Association between serum uric acid levels and clinical outcomes in patients with acute kidney injury

AbstractBackground The effects of serum uric acid (SUA) on clinical outcomes in patients with acute kidney injury (AKI) are unclear. The aim of this study was to investigate the association of SUA levels with clinical outcomes of AKI patients.Methods The data of AKI patients hospitalized in the Affiliated Hospital of Qingdao University were retrospectively reviewed. Multivariable logistic regression was utilized to assess the association between SUA levels and the clinical outcomes of AKI patients. Receiver operating characteristic (ROC) analysis was applied to assess the predictive ability of SUA levels for in-hospital mortality in patients with AKI.Results A total of 4,646 AKI patients were eligible for study inclusion. In multivariable analysis, after adjustment for various confounding factors in the fully adjusted model, a higher SUA level was found to be associated with increased in-hospital mortality of AKI patients with an odds ratio (OR) of 1.72 (95% CI, 1.21–2.33, p = 0.005) for the SUA level >5.1–6.9 mg/dl group and 2.75 (95% CI, 1.78–4.26, p 6.9 mg/dl group compared with the reference group (SUA ≤3.6 mg/dl). In the ROC analysis, the area under the curve (AUC) of SUA was 0.65 with a sensitivity of 51% and a specificity of 73%.Conclusions An elevated SUA level is associated with an increased risk of in-hospital mortality in patients with AKI, and it appears to be an independent prognostic marker for these patients

Mesenchymal stem cells protect against sepsis-associated acute kidney injury by inducing Gal-9/Tim-3 to remodel immune homeostasis

AbstractObjective The present study investigated the specific mechanism by which mesenchymal stem cells (MSCs) protect against sepsis-associated acute kidney injury (SA-AKI).Methods Male C57BL/6 mice underwent cecal ligation and puncture surgery to induce sepsis and then received either normal IgG or MSCs (1 × 106 cells, intravenously) plus Gal-9 or soluble Tim-3 3 h after surgery.Results After cecal ligation and puncture surgery, the mice injected with Gal-9 or MSCs plus Gal-9 had a higher survival rate than the mice in the IgG treatment group. Treatment with MSCs plus Gal-9 decreased serum creatinine and blood urea nitrogen levels, improved tubular function recovery, reduced IL-17 and RORγt levels and induced IL-10 and FOXP3 expression. Additionally, the Th17/Treg cell balance was altered. However, when soluble Tim-3 was used to block the Gal-9/Tim-3 pathway, the septic mice developed kidney injury and exhibited increased mortality. Treatment with MSCs plus soluble Tim-3 blunted the therapeutic effect of MSCs, inhibited the induction of Tregs, and suppressed the inhibition of differentiation into Th17 cells.Conclusion Treatment with MSCs significantly reversed the Th1/Th2 balance. Thus, the Gal-9/Tim-3 pathway may be an important mechanism of MSC-mediated protection against SA-AKI