Rongyi Chen

Global Incidence and Outcomes of Adult Patients With Acute Kidney Injury After Cardiac Surgery: A Systematic Review and Meta-Analysis.

OBJECTIVES To estimate the global incidence and outcomes of acute kidney injury (AKI) after cardiac surgery in adult patients. DESIGN A systematic review and meta-analysis. SETTING Cardiac surgery wards. PARTICIPANTS Adult patients after cardiac surgery INTERVENTIONS None. MEASUREMENTS AND MAIN RESULTS The authors searched PubMed, Web of Science, Cochrane Library, OVID, and EMBASE databases for all articles on cardiac surgery patients published during 2004 to 2014. Meta-analyses were conducted to generate pooled incidence, mortality, ICU length of stay, and length of hospital stay. The authors also described the variations according to study design, criteria of AKI, surgical methods, countries, continents, and their economies. After a primary and secondary screen, 91 observational studies with 320,086 patients were identified. The pooled incidence rates of AKI were 22.3% (95% confidence interval [CI], 19.8 to 25.1) in total and 13.6%, 3.8%, and 2.7% at stages 1, 2, and 3, respectively, whereas 2.3% of patients received renal replacement therapy. The pooled short-term and long-term mortality were 10.7% and 30%, respectively, and increased along with the severity of stages. The pooled unadjusted odds ratio for short-term and long-term mortality in patients with AKI relative to patients without AKI was 0.144 (95% CI, 0.108 to 0.192, p<0.001) and 0.342 (95% CI 0.287-0.407, p<0.001), respectively. The pooled average ICU length of stay and length of hospital stay in the AKI group were 5.4 and 15 days, respectively, while they were 2.2 and 10.5 days in the no-AKI group. CONCLUSIONS AKI is a great burden for patients undergoing cardiac surgery and can affect short-term and long-term prognoses of these patients.

Augmented O-GlcNAc signaling via glucosamine attenuates oxidative stress and apoptosis following contrast-induced acute kidney injury in rats

ABSTRACT Contrast‐induced acute kidney injury (CI‐AKI) is an iatrogenic renal injury and associated with substantial morbidity and mortality in susceptible individuals. Despite extensive study of a variety of agents for renal protection, limited strategies have been shown to be effective in the reduction of CI‐AKI. O‐linked &bgr;‐N‐acetylglucosamine (O‐GlcNAc) is a post‐translational regulatory modification of intracellular proteins and governs the function of numerous proteins, both cytosolic and nuclear. Increasing evidence suggests that O‐GlcNAc levels are increased in response to stress and that acute augmentation of this reaction is cytoprotective. However, the underlying mechanisms by which augmented OGlcNAc signaling provides renoprotection against contrast media insults is still unknown. Here, we investigated the effect of augmented O‐GlcNAc signaling via glucosamine on CI‐AKI and explored the underlying molecular mechanisms, particularly its relationship with PI3‐kinase (PI3K)/Akt signaling. We used a novel and reliable CI‐AKI model consisting of 5/6 nephrectomized (NE) rats, and a low‐osmolar contrast media (iohexol, 10 mL/kg, 3.5gI) injected via the tail vein after dehydration for 48 h. The results showed that augmented O‐GlcNAc signaling by glucosamine prevented the kidneys against iohexol‐induced injury characterized by the attenuation of renal dysfunction, tubular damage, apoptosis and oxidative stress. Furthermore, this renoprotection was blocked by treatment with alloxan, an O‐GlcNAc transferase inhibitor. Augmented O‐GlcNAc signaling also increased the protein expression levels of phospho‐Akt (Ser473, but not Thr308 and Thr450), phospho‐GSK‐3&bgr;, Nrf2, and Bcl‐2, and decreased the levels of Bax and cleaved caspase‐3. Both alloxan and specific inhibitors of PI3K (Wortmannin and LY294002) blocked the protection of glucosamine via inhibiting Akt signaling pathway. We further identified O‐GlcNAcylated Akt through immunoprecipitation and western blot. We confirmed that Akt was modified by O‐GlcNAcylation, and glucosamine pretreatment increased the O‐GlcNAcylation of Akt. Collectively, the results demonstrate that glucosamine induces renoprotection against CI‐AKI through augmented O‐GlcNAc and activation of PI3K/Akt signaling, making it a promising strategy for preventing CI‐AKI. HighlightsIncreasing evidence suggests that O‐linked &bgr;‐N‐acetylglucosamine (O‐GlcNAc) levels are increased in response to stress and that acute augmentation of this reaction is cytoprotective.We used a novel and reliable contrast‐induced acute kidney injury (CI‐AKI) model and the results showed that augmented O‐GlcNAc signaling by glucosamine prevented the kidneys against iohexol‐induced injury by the attenuation of apoptosis and oxidative stress.Furthermore, both alloxan and specific inhibitors of PI3K (Wortmannin and LY294002) blocked the protection of glucosamine via inhibiting Akt signaling pathway.

Monocyte/lymphocyte ratio as a better predictor of cardiovascular and all-cause mortality in hemodialysis patients: A prospective cohort study

Introduction: Patients with chronic kidney disease, especially those with end‐stage renal disease, have an increased risk of death. Previous studies have suggested neutrophil/lymphocyte ratio (NLR) was related to worse outcome in patients undergoing hemodialysis (HD). However, monocyte/lymphocyte ratio (MLR) has not been evaluated in HD patients. In this study, we prospectively studied the predictive value of MLR for all‐cause and cardiovascular mortality in HD patients and compared it with NLR.

Factors associated with the elevated percentage of CD4CD69 T cells in maintained hemodialysis patients

Abstract Background: CD4 T-cell abnormality, influencing the outcome of the maintained hemodialysis (MHD), is common in patients on dialysis. We try to find out factors associated with the activated CD4 T cells, CD4CD69 T cells, to improve the dialysis quality. Methods: A cross-sectional study was conducted to evaluate the change of CD4CD69 in MHD patients and healthy controls in our hospital from September 2015 to May 2016. A total of 164 MHD patients and 24 healthy controls were included according to the criteria. Univariate and multivariate logistic regression models after correlation analysis were executed to discover the related factors of CD4CD69 T-cell posterior to the division of the CD4CD69 T cell according to its median. Results: The lymphocytes were lower, but the percentage of CD4CD69 T cells was higher in MHD patients compared with healthy controls, even after the propensity score matching based on age and sex. The percentage of CD4 T cells showed no significant difference between the two groups. Further multivariate logistic regression models revealed that CD4CD69 T cell was independently associated with serum total protein (OR 95%CI: 0.830[0.696, 0.990], p = .038), transferrin (OR 95%CI: 3.072[1.131, 8.342], p = .028) and magnesium (OR 95%CI: 16.960[1.030, 279.275], p = .048). Conclusion: The percentage of CD4CD69 T cells, activated CD4 T cells, elevated in hemodialysis patients despite the decrease in lymphocytes. The elevated CD4CD69 T cells were independently associated with serum total protein negatively, but transferrin and magnesium positively. Strengthening nutrition, reducing the concentration of transferrin and magnesium might be beneficial to reduce the activation of CD4 T cells and improve the outcome of MHD patients.

Dysnatremia is an Independent Indicator of Mortality in Hospitalized Patients

Background Dysnatremia is a risk factor for poor outcomes. We aimed to describe the prevalence and outcomes of various dysnatremia in hospitalized patients. High-risk patients must be identified to improve the prognosis of dysnatremia. Material/Methods This prospective study included all adult patients admitted consecutively to a university hospital between October 1, 2014 and September 30, 2015. Result All 90 889 patients were included in this study. According to the serum sodium levels during hospitalization, the incidence of hyponatremia and hypernatremia was 16.8% and 1.9%, respectively. Mixed dysnatremia, which was defined when both hyponatremia and hypernatremia happened in the same patient during hospitalization, took place in 0.3% of patients. The incidence of dysnatremia was different in various underlying diseases. Multiple logistic regression analyses showed that all kinds of dysnatremia were independently associated with hospital mortality. The following dysnatremias were strong predictors of hospital mortality: mixed dysnatremia (OR 22.344, 95% CI 15.709–31.783, P=0.000), hypernatremia (OR 13.387, 95% CI 10.642–16.840, P=0.000), and especially hospital-acquired (OR 16.216, 95% CI 12.588–20.888, P=0.000) and persistent (OR 22.983, 95% CI 17.554–30.092, P=0.000) hypernatremia. Hyponatremia was also a risk factor for hospital mortality (OR 2.225, 95% CI 1.857–2.667). However, the OR increased to 56.884 (95% CI 35.098–92.193) if hyponatremia was over-corrected to hypernatremia. Conclusions Dysnatremia was independently associated with poor outcomes. Hospital-acquired and persistent hypernatremia were strong risk factors for hospital mortality. Effective prevention and proper correction of dysnatremia in high-risk patients may reduce the hospital mortality.

Delayed Ischemic Preconditioning Attenuated Renal Ischemia-Reperfusion Injury by Inhibiting Dendritic Cell Maturation

Background/Aims: Even though delayed ischemic preconditioning (DIPC) has been reported to produce renal protection, the underlying mechanism remains poorly understood. We reported that a 15-minute renal ischemic preconditioning (IPC) 4 days before subsequent ischemia-reperfusion attenuated renal injury Kidney dendritic cells (DCs) are abundant in the renal tubulointerstitium and, depending on their status, can induce immune activation or tolerance. The aim of the present study was to investigate the role of DCs in IPC of the kidney. Methods: Mouse kidneys were challenged by transient brief episodes of sublethal ischemia followed by subsequent prolonged ischemia. DC abundance and maturation in the spleen and kidney were measured by flow cytometry and immunohistochemical staining. To confirm the function of mature DCs in the renoprotective effect of IPC on renal ischemia-reperfusion injury the A2 adenosine receptor (A2AR) antagonist SCH58261 was administered to stimulate DC maturation prior to assessment of renal functional and histological injury and the inflammatory reaction. Results: Compared with sham-operated animals, preconditioned mice had a reduced injury with less CD11c+ cells, lower levels of the pro-inflammatory cytokine IL-17 and reduced expression of the mature DC marker CCR7. Preconditioned mice also produced more of the anti-inflammatory cytokine IL-10. Both renal cells and splenocytes from these mice had more DCs (CD45+/CD11c+/F4/80-), but fewer of these DCs were mature (CD45+/CD11c+/ F4/80-/MHC-II+/CD80+) compared with those from sham-treated animals, suggesting that the immunomodulatory effect of renal ischemic preconditioning is both local and systemic. Additionally, injection of the A2AR antagonist SCH58261 reversed IPC-induced inhibition of DC maturation and mitigated the protective effect of preconditioning, suggesting that DC maturation contributes to immune cell-mediated ischemic preconditioning. Conclusion: Our results show that DIPC of the kidney provides local and systemic immunosuppression by inhibiting DC maturation and hence mediates a renal protective effect.

Metabolic acidosis as a risk factor for the development of acute kidney injury and hospital mortality

Metabolic acidosis has been proved to be a risk factor for the progression of chronic kidney disease, but its relation to acute kidney injury (AKI) has not been investigated. In general, a diagnosis of metabolic acidosis is based on arterial blood gas (ABG) analysis, but the diagnostic role of carbon dioxide combining power (CO2CP) in the venous blood may also be valuable to non-respiratory patients. This retrospective study included all adult non-respiratory patients admitted consecutively to our hospital between October 01, 2014 and September 30, 2015. A total of 71,089 non-respiratory patients were included, and only 4,873 patients were evaluated by ABG analysis at admission. In patients with ABG, acidosis, metabolic acidosis, decreased HCO3− and hypocapnia at admission was associated with the development of AKI, while acidosis and hypocapnia were independent predictors of hospital mortality. Among non-respiratory patients, decreased CO2CP at admission was an independent risk factor for AKI and hospital mortality. ROC curves indicated that CO2CP was a reasonable biomarker to exclude metabolic acidosis, dual and triple acid-base disturbances. The effect sizes of decreased CO2CP on AKI and hospital mortality varied according to age and different underlying diseases. Metabolic acidosis is an independent risk factor for the development of AKI and hospital mortality. In non-respiratory patient, decreased CO2CP is also an independent contributor to AKI and mortality and can be used as an indicator of metabolic acidosis.