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We aim to develop and validate a nomogram model for predicting severe acute kidney injury (AKI) after orthotopic liver transplantation (OLT). A total of 576 patients who received OLT in our center were enrolled. They were assigned to the development and validation cohort according to the time of inclusion. Univariable and multivariable logistic regression using the forward variable selection routine were applied to find risk factors for post-OLT severe AKI. Based on the results of multivariable analysis, a nomogram was developed and validated. Patients were followed up to assess the long-term mortality and development of chronic kidney disease (CKD). Overall, 35.9% of patients were diagnosed with severe AKI. Multivariable logistic regression analysis revealed that recipients' BMI (OR 1.10, 95% CI 1.04–1.17, p = 0.012), hypertension (OR 2.32, 95% CI 1.22–4.45, p = 0.010), preoperative serum creatine (sCr) (OR 0.96, 95% CI 0.95–0.97, p < 0.001), and intraoperative fresh frozen plasm (FFP) transfusion (OR for each 1000 ml increase 1.34, 95% CI 1.03–1.75, p = 0.031) were independent risk factors for post-OLT severe AKI. They were all incorporated into the nomogram. The area under the ROC curve (AUC) was 0.73 (p < 0.05) and 0.81 (p < 0.05) in the development and validation cohort. The calibration curve demonstrated the predicted probabilities of severe AKI agreed with the observed probabilities (p > 0.05). Kaplan-Meier survival analysis showed that patients in the high-risk group stratified by the nomogram suffered significantly poorer long-term survival than the low-risk group (HR 1.92, p < 0.01). The cumulative risk of CKD was higher in the severe AKI group than no severe AKI group after competitive risk analysis (HR 1.48, p < 0.05). With excellent predictive abilities, the nomogram may be a simple and reliable tool to identify patients at high risk for severe AKI and poor long-term prognosis after OLT. [ABSTRACT FROM AUTHOR]

It is well known that the progression of hyperuricemia disease often contributes to renal dysfunction. However, there have been few studies on uric acid nephropathy (UAN), especially its relationship with gut microbiota. UAN is usually accompanied by disordered intestinal flora, and damaged gut barrier, which are closely related to tubulointerstitial fibrosis, and systemic inflammation. In previous studies, it has been confirmed that curcumin could alleviate tubulointerstitial fibrosis, and improve renal function through its antioxidant, anti-apoptotic, and anti-inflammatory efficacies. However, the effects curcumin exerts on intestinal flora in uric acid nephropathy are still unknown. Therefore, we used next-generation sequencing technology to investigate the effects of curcumin on gut microbiota in a rat model of UAN induced by adenine and potassium oxonate, and rats were randomly divided into control, model or curcumin treatment groups. The results demonstrated that, compared to the model group, the treatment group showed decreased serum uric acid (156.80 ± 11.90 μmol/L vs. 325.60 ± 18.65 μmol/L, p < 0.001), serum creatinine (66.20 ± 11.88 μmol/L vs. 182.20 ± 8.87 μmol/L, p < 0.001) and BUN level (13.33 ± 3.16 mmol/L vs. 36.04 ± 6.60 mmol/L, p < 0.001). The treatment group also displayed attenuated renal pathological lesions and metabolic endotoxemia (25.60 ± 5.90 ng/mL vs. 38.40 ± 4.98 ng/mL, p < 0.01), and improved tightly linked proteins expression. Besides, curcumin altered the gut microbiota structure in UAN rats. More specifically, curcumin treatment protected against the overgrowth of opportunistic pathogens in UAN, including Escherichia-Shigella and Bacteroides, and increased the relative abundance of bacteria producing short‐chain fatty acids (SCFAs), such as Lactobacillus and Ruminococcaceae. These results suggest that curcumin could modulate gut microbiota, fortify the intestinal barrier, attenuate metabolic endotoxemia, and consequently protect the renal function in UAN rats. [ABSTRACT FROM AUTHOR]