Background There are still limited studies comprehensively examining the diagnostic performance of neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C in contrast-induced nephropathy (CIN). The study aimed to investigate and compare the predictive value of NGAL and cystatin C in the early diagnosis of CIN. Methods and materials We searched the PubMed, EMBASE and Cochrane Library databases until November 10, 2019. The methodological quality of the included studies was assessed by the Quality Assessment of Diagnostic Accuracy Studies 2 (QUADAS-2) tool. Bivariate modeling and hierarchical summary receiver operating characteristic (HSROC) modeling were performed to summarize and compare the diagnostic performance of blood/urine NGAL and serum cystatin C in CIN. Subgroup and meta-regression analyses were performed according to the study and patient characteristics. Results Thirty-seven studies from thirty-one original studies were included (blood NGAL, 1840 patients in 9 studies; urine NGAL, 1701 patients in 10 studies; serum cystatin C, 5509 patients in 18 studies). Overall, serum cystatin C performed better than serum/urine NGAL (pooled DOR: 43 (95%CI: 12-152); AUROC: 0.93; λ: 3.79); serum and urine NGAL had a similar diagnostic performance (pooled DOR: 25 (95%CI: 6-108)/22(95%CI: 8-64); AUROC: 0.90/0.89; λ: 3.20/3.08). Meta-regression analysis indicated that the sources of heterogeneity might be CIN definition, assays, and nationalities. Conclusion Both NGAL and cystatin C can serve as early diagnostic indicators of CIN, while cystatin C may perform better than NGAL.

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Aims: We aimed to evaluate risk factors influencing adverse short-term outcomes in contrast-induced acute kidney injury (CI-AKI) patients after coronary angiography (CA) or percutaneous coronary intervention (PCI). Materials and methods: We retrospectively collected 64 consecutive CI-AKI patients after CA/PCI procedure from January 2014 to November 2019. The clinical outcomes were in-hospital mortality and persistent renal dysfunction (RD). Univariable and multivariable analyses were used to identify the risk factors for in-hospital mortality and persistent RD. Results: The incidence of in-hospital mortality was 7.8% in CI-AKI patients. After adjusting potential confounders, cardiogenic shock (OR=40.5, 95% CI, 4.147–395.494, P=0.001) was the independent risk factor for in-hospital mortality. Persistent RD occurred in 35 (59%) of survival patients. After adjusting potential confounders, eGFR (OR=3.553, 95% CI, 1.497–25.416, P=0.027), duration of procedure (OR=1.037, 95% CI, 1.002–1.073, P=0.038) and contrast media category (OR=7.189, 95% CI, 1.202–42.982, P=0.031) were independent risk factors for persistent RD. Conclusion: In-hospital mortality of CI-AKI patients was associated with severe systemic hemodynamic alteration. Patients with existing renal impairment before CA/PCI were more likely to develop persistent RD, while reducing CA/PCI procedure time and use of isotonic contrast media (IOCM) might help decreasing the risk.

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Objective: This study investigated the impact of 24-hour urinary calcium excretion (UCaE) on renal function decline in hospitalized patients with and without chronic kidney disease (CKD). Methods: This study enrolled 3,815 CKD patients with stages 1-4, and 1,133 Non-CKD patients admitted to the First Center of the Chinese PLA General Hospital between January 2014 and July 2022. The primary outcome for CKD was a composite of CKD progression defined as a 40% decline in estimated glomerular filtration rate (eGFR) and end-stage kidney disease and rapid kidney function decline [RKFD, defined as annual eGFR decline of ≥ 5 ml/min/1.73m 2/yr] as the secondary outcome. For Non-CKD patients, an eGFR decline of ≥ 20%, incidence of CKD, and a declining slope of ≥3 ml/min/1.73m 2/yr were the outcomes. The association between UCaE and kidney function decline was assessed using Cox proportional hazards and generalized linear models. Results: The primary outcome was observed in 813 CKD and 109 without CKD over a median follow-up of 3.0 and 4.1 years, respectively. For CKD patients, every 1-mmol/d increase in UCaE was associated with a 15% decreased risk of CKD progression. The hazard ratio (HR) was 0.85, with a 95% confidence interval (CI) of 0.77-0.93. And, for Non-CKD patients, the risk of renal function decline decreased by 11%. The multivariate models indicated that there was an annual decrease of eGFR in both CKD and Non-CKD, with a reduction of 0.122 ml/min/1.73m2/yr (P < 0.001) and 0.046 ml/min/1.73m2/yr (P = 0.004), respectively, for every 1-mmol/d increase of UCaE. Conclusions: CKD experiences a decrease in 24-hour UCaE as early as stage 1, with a significant decline in stage 4. CKD and Non-CKD patients with lower UCaE levels are at an increased risk of renal decline, regardless of other variables.

Acute kidney injury (AKI) is one of a complex clinical syndrome with various causes and poor efficacy. The pathophysiology of AKI includes inflammation, cell apoptosis and cell death. Long noncoding RNAs (lncRNAs) represent a class of functional RNA molecules with a length of more than 200 nucleotide units (NT) and no ability to encode proteins. To identify novel molecular mechanism and potential targets for AKI, the differential expressed lncRNAs between normal and AKI tissues were analyzed with bioinformatics tool. In the present study, the mouse kidney ischemia/reperfusion injury (IRI) model and cell oxygen and glucose deprivation/ reperfusion (OGD/R) model were established. The expression levels of lncRNAs, miRNAs and mRNAs were detected by high-throughput sequencing technology. Meanwhile, lncRNA, miRNA expression levels were detected by quantitative real-time PCR. Luciferase analysis was used to further investigate the interaction between lncRNA AK154753 and miRNA, miRNA and mRNA. Western-blot were performed to test the expression of apoptosis related proteins. Furthermore, TUNEL assay was united with flow cytometry to detect cell apoptosis rate. We found lncRNA AK154753 was significantly up-regulated, while miR-345-3p and miR-708-5p were significantly down-regulated during IRI. At the same time, IRI triggered cell apoptosis both in vivo and in vitro as the evidence by upregulation of Bim/Bak/cleaved-caspase3. Luciferase analysis showed that lncRNA AK154753 could both interacted with miR-345-3p and miR-708-5p, miR-345-3p could interacted with Bak, miR-708-5p could interacted with Bim respectively. Inhibition of lncRNA AK154753 alleviated cell apoptosis along with miR-345-3p/miR-708-5p up-regulated during IRI. In conclusion, the results suggest that lncRNA AK154753 participates in the occurrence and development of acute kidney ischemia-reperfusion injury by regulating miR-345-3p/Bak, miR-708-5p/Bim axes. Inhibiting lncRNA AK154753 may represent new therapeutic modalities for renal IR injury.