Ochsner Medical Center

About: Ochsner Medical Center is a healthcare organization based out in New Orleans, Louisiana, United States. It is known for research contribution in the topics: Population & Heart failure. The organization has 980 authors who have published 1159 publications receiving 49961 citations. The organization is also known as: Ochsner Hospital & Ochsner Foundation Hospital.

Treatment of C3 Glomerulopathy in Adult Kidney Transplant Recipients: A Systematic Review

Abstract: Background: C3 glomerulopathy (C3G), a rare glomerular disease mediated by alternative complement pathway dysregulation, is associated with a high rate of recurrence and graft loss after kidney transplantation (KTx). We aimed to assess the efficacy of different treatments for C3G recurrence after KTx. Methods: Databases (MEDLINE, EMBASE, and Cochrane Database) were searched from inception through 3 May, 2019. Studies were included that reported outcomes of adult KTx recipients with C3G. Effect estimates from individual studies were combined using the random-effects, generic inverse variance method of DerSimonian and Laird., The protocol for this meta-analysis is registered with PROSPERO (no. CRD42019125718). Results: Twelve studies (7 cohort studies and 5 case series) consisting of 122 KTx patients with C3G (73 C3 glomerulonephritis (C3GN) and 49 dense deposit disease (DDD)) were included. The pooled estimated rates of allograft loss among KTx patients with C3G were 33% (95% CI: 12–57%) after eculizumab, 42% (95% CI: 2–89%) after therapeutic plasma exchange (TPE), and 81% (95% CI: 50–100%) after rituximab. Subgroup analysis based on type of C3G was performed. Pooled estimated rates of allograft loss in C3GN KTx patients were 22% (95% CI: 5–46%) after eculizumab, 56% (95% CI: 6–100%) after TPE, and 70% (95% CI: 24–100%) after rituximab. Pooled estimated rates of allograft loss in DDD KTx patients were 53% (95% CI: 0–100%) after eculizumab. Data on allograft loss in DDD after TPE (1 case series, 0/2 (0%) allograft loss at 6 months) and rituximab (1 cohort, 3/3 (100%) allograft loss) were limited. Among 66 patients (38 C3GN, 28 DDD) who received no treatment (due to stable allograft function at presentation and/or clinical judgment of physicians), pooled estimated rates of allograft loss were 32% (95% CI: 7–64%) and 53% (95% CI: 28–77%) for C3GN and DDD, respectively. Among treated C3G patients, data on soluble membrane attack complex of complement (sMAC) were limited to patients treated with eculizumab (N = 7). 80% of patients with elevated sMAC before eculizumab responded to treatment. In addition, all patients who responded to eculizumab had normal sMAC levels after post-eculizumab. Conclusions: Our study suggests that the lowest incidence of allograft loss (33%) among KTX patients with C3G are those treated with eculizumab. Among those who received no treatment for C3G due to stable allograft function, there is a high incidence of allograft loss of 32% in C3GN and 53% in DDD. sMAC level may help to select good responders to eculizumab.

Accuracy and Clinical Utility of a Peri-Operative Risk Calculator for Total Knee Arthroplasty

Abstract: Utilizing the Medicare Provider Analysis and Review dataset, a, peri-operative total knee arthroplasty (TKA) risk calculator was created based on select preoperative comorbidities. We retrospectively identified and reviewed 2284 primary TKAs at a single institution from 2000-2008. A numerical, predicted complication risk was established for each patient. Actual complications occurring within the first 14 post-operative days were recorded. Statistical analysis was performed using the C-statistic and ANOVA test. Patients with higher predicted probability of a complication did show higher complication rates. The corresponding C-statistic was 0.609. (95% Confidence Interval: 0.542-0.677). When the patients were divided into 4 groups based on their calculated complication risk (0-5%, 5-10%, 10-25%, >25%) the statistical significance of the associated ANOVA was P < .001, showing that patients with higher predicted risk experienced more complications, and those with lower predicted risk experienced fewer complications. Based on our results, the calculator has predictive value and is clinically relevant.

MicroRNA Profile in Cerebrospinal Fluid and Plasma of Patients with Spontaneous Intracerebral Hemorrhage

Abstract: Spontaneous intracerebral hemorrhage (ICH) accounts for 15–20% of “acute stroke” with a significant morbidity and mortality [1]. Following ICH, pathobiological processes (blood–brain barrier (BBB) damage, cerebral edema, and inflammation) are activated [1,2]. The molecular changes associated with these processes could be a target for therapeutic interventions or potential biomarkers. Gene expression profiling of human tissues and experimental models of ICH have identified potential candidate genes [3]. MicroRNAs (miRNAs) are important gene regulators and primarily identified in tissues encapsulated in microvesicles [2,4]. Following tissue injury, miRNAs are released into the extracellular space [4]. Comparison of miRNAs from cerebrospinal fluid (CSF) and blood from the same patient is unique as CSF likely reflects the local events of injured brain tissue compared to miRNAs in the bloodstream. This study was approved by the Ochsner Medical Center Institution Review Board. Patients with ICH confirmed on computed tomography (CT) scan who required a ventricular drain were consented for CSF and blood sample collection. We enrolled five male subjects with a median age of 54 years (range, 37–78 years). The basic clinical information is provided (Table S1). Blood samples (10 mL) were collected in sodium citrate tubes, and CSF samples (3–5 mL) were collected within 24 h of presentation. The study was designed such that each patient serves as an intrinsic control in comparing CSF and blood miRNA expression patterns. Total RNA containing miRNAs was isolated from plasma and CSF (200 lL) for profiling of 782 known miRNAs (Exiqon). The real-time PCR was run for 40 cycles in a CFX-384 thermal cycler (Bio-Rad, Hercules, CA, USA). Cycle threshold (Ct) data were obtained using the regression method. Data were normalized using the global mean and log2-transformed using the GenEx software (Exiqon, Vedbaek, Denmark). Using a Ct value cutoff of 39, 423 miRNAs were reliably expressed in CSF and plasma. Of these, 128 miRNAs were detected in CSF, 14 miRNAs in plasma, and 281 miRNAs in both CSF and plasma. Differential miRNA expression analysis found 242 significantly expressed miRNAs (P < 0.05). Of these, 139 miRNAs were found at 2-fold higher in CSF and 94 miRNAs at 2-fold lower in CSF compared to plasma. When the P-values were adjusted for multiple testing correction using the Benjamin–Hochberg method, 211 miRNAs were statistically significant (P < 0.05; Table S2). The heat map of the top 25 significantly expressed miRNAs is shown with the corresponding fold change and significance value (Figure 1A, B). The highly expressed miR-204-5p (2075-fold), miR-125b-5p (108-fold), miR-9-5p (299-fold), miR-338-3p (146fold), miR-187-3p (21-fold), and miR-9-3p (42-fold) in CSF are associated with the regulation of matrix metalloproteinase-9 (MMP-9), IL-1b, IL-6, occludin, and SELE, to name a few. In the case of miR-204-5p, miR-9-3p, and miR-338-3p, which target MMP-9, their expressions in plasma were decreased, suggesting an increased expression and activation of pro-MMP-9 in plasma. However, the expression in CSF is decreased. In animal and human studies, elevated MMP-9 in plasma during the acute phase of ICH was associated with increased BBB damage, hematoma growth, and perihematomal edema [5]. MiR-126-5p expression was downregulated ( 8.3-fold) in CSF compared to plasma. miRNA-126 regulates vascular cell adhesion molecule 1 (VCAM-1) expression in endothelial cells. Decreased expression of miRNA-126 may lead to VCAM-1 expression and promotes immune cell localization at the site of injury. Zhu et al. [6] found miRNA levels in serum were mostly downregulated