Relation Between Exposure to Tobacco Smoke Assessed by Serum Cotinine Concentration and Questionnaire Method, and Serum Renalase Concentration-the Importance of the Coexistence of Arterial Hypertension and Other Cardiovascular Diseases.

Exposure to tobacco smoke (ETS) is one of the main risk factors for cardiovascular disease (CVD). Renalase is a protein that may play a role in the pathogenesis of CVD. The aim of the study was to assess the relationship between ETS and serum renalase concentration. A group of 109 patients was recruited for this study (49.7 ± 14.7 years). In accordance with the questionnaire, patients were divided into the following subgroups: subgroup A- declaring themselves active smokers (n = 36), subgroup B- declaring themselves non-smokers and exposed to environmental tobacco smoke (n = 35), subgroup C- declaring themselves non-smokers and not exposed to environmental tobacco smoke (n = 38). The same patients were divided based on cotinine concentration into the following subgroups: subgroup D- active smokers (n = 42), subgroup E- non-smokers exposed to environmental tobacco smoke (n = 66), and subgroup F- non-smokers not exposed to environmental tobacco smoke (n = 1). Serum cotinine concentration and serum renalase concentration were measured using ELISA tests. Serum renalase concentration was statistically significantly higher in subgroup C than in subgroups A and B and in subgroup E and F than in D. There was a negative correlation between serum cotinine concentration and serum renalase concentration (r = -0.41, p < 0.05). Regression analysis showed that higher BMI, higher diastolic blood pressure, coronary artery disease and higher serum cotinine concentration are independent risk factors of lower serum renalase concentration. The questionnaire method of assessing exposure to tobacco smoke was characterized by high sensitivity, but only moderate specificity, especially in terms of assessing environmental exposure to tobacco smoke. In summary, the study showed an independent relationship between exposure to tobacco smoke and lower serum renalase concentration.

Association of renalase with clinical outcomes in hospitalized patients with COVID-19.

Renalase is a secreted flavoprotein with anti-inflammatory and pro-cell survival properties. COVID-19 is associated with disordered inflammation and apoptosis. We hypothesized that blood renalase levels would correspond to severe COVID-19 and survival. In this retrospective cohort study, clinicopathologic data and blood samples were collected from hospitalized COVID-19 subjects (March-June 2020) at a single institution tertiary hospital. Plasma renalase and cytokine levels were measured and clinical data abstracted from health records. Of 3,450 COVID-19 patients, 458 patients were enrolled. Patients were excluded if <18 years, or opted out of research. The primary composite outcome was intubation or death within 180 days. Secondary outcomes included mortality alone, intensive care unit admission, use of vasopressors, and CPR. Enrolled patients had mean age 64 years (SD±17), were 53% males, and 48% non-whites. Mean renalase levels was 14,108·4 ng/ml (SD±8,137 ng/ml). Compared to patients with high renalase, those with low renalase (< 8,922 ng/ml) were more likely to present with hypoxia, increased ICU admission (54% vs. 33%, p < 0.001), and cardiopulmonary resuscitation (10% vs. 4%, p = 0·023). In Cox proportional hazard model, every 1000 ng/ml increase in renalase decreased the risk of death or intubation by 5% (HR 0·95; 95% CI 0·91-0·98) and increased survival alone by 6% (HR 0·95; CI 0·90-0·98), after adjusting for socio-demographics, initial disease severity, comorbidities and inflammation. Patients with high renalase-low IL-6 levels had the best survival compared to other groups (p = 0·04). Renalase was independently associated with reduced intubation and mortality in hospitalized COVID-19 patients. Future studies should assess the pathophysiological relevance of renalase in COVID-19 disease.

Renalase is a novel tissue and serological biomarker in pancreatic ductal adenocarcinoma.

Dysregulated expression of the secretory protein renalase can promote pancreatic ductal adenocarcinoma (PDAC) growth in animal models. We characterized renalase expression in premalignant and malignant PDAC tissue and investigated whether plasma renalase levels corresponded to clinical PDAC characteristics. Renalase immunohistochemistry was used to determine the presence and distribution of renalase in normal pancreas, chronic pancreatitis, PDAC precursor lesions, and PDAC tissues. Associations between pretreatment plasma renalase and PDAC clinical status were assessed in patients with varied clinical stages of PDAC and included tumor characteristics, surgical resection in locally advanced/borderline resectable PDAC, and overall survival. Data were retrospectively obtained and correlated using non-parametric analysis. Little to no renalase was detected by histochemistry in the normal pancreatic head in the absence of abdominal trauma. In chronic pancreatitis, renalase immunoreactivity localized to peri-acinar spindle-shaped cells in some samples. It was also widely present in PDAC precursor lesions and PDAC tissue. Among 240 patients with PDAC, elevated plasma renalase levels were associated with worse tumor characteristics, including greater angiolymphatic invasion (80.0% vs. 58.1%, p = 0.012) and greater node positive disease (76.5% vs. 56.5%, p = 0.024). Overall survival was worse in patients with high plasma renalase levels with median follow-up of 27.70 months vs. 65.03 months (p < 0.001). Renalase levels also predicted whether patients with locally advanced/borderline resectable PDAC underwent resection (AUC 0.674; 95%CI 0.42-0.82, p = 0.04). Overall tissue renalase was increased in both premalignant and malignant PDAC tissues compared to normal pancreas. Elevated plasma renalase levels were associated with advanced tumor characteristics, decreased overall survival, and reduced resectability in patients with locally advanced/borderline resectable PDAC. These studies show that renalase levels are increased in premalignant pancreatic tissues and that its levels in plasma correspond to the clinical behavior of PDAC.

Simultaneously Detecting Monoamine Oxidase A and B in Disease Cell/Tissue Samples Using Paper-Based Devices.

As enzymes in the outer membrane of the mitochondrion, monoamine oxidases (MAOs) can catalyze the oxidative deamination of monoamines in the human body. According to different substrates, MAOs can be divided into MAO-A and MAO-B. The imbalance of the MAO-A is associated with neurological degeneration, while excess MAO-B activity is closely connected with Parkinson's disease (PD) and Alzheimer's disease (AD); therefore, detection of MAOs is of great significance for the diagnosis and treatment of these diseases. This work reports the multiplexed detection of MAO-A and MAO-B using paper-based devices based on chemiluminescence (CL). The detection limits were 5.01 pg/mL for MAO-A and 8.50 pg/mL for MAO-B in human serum. In addition, we used paper-based devices to detect MAOs in human cells and tissue samples and found that the results of paper-based detection and Western blotting (WB) showed the same trend. While only one antibody can be incubated on the same membrane by WB, multiple antibodies incubated on the same paper enabled simultaneous detection of MAO-A and MAO-B by paper-based devices. The paper-based assay could be used for preliminary early screening of clinical samples for MAOs and can be extended as an alternative to WB for multiplexed detection of various proteins in disease cell or tissue samples.

Detention in Juvenile Correctional Facilities Is Associated with Higher Platelet Monoamine Oxidase B Activity in Males.

Juvenile delinquency is related to several biological factors, yet very few vulnerability biomarkers have been identified. Previous data suggest that the enzyme monoamine oxidase B (MAO-B) influences several personality traits linked to the propensity to engage in delinquent behavior. Building on this evidence, we assessed whether conduct disorder (CD), juvenile delinquency adjudications, or detention in a correctional facility were associated with either platelet MAO-B activity or the MAOB rs1799836 polymorphism. The study enrolled 289 medication-free male youths, including 182 individuals detained in a correctional facility (with or without a diagnosis of CD). Of the remaining 107 participants, 26 subjects had a diagnosis of CD, and 81 were mentally healthy controls. Platelet MAO-B activity was determined by spectrophotofluorometry, while MAOB rs1799836 was genotyped using qPCR. Platelet MAO-B activity, corrected for age and smoking, was significantly higher in juvenile detainees (p < 0.001), irrespective of CD diagnosis. MAOB rs1799836 was not associated with platelet MAO-B activity or with detention in a correctional facility, CD diagnosis, or delinquent behavior. These data suggest that detention in a juvenile correctional facility increases platelet MAO-B activity in male adolescents. Future studies are needed to determine the mechanisms and functional significance of MAO-B peripheral elevation in juvenile male detainees.

Novel biomarkers of acute kidney injury following living donor liver transplantation.

Urinary biomarkers such as neutrophil gelatinase-associated lipocalin (NGAL) and renalase were recently studied for their potential role in the early detection of acute kidney injury (AKI) in patients with cirrhosis. Our study was conducted on 50 patients with end-stage liver disease undergoing living donor liver transplantation. The patients were divided into two groups: Group I contained 23 patients with AKI who had undergone liver transplantation and Group II included 27 non-AKI patients who had undergone liver transplantation. Serum renalase and NGAL levels were measured by ELISA; renalase was measured on day 1, day 7, and three months after liver transplantation. NGAL was measured on day 1 postliver transplantation. There was an improvement in liver function, kidney functions, hemoglobin level, platelet count, and C- reactive protein levels in patients at three months posttransplantation when compared to day 1, day 3, and day 7 (P < 0.01). Comparison of the renalase level at day 1, day 7, and three months showed that there was a highly significant decline at three months in the AKI group compared to the non-AKI group (P < 0.01). Regarding the NGAL level at day 1, there was no significant difference between the AKI and non-AKI groups (P > 0.05). The receiver operating characteristic curve for the renalase biomarker showed a borderline significant change between the AKI and non-AKI groups at day 1 [area under the curve (AUC): 0.54, P = 0.08], day 7 (AUC: 0.605, P = 0.08), and three months (AUC: 0.605, P = 0.08). However, the NGAL biomarker level was not significantly different between the AKI and non-AKI groups. Our study suggests that renalase showed a better predictive value and a higher accuracy in identifying postliver transplantation patients with AKI than NGAL.

The partnership between renalase and ejection fraction as a risk factor for increased cardiac remodeling biomarkers in chronic heart failure patients.

Objective: Heart failure (HF) represents a huge socio-economic burden. It has been demonstrated, experimentally, that renalase, a newly discovered protein, prevents cardiac hypertrophy and adverse remodeling, which is seen in HF. We postulated the following aims: to investigate associations of renalase with biomarkers of cardiac remodeling: galectin-3, soluble suppression of tumorigenicity, (sST2), growth differentiation factor 15 (GDF-15) and syndecan-1, myocardial stretch (BNP) and cardio-renal axis (cystatin C) in HF patients with reduced ejection fraction (HFrEF) and preserved ejection fraction (HFpEF) to determine whether renalase, in combination with left ventricular ejection fraction (LVEF), represents a risk factor for plasma elevation in biomarkers.Methods: We classified HF patients (n = 76) according to LVEF (preserved/reduced), applied a median plasma renalase (113 ng/mL) as a cut-off value (low/high) and created four subgroups of HF patients: HFpEF/low renalase (n = 19), HFrEF/low renalase (n = 19), HFrEF/high renalase (n = 32) and HFpEF/high renalase (n = 6). A control group (n = 35) consisted of healthy volunteers.Results: Plasma concentrations of evaluated biomarkers were determined using an ELISA technique and were highest in HF patients with reduced EF (p < .001, respectively), and renalase's positive correlations were obtained relating to all biomarkers: galectin-3 (r = 0.913; p < .001), sST2 (r = 0.965; p < .001), GDF-15 (r = 0.887; p < .001), syndecan-1 (r = 0.922; p < .001), BNP (r = 0.527; p < .001) and cystatin C (r = 0.844; p < .001) and strong and negative correlation with LVEF (r = -0.456, p < .001). Increased renalase, regardless of the EF (preserved/reduced), was shown to be an independent risk factor for an increase in all evaluated cardiac remodeling biomarkers, p < .001, respectively. However, increased renalase and reduced EF was the only independent risk factor for BNP and cystatin C elevation, p < .001, respectively. Results after multivariable adjustments (age/gender) were identical.Conclusion: When elevated plasma renalase and HF are present, regardless of EF being reduced or preserved, that represents a significant risk factor for increase in cardiac remodeling biomarker plasma concentrations. However, only elevated renalase and reduced EF demonstrated significance as a risk factor for BNP and cystatin C plasma elevation. Renalase may be considered a promising molecule for the improved predictive abilities of conventional biomarkers and is worthy of further investigation.

Elevated renalase levels in patients with acute coronary microvascular dysfunction - A possible biomarker for ischemia.

AIMS: We explored the relationship between inflammation, renalase an anti-inflammatory protein, and acute chest pain with coronary microvascular dysfunction (CMD). METHODS AND RESULTS: We used cardiac Rb-82 PET/CT imaging to diagnose coronary artery disease (CAD/CALC) (defect or coronary calcification) and CMD (depressed coronary flow reserve without CAD) in patients with chest pain in an emergency department (ED). Blood samples were collected pre-imaging within 24 h of ED presentation and were analyzed for renalase and inflammatory markers including C-reactive protein, interleukins, interferon gamma, tumor necrosis factor, vascular endothelial growth factor, and metalloproteinases. Exclusions were age ≤30 years, myocardial infarction, hemodynamic instability, hypertensive crisis, heart failure or dialysis. Between 6/2014 and 11/2015, 80 patients undergoing PET/CT provided blood and were categorized as normal (18%), CAD/CALC (27%) and CMD (55%). Median renalase values were highest in patients with CMD (5503 ng/ml; IQR 3070) compared to patients with normal flows (4266 ng/ml; IQR 1503; p = 0.02) or CAD/CALC (4069 ng/ml IQR 1850; p = 0.004). CMD patients had similar median values for inflammatory markers as normal patients (p > 0.05). Renalase remained an independent predictor of CMD (OR 1.34; 95% CI = 1.1-1.7, per 1000 ng/ml) after adjustment for smoking, family history, obesity and Framingham risk score. In a model for CMD diagnosis with Framingham risk score, typical angina history and CRP, renalase improved discrimination from C-statistic = 0.60 (95% CI 0.47, 0.73) to 0.70 (95% CI, 0.59-0.82). CONCLUSION: We found elevated renalase in response to ischemia from acute CMD. Its role as a biomarker needs validation in larger trials.

Renalase, Catecholamine and Nitric Oxide Changes Before and After Sodium Nitroprusside Administration to Patients who Develop Post-Coronary Artery By-Pass (CABG) Hypertension.

BACKGROUND: Hypertension develops at a rate of 33 to 70% after Coronary artery bypass grafting (CABG) operations. One of the most commonly used drugs to control hypertension is sodium nitroprusside (SNP). Additionally, renalase enzyme destroys catecholamines and mediates the regulation (reduction) of blood pressure. Thus, this clinical study aims to reveal how renalase, catecholamines and nitric oxide (NO) change and how certain hemodynamic parameters are affected in randomly and prospectively selected cases who are administered SNP for the treatment of blood pressure elevation within 6 to 8 hours after CABG surgery. METHODS: The study included 26 patients who developed hypertension after CABG, 12 patients who had normal blood pressure after CABG, and 22 healthy individuals. Renalase and catecholamine levels of the patients were measured using ELISA method and NO levels were determined by spectrophotometry. RESULTS: Renalase and NO levels of the patients who developed hypertension after CABG were found statistically significantly lower than those of healthy controls and patients who did not develop hypertension after CABG, while catecholamine levels were significantly higher in the former. After SNP was started, renalase and NO levels increased, and a significant decrease was observed in the catecholamine levels. Additionally, administration of SNP produced a slight increase in the heart rate and a decrease in systolic arterial pressure (SAP), diastolic arterial pressure (DAP) and means arterial pressure (MAP). CONCLUSION: SNP elevates NO and renalase levels; thus, administration of renalase preparations, which act in the destruction of catecholamines to contain persistent hypertension that develops in association with catecholamine elevation after CABG surgery, along with SNP and other medications used to lower blood pressure can be an effective therapeutic method to control hypertension.

Endocan Concentration in Patients With Primary Hypertension.

Inflammation and endothelial dysfunction may play an important role in the multifactorial pathogenesis of hypertension. Endocan is also thought to play a role in cell adhesion and inflammatory disorders. The aim of the study was to compare endocan concentrations in patients with primary hypertension and healthy volunteers. There were 104 patients with hypertension (study group) and 21 healthy volunteers (control group). The correlation between endocan, catecholamines, and blood pressure control in patients with primary hypertension and the control group was analyzed. The median endocan concentration in the study group (2.03 ng/mL) was significantly higher than in the control group (1.09 ng/mL, P = .0001). Endocan concentration was correlated positively with renalase ( r = .2, P = .047) and norepinephrine ( r = .25, P = .02). Negative correlation was observed between endocan and body mass index ( r = -.25, P = .016) and leukocyte count ( r = -.36, P = .0004). The present study reports higher plasma endocan concentration in patients with treated, well-controlled primary hypertension compared with healthy volunteers. The higher endocan concentration in the study group may reflect endothelial dysfunction in this population.

The association of measures of the serotonin system, personality, alcohol use, and smoking with risk-taking traffic behavior in adolescents in a longitudinal study.

Studies on the neurobiological basis of risk-taking behavior have most often focused on the serotonin system. The promoter region of the gene encoding the serotonin transporter contains a polymorphic site (5-HTTLPR) that is important for the transcriptional activity, and studies have demonstrated its association with brain activity and behavior. Another molecular mechanism that reflects the capacity of the central serotonin system is the activity of the enzyme monoamine oxidase (MAO) as measured in platelets. The purpose of the present study was to examine how measures of the serotonin system (platelet MAO activity and the 5-HTTLPR polymorphism), personality variables, alcohol use and smoking are associated with risk-taking traffic behavior in schoolchildren through late adolescence. The younger cohort of the longitudinal Estonian Children Personality Behaviour and Health Study (originally n = 583) filled in questionnaires about personality traits, smoking status, alcohol use and traffic behavior at age 15 and 18 years. From venous blood samples, platelet MAO activity was measured radioenzymatically and 5-HTTLPR was genotyped. During late adolescence, subjects with lower platelet MAO activity were more likely to belong to the high-risk traffic behavior group. Male 5-HTTLPRs'-allele carriers were more likely to belong to the high-risk traffic behavior group compared to the l'/l' homozygotes. Other variables predicting risk group were alcohol use, smoking and Maladaptive impulsivity.The results suggest that lower capacity of the serotoninergic system is associated with more risky traffic behavior during late adolescence, but possibly by different mechanisms in boys and girls.

The serum protein renalase reduces injury in experimental pancreatitis.

Acute pancreatitis is a disease associated with inflammation and tissue damage. One protein that protects against acute injury, including ischemic injury to both the kidney and heart, is renalase, which is secreted into the blood by the kidney and other tissues. However, whether renalase reduces acute injury associated with pancreatitis is unknown. Here, we used both in vitro and in vivo murine models of acute pancreatitis to study renalase's effects on this condition. In isolated pancreatic lobules, pretreatment with recombinant human renalase (rRNLS) blocked zymogen activation caused by cerulein, carbachol, and a bile acid. Renalase also blocked cerulein-induced cell injury and histological changes. In the in vivo cerulein model of pancreatitis, genetic deletion of renalase resulted in more severe disease, and administering rRNLS to cerulein-exposed WT mice after pancreatitis onset was protective. Because pathological increases in acinar cell cytosolic calcium levels are central to the initiation of acute pancreatitis, we also investigated whether rRNLS could function through its binding protein, plasma membrane calcium ATPase 4b (PMCA4b), which excretes calcium from cells. We found that PMCA4b is expressed in both murine and human acinar cells and that a PMCA4b-selective inhibitor worsens pancreatitis-induced injury and blocks the protective effects of rRNLS. These findings suggest that renalase is a protective plasma protein that reduces acinar cell injury through a plasma membrane calcium ATPase. Because exogenous rRNLS reduces the severity of acute pancreatitis, it has potential as a therapeutic agent.

Enzyme-induced dual-network ε-poly-l-lysine-based hydrogels with robust self-healing and antibacterial performance.

An enzyme-induced strategy is reported to construct novel self-mending hydrogels based on ε-poly-l-lysine with both excellent self-healing properties (95%) and antibacterial capacity. Most importantly, the hydrogels are able to accelerate wound healing efficiently, which shows great potential in myriad biomedical fields, such as wound repair, artificial skin, and tissue engineering.

Renalase Protects against Renal Fibrosis by Inhibiting the Activation of the ERK Signaling Pathways.

Renal interstitial fibrosis is a common pathway for the progression of chronic kidney disease (CKD) to end-stage renal disease. Renalase, acting as a signaling molecule, has been reported to have cardiovascular and renal protective effects. However, its role in renal fibrosis remains unknown. In this study, we evaluated the therapeutic efficacy of renalase in rats with complete unilateral ureteral obstruction (UUO) and examined the inhibitory effects of renalase on transforming growth factor-ß1 (TGF-ß1)-induced epithelial-mesenchymal transition (EMT) in human proximal renal tubular epithelial (HK-2) cells. We found that in the UUO model, the expression of renalase was markedly downregulated and adenoviral-mediated expression of renalase significantly attenuated renal interstitial fibrosis, as evidenced by the maintenance of E-cadherin expression and suppressed expression of α-smooth muscle actin (α-SMA), fibronectin and collagen-I. In vitro, renalase inhibited TGF-ß1-mediated upregulation of α-SMA and downregulation of E-cadherin. Increased levels of Phospho-extracellular regulated protein kinases (p-ERK1/2) in TGF-ß1-stimulated cells were reversed by renalase cotreatment. When ERK1 was overexpressed, the inhibition of TGF-ß1-induced EMT and fibrosis mediated by renalase was attenuated. Our study provides the first evidence that renalase can ameliorate renal interstitial fibrosis by suppression of tubular EMT through inhibition of the ERK pathway. These results suggest that renalase has potential renoprotective effects in renal interstitial fibrosis and may be an effective agent for slowing CKD progression.

Plasma Catecholamine Levels on the Morning of Surgery Predict Post-Operative Atrial Fibrillation.

OBJECTIVES: This study sought to determine whether plasma catecholamines and monoamine oxidase-B (MOA-B) are associated with post-operative atrial fibrillation (POAF) in patients undergoing elective cardiac surgery. BACKGROUND: Although intra- and post-operative adrenergic tone has been demonstrated to be an causative factor for POAF, the role and association of pre-operative plasma catecholamines remains unclear. METHODS: Prior to administration of anesthesia on the morning of surgery, blood samples were obtained from 324 patients undergoing nonemergent coronary artery bypass graft and/or aortic valve surgery with cardiopulmonary bypass at East Carolina Heart Institute. The concentrations of norepinephrine (NE), dopamine (DA), epinephrine (EPI), and enzyme MAO-B were assessed in platelet-rich plasma. A log-binomial regression model was used to determine the association between quartiles of these variables and POAF. RESULTS: Levels of NE (p = 0.0006) and EPI (p = 0.047) in the 4th quartile [Formula: see text] were positively associated with POAF, whereas DA (p = 0.0034) levels in the 4th quartile [Formula: see text] were inversely associated with POAF. Adjusting for age, heart failure (HF), and history of atrial fibrillation, the composite pre-operative (adrenergic) plasma marker [Formula: see text] was associated with a 4-fold increased occurrence of POAF (adjusted p = 0.0001). No association between plasma MAO-B and POAF was observed. CONCLUSIONS: Our results suggest that pre-operative adrenergic tone is an important factor underlying POAF. This information provides evidence that assessment of plasma catecholamines may be a low-cost method that is easy to implement for predicting which patients are likely to develop POAF. More investigation in a multicentric setting is needed to validate our results.

Serum levels of 12 renal function and injury markers in patients with glomerulonephritis.

INTRODUCTION    Glomerulonephritis (GN) is a complex disease that affects the function of the whole nephron. There are few data on the serum levels of the most common biomarkers of kidney function and injury in GN, or the studies provide ambiguous results. OBJECTIVES    The aim of the study was to evaluate the levels of known kidney-specific and nonspecific markers of renal function or injury in the serum of patients with diagnosed primary or secondary GN, with or without the presence of nephrotic syndrome (NS) and arterial hypertension (AH). PATIENTS AND METHODS    The study included 58 patients with diagnosed GN and 6 patients with congenital defects (CD) of the kidney and AH (CD+AH). The serum levels of ß2-microglobulin (ß2M), neutrophil­gelatinase associated lipocalin (NGAL), osteopontin, trefoil factor 3 (TFF-3), calbindin, glutathione-S­transferase- π (GST-π), interleukin 18 (IL-18), kidney injury molecule 1 (KIM-1), and monocyte chemoattractant protein 1 (MCP-1) were measured with Kidney Toxicity Panels 1 and 2 using the Bio-Plex method. Renalase levels were measured using an enzyme-linked immunosorbent assay. RESULTS    In the whole group and in the subgroups (GN, GN+AH, GN+NS, CD+AH), NGAL, KIM-1, TFF-3, IL-18, ß2M, and calbindin levels correlated with estimated glomerular filtration rate (eGFR). In patients with NS, this correlation for calbindin was reversed. Renalase, MCP-1, GST-π, and osteopontin levels were independent of eGFR. Increase in IL-18 levels in the group with GN was assiociated with lower odds of the kidney disease. When this group was divided according to eGFR into subgroups G1-G5, TFF-3, NGAL, and ß2M levels increased with the stage of the disease. CONCLUSIONS In patients with NS, renalase and MCP-1 might regulate each other's levels. Further studies are needed to investigate associations between renalase, MCP-1, and osteopontin as factors unrelated to eGFR in GN. NS may contribute to the loss of calbindin from serum. NGAL, KIM-1, TFF-3, IL-18, ß2M, and calbindin are good indicators of kidney function loss in patients with GN.

A New Risk Factor for Traumatic Spinal Cord Injury.

Several behavioral factors such as violence, impulsivity, and alcohol-related problems are associated with traumatic spinal cord injury (TSCI). Such factors have been associated with inherently low neuronal serotonergic capacity that in turn is reflected in low activity of monoamine oxidase (MAO) as measured in platelets. The aim of the study was to characterize platelet MAO activity and impulsivity in persons with TSCI. Data were collected from 93 patients with TSCI and compared with 93 age- and gender-matched control subjects. Platelet MAO activity was measured radioenzymatically and expressed as nanomoles of beta-phenylethylamine oxidized per 10 to the tenth power platelets per minute. Facets of impulsivity were self-reported using Barratt Impulsiveness Scale (BIS-11). Most of the patients were men (87%). The mean time from TSCI was 4.3 ± 3.7 years. Twenty-one (24%) patients reported social problems associated with alcohol, and 30 (39%) patients had consumed alcohol before the trauma. Platelet MAO activity was significantly lower among the patients with TSCI (6.4 ± 3.2 vs.10.8 ± 5.2, p < 0.0001). This difference was not affected by consideration of their smoking status. The patients with TSCI had significantly higher BIS-11 impulsivity compared with the controls (62.8 ± 10.0 vs. 55.4 ± 8.6, p = 0.0001). The patients with TSCI have lower platelet MAO activity, and they are more impulsive compared with the healthy controls. Our results indicate that both low platelet MAO activity and high impulsivity are important risk factors for TSCI that can have predictive value and aid in undertaking preventive measures.

Monoamine oxidase and agitation in psychiatric patients.

Subjects with schizophrenia or conduct disorder display a lifelong pattern of antisocial, aggressive and violent behavior and agitation. Monoamine oxidase (MAO) is an enzyme involved in the degradation of various monoamine neurotransmitters and neuromodulators and therefore has a role in various psychiatric and neurodegenerative disorders and pathological behaviors. Platelet MAO-B activity has been associated with psychopathy- and aggression-related personality traits, while variants of the MAOA and MAOB genes have been associated with diverse clinical phenotypes, including aggressiveness, antisocial problems and violent delinquency. The aim of the study was to evaluate the association of platelet MAO-B activity, MAOB rs1799836 polymorphism and MAOA uVNTR polymorphism with severe agitation in 363 subjects with schizophrenia and conduct disorder. The results demonstrated significant association of severe agitation and smoking, but not diagnosis or age, with platelet MAO-B activity. Higher platelet MAO-B activity was found in subjects with severe agitation compared to non-agitated subjects. Platelet MAO-B activity was not associated with MAOB rs1799836 polymorphism. These results suggested the association between increased platelet MAO-B activity and severe agitation. No significant association was found between severe agitation and MAOA uVNTR or MAOB rs1799836 polymorphism, revealing that these individual polymorphisms in MAO genes are not related to severe agitation in subjects with schizophrenia and conduct disorder. As our study included 363 homogenous Caucasian male subjects, our data showing this negative genetic association will be a useful addition to future meta-analyses.

Renalase: Another puzzle piece between hypertension and simple renal cysts?

BACKGROUND AND AIM: Since renalase is mostly expressed in kidney tubules, simple renal cyst (SRC) originates from the kidney tubules, and both conditions are related to hypertension, it may be possible that SRC is associated with increased renalase levels. Therefore, in the current study we aimed to confirm the relation between renalase and epinephrine levels, the association between SRC and renalase levels and the association between renalase, blood pressure levels and endothelial dysfunction. MATERIALS AND METHODS: We made a cross-sectional study including 75 patients with SRC, and 51 controls were included to the study. Flow-mediated dilatation (FMD) was assessed, and serum renalase and epinephrine levels were determined. RESULTS: Patient with SRC had lower renalase, higher epinephrine and lower FMD levels when compared to patients without SRC (p < 0.05). Log renalase was correlated with log epinephrine (r = -0.302, p = 0.001) and log FMD (r = 0.642, p < 0.0001). There was no correlation between renalase and urine albumin/creatinine ratio and glomerular filtration rate. In univariate analysis, age, glomerular filtration rate, renalase and FMD were associated with the presence of SRC. Multivariate regression analysis of factors which are statistically significant in univariate analysis showed that age and renalase was associated with the presence of SRC. CONCLUSION: We have demonstrated that renalase levels were associated with the presence of SRC and endothelial dysfunction. Further research is necessary to highlight underlying mechanisms.