 4%; P = .0006). EVAR-c was associated with a higher incidence of retroperitoneal aortic exposure (41%; n = 64 vs PAR, 26%, n = 976; P < .0001), use of a bifurcated graft (65%; n = 101 vs PAR, 52%; n = 1923; P = .001), greater blood loss (median [interquartile range], 2000 mL [1010-3500] vs PAR, 1200 mL [750-2000]; P < .0001) and longer procedure times (EVAR-c, 275 ± 122 minutes vs PAR, 232 ± 9 minutes; P < .0001). However, PAR more frequently was completed with a suprarenal and/or mesenteric cross-clamp (74%, n = 2749 vs EVAR-c, 53%, n = 83; P < .0001) and had a higher incidence of concomitant procedures (26%; n = 972 vs EVAR-c, 18%; n = 28; P = .03). Nonadjusted 30-day mortality was greater after EVAR-c: EVAR-c, 8% (n = 10) vs PAR, 3% (n = 105); P = .009. There was no difference in complication rates: EVAR-c, 33% (n = 52) vs PAR, 28% (n = 1056); P =.3. Preoperative 30-day mortality predictors included age (odds ratio [OR], 1.06/y, 95% confidence interval [CI], 1.04-1.1; P < .0001), chronic obstructive pulmonary disease (OR, 2.4; 95% CI, 1.6-3.5; P < .0001), history of leg bypass (OR, 2.3, 1.2-4.4;P =.01), suprarenal cross-clamp (OR 2.2, 1.2-4.1;P =.01), prior carotid revascularization (OR 2.2; 95% CI, 1.3-3.8; P = .0004), congestive heart failure (OR, 1.8; 95% CI, 0.9-3.5; P = .08), and female sex (OR, 1.6; 95% CI, 1.1-2.3; P = .02; area under the curve, 0.75). When controlling for covariates, EVAR-c was not significantly associated with MACE (OR, 1.2; 95% CI, 0.7-2.0; P = .4) or 30-day mortality (OR, 2.0; 0.9-4.2; P = .08).EVAR-c patients are typically older, have more comorbidities, and experience greater blood loss and longer procedure times compared with PAR patients. However, postoperative morbidity and mortality are primarily driven by patient covariates and intraoperative factors, rather than the need for endograft explantation. Several preoperative variables were identified as predictors of 30-day mortality after elective EVAR-c and should be considered during the decision-making process for remedial treatment of failed endovascular PAR.

Dataset Information

SLPI - a Biomarker of Acute Kidney Injury after Open and Endovascular Thoracoabdominal Aortic Aneurysm (TAAA) Repair.

Publications

SLPI - a Biomarker of Acute Kidney Injury after Open and Endovascular Thoracoabdominal Aortic Aneurysm (TAAA) Repair.

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