Predictive value of renal resistive index for the onset of acute kidney injury and its non-recovery: A systematic review and meta-analysis
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BACKGROUND: The predictive value of Doppler-based renal resistive index (RRI) for acute kidney injury (AKI) has not been fully elucidated. The present meta-analysis was carried out to disclose the correlation between AKI and RRI, and to investigate the predictive value of RRI for the onset of AKI and its recovery. MATERIALS AND METHODS: We searched PubMed, Embase, and Cochrane Library databases from inception to March 2019. The weighted mean difference (WMD) with a 95% confidence interval (CI) was used to assess the difference in RRIs between AKI and non-AKI patients. Moreover, the sensitivity and specificity were calculated, and summary receiver operating characteristic (SROC) curves were constructed. Meta-Disc and STATA were used for all statistical analyses. RESULTS: A total of 20 studies (14 for prediction of the onset of AKI and 6 for prediction of AKI short-term non-recovery) were included in our meta-analysis. The values of RRI (WMD = 0.07; 95% CI: 0.05 - 0.09; p < 0.0001) were significantly higher in AKI patients compared with non-AKI patients. The overall sensitivity and specificity of RRI for prediction of the onset of AKI were 72% (95% CI, 64 - 80%) and 79% (95% CI, 71 - 85%), respectively. As for prediction of AKI short-term non-recovery, the pooled sensitivity was 81% (95% CI: 64 - 91), and the pooled specificity was 80% (95% CI: 72 - 85). For the onset of AKI, the best predictive performance was observed for the RRI measured immediately after major surgery, and a cut-off value ≥ 0.715 also achieved superior predictive value. CONCLUSION: This study showed that the elevation of RRI may be related to the progression of AKI, and RRI could have good overall predictive value for the onset of AKI and its short-term non-recovery. Further studies in different clinical settings and patient groups are warranted before it could be widely used in clinical practice.

Colitis after polytrauma: case report.

Across the medical literature, delayed diagnosis and treatment leads to more costly and worse outcomes. Rehabilitation patients, especially those with polytrauma, often have a complex mixture of medical, social, and psychological health problems that can impair effective diagnosis and treatment. The case presentation describes the procession toward the diagnosis of ulcerative colitis in a preinjury asymptomatic male, suggesting a potential mechanism for its emergence and describing the effect of delayed diagnosis on the efficiency of rehabilitative care. As such, the differential diagnosis for early posttraumatic diarrhea should remain broad, particularly if unexplained or ineffectively controlled.

Addiction to elevated insulin-like growth factor I receptor and initial modulation of the AKT pathway define the responsiveness of rhabdomyosarcoma to the targeting antibody.

Insulin-like growth factor I receptor (IGF-IR) and its ligands are overexpressed by tumors, mediating proliferation and protecting against stress-induced apoptosis. Accordingly, there has been a considerable amount of interest in developing therapeutic agents against IGF-IR. IGF-IR is believed to be ubiquitously expressed without detectable mutation or amplification in cancer. We explored the determinants of cellular response to a humanized anti-IGF-IR antibody. Our results showed a large variation in IGF-IR levels in rhabdomyosarcoma tumor specimens that were comparable with those in rhabdomyosarcoma cell lines. In vitro analysis revealed a direct and very significant correlation between elevated IGF-IR levels and antiproliferative effects of the antibody and defined a receptor number that would predict sensitivity. Our data further suggested a strong dependence on IGF-IR for AKT signaling in cells with elevated IGF-IR. The sensitivity of the high IGF-IR-expressing cells was blocked with a constitutively active AKT. The extracellular signal-regulated kinase pathway was not affected by the antibody. In vivo studies showed that anti-IGF-IR had single-agent antitumor activity; furthermore, predictions of responses based on IGF-IR levels were accurate. In vivo biomarker analysis suggested that h7C10 down-regulated both IGF-IR and p-AKT initially, concordant with antitumor activity. Subsequent progression of tumors was associated with reactivation of p-AKT despite sustained suppression of IGF-IR. These results identified the first predictive biomarker for anti-IGF-IR therapies in cancer.