OBJECTIVETo determine the levels of urinary soluble intercellular adhesion molecule-1 (sICAM-1) and vascular cellular adhesion molecule-1 (VCAM-1) in patients with lupus nephritis (LN), and explore their correlation with renal disease activity.

METHODSUrine samples were collected from 92 renal biopsy-proven LN patients and 20 healthy controls. Renal disease activity was determined according to the ISN/RPS 2003 Revised Classification of Lupus Nephritis. The urine levels of sICAM-1 and VCAM-1 were detected by enzyme-linked immunosorbent assay, and the expressions of intrarenal ICAM-1 and VCAM-1 were evaluated by immunohistochemisty staining.

RESULTSUrinary sICAM-1 and VCAM-1 levels were elevated in LN patients compared with the controls. Significantly higher levels of urinary sICAM-1 and VCAM-1 were found in patients with active LN, who had also significantly increased intrarenal expressions of ICAM-1 and VCAM-1 compared with patients in remission. A strong positive correlation was noted between intrarenal expression and urine levels of ICAM-1 and VCAM-1. The receiver-operating characteristic (ROC) curve of urine sICAM-1 showed tan area under ROC curve of 0.874 for all participants in the test. A cutoff of 1095.00 pg/mg creatinine yielded a good sensitivity (0.945) and specificity (0.789). The ROC curve of urine VCAM-1 showed an area under ROC of 0.882 for all the participants, and a cutoff of 898.11 pg/mg creatinine yielded a good sensitivity (0.982) and specificity (0.667).

CONCLUSIONUrine sICAM-1 and VCAM-1 levels are positively correlated with their intrarenal expressions and reflect the activity of the nephritis, and therefore they may serve as potential biomarkers for early diagnosis of active LN.

Biomarkers ; urine ; Case-Control Studies ; Early Diagnosis ; Enzyme-Linked Immunosorbent Assay ; Humans ; Intercellular Adhesion Molecule-1 ; urine ; Kidney ; metabolism ; Lupus Nephritis ; diagnosis ; urine ; ROC Curve ; Sensitivity and Specificity ; Vascular Cell Adhesion Molecule-1 ; urine

Objective: To investigate the effects of glutamate (Glu) injected into hypothalamic paraventricular nucleus (PVN) on visceral pain of chronic visceral hypersensitivity (CVH) rats and its possible mechanism. Methods: Newborn SD rats were given CVH rat model by colorectal distension (CRD) on the 8th, 10th and 12th day after birth. Thirty rats with successful CVH model were randomly divided into CVH model group (CVH group), CVH + injection of saline into PVN group (NS group), CVH+ injection of Glu into PVN (3, 6, and 12 μg Glu, namely G3, G6, and G12, respectively), 6 rats in each group, and 6 SD rats with matching body mass were taken as sham operation group (Sham group). The pain behavior of the rats was evaluated by pain threshold, abdominal withdrawal reflex (AWR) score, and abdominal external oblique muscle electromyography (EMG). The expression of arginine vasopressin (AVP) and the proliferation of colon tissue were detected by immunohistochemical staining. The apoptosis of colon tissue was detected by TUNEL. Results: Compared with the NS group, the pain thresholds of the G3, G6 and G12 groups increased, and the AWR scores and EMG amplitudes decreased. The differences were statistically significant(Pain threshold: t=7.65, 16.31, 24.78, both P<0.05; AWR scores: t=-2.98, -4.77, -7.29, both P<0.05; EMG amplitudes: t=-3.06, -5.75, -8.92, both P<0.05). Compared with the Sham group, the expression of AVP in PVN of the CVH group and NS group decreased ((42.63±5.20) %, (18.67±2.94) %, (17.53±2.47) %; t=6.95, t=7.56, both P<0.05). The expression of AVP was increased after different doses of Glu into PVN, and the AVP level in G12 group ((18.15±6.49)%) was higher than that of NS group, the difference was statistically significant (t=-4.21, P<0.05). Compared with the Sham group, the expression of PCNA in colonic mucosal cells of the CVH group and NS group decreased ((65.48±1.68) %, (18.39±1.67) %, (17.69±1.68) %; t=34.35, t=34.80, both P<0.05). The expression of PCNA was increased after different doses of Glu injected into PVN, and the PCNA level in G12 group ((59.91±5.63)%) was higher than that of NS group, the difference was statistically significant (t=-12.44, P<0.05). Compared with the Sham group, the expression of apoptotic cells in colonic mucosal cells of the CVH group and NS group increased ((23.38±11.40)%, (83.79±3.57)%, (80.91±2.47)%; t=-8.77, t=-8.54, both P<0.05). The expression of apoptotic cells was decreased after different doses of Glu into PVN, and the G12 group was ((18.15±6.49) %). Compared with NS group, the difference was statistically significant (t=15.65, P<0.05). Conclusion Injection of Glu into hypothalamic PVN can alleviate the visceral pain behaviors in CVH rats, and its mechanism may be related to arginine vasopressin.

Objective: To explore the association between coagulation indicators and all-cause mortality in sepsis-related acute kidney injury (AKI) patients. Methods: Clinical data of patients with sepsis-related AKI admitted to the First Affiliated Hospital of Guangxi Medical University from June 10, 2016 to June 10, 2018 were retrospectively analyzed. The patients were divided into death group and survival group according to the outcome of 28 d. The risk factors of all-cause mortality in sepsis-related AKI patients were analyzed. Receiver operating characteristic curve (ROC) was used to evaluate the prognostic value of independent risk factor for the death of sepsis-related AKI patients and Kaplan-Meier method was used to draw the survival curve. Results: A total of 214 patients with sepsis-related AKI were enrolled into this study. Their age was (57.90±16.96) years old, and the ratio of male to female was 2.57∶1. There was at least one abnormal coagulation indicator in 74.77%(160/214) of patients, and multiple organ dysfunction syndrome (MODS) in 37.38% of patients. The 28-day all-cause mortality was 28.04%(60/214). Prothrombin time, activated partial thrombin time (APTT), international standardized ratio, thrombin time, procalcitonin, abnormal coagulation indicators and the incidence of MODS in the death group were higher than those in the survival group, while body weight, hemoglobin, the percent of neutrophile granulocyte, platelet count, prothrombin activity, serum albumin and the proportion of renal replacement therapy (RRT) were lower than those in the survival group (all P<0.05). Cox regression analysis suggested that sepsis-related AKI patients with prolonged APTT had a higher risk for all-cause death (HR=2.610, 95%CI 1.077-6.326, P=0.034). The Kaplan-Meier survival curve indicated that 28 d survival rate of APTT extension group was lower than that of the non-APTT extension group (37.1% vs 70.6%, Log-rank χ²=16.881, P<0.001), and the average survival time was shorter than that of the non-APTT extension group (21.79 d vs 24.73 d). Conclusions Coagulation abnormalities are common in patients with sepsis-related AKI, which are also correlated to the all-cause death. APTT extension is an independent risk factor for the all-cause death in sepsis-related AKI patients.