A novel risk factor of contrast associated acute kidney injury in patients after enhanced computed tomography: a retrospective study.

Background: Contrast associated acute kidney injury (CA-AKI) is a major cause of acute renal failure and the incidence of CA-AKI is still high in recent years. Risk stratification is traditionally based on glomerular filtration rate(GFR). Hence, the aim of this study was to explore the novel risk factors for CA-AKI after enhanced computed tomography (CT). Methods: A retrospective cohort study was conducted in 632 in-hospital patients undergoing enhanced CT. The patients were divided into CA-AKI and no-CA-AKI groups. For comparative analyses, we applied one-to-four cohorts of those two groups using propensity score-matching methods addressing the imbalances of age, gender, weight, and smoking. The baseline clinical and biochemical data were compared. Logistic regression analysis was employed to investigate the CA-AKI risk factors. The receiver operating characteristic (ROC) curve was adopted to test the value of RDW in predicting CA-AKI after enhanced CT. Results: 25 (3.96%) patients suffered from CA-AKI. Those subjects who developed CA-AKI had advanced age, severer renal functional injury, lower albumin, higher baseline RDW, neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ratio (PLR) than those without CA-AKI. It also exhibited more severe anemia including decreased hemoglobin and red blood cell count (all p < 0.05). The baseline RDW, albumin and PLR between the two groups were statistically significant different after PSM. Binary logistic regression analysis showed that baseline RDW, albumin and eGFR were correlated with CA-AKI after contrast-enhanced CT examination. The RDW exhibited moderated discrimination ability for predicting CA-AKI beyond eGFR, with an AUC of 0.803 (95% CI [0.702-0.90]) vs 0.765 (95% CI [0.70-0.83]). Conclusion: Increased baseline RDW and decreased eGFR are risk factors for CA-AKI after enhanced CT. RDW exhibited good predictive value and can be used as an early warning marker for patients suffering from CA-AKI after enhanced CT.

Emergency irradiation with 3.4 Gy/2f in sellar/suprasellar germinoma patients with rapid visual acuity decline.

BACKGROUND: Rapid visual acuity (VA) decline was a common complaint in patients with sellar/suprasellar germinoma. In our hospital, 3.4 Gy/2f of emergency irradiation was applied to save patient VA and enable subsequent chemoradiotherapy. This study aimed to investigate the efficacy of emergency irradiation with 3.4 Gy/2f in patients with sellar/suprasellar germinoma who had rapid VA decline. METHODS: From January 2014 to December 2017, 33 patients with sellar/suprasellar germinoma who complained of VA decline within 3 months received 3.4 Gy/2f of emergency irradiation in Beijing Tiantan Hospital. The best-corrected VA (BCVA) and mean deviation (MD) were measured. Correlations between visual function change and clinical factors, including age at diagnosis, duration of VA decline, extent of tumor regression, serum level of tumor markers, were analyzed. RESULTS: Among 33 patients with sellar/suprasellar germinoma, the median diameter and volume of sellar/suprasellar lesions were 32 mm (range: 5-55 mm) and 12.9 cm (range 0.6-58.5 cm), respectively. Data on pre- and post-emergency-irradiation BCVA were obtained in 32 patients. For the right eyes, BCVA was improved in 23 patients (71.9%), unchanged in 7 (21.9%), and worsened in 2 (6.2%); and for the left eyes, these numbers were 27 (84.4%), 4 (12.5%), and 1 (3.1%), respectively. In terms of the logarithm of the minimum angle of resolution (logarithm of the minimum angle of resolution = Log (1/BCVA) score, the improvement was significant in both eyes (P < 0.001). In terms of MD, six patients had paired data and the improvement was marginal in the right eyes (P = 0.068) and significant in the left eyes (P = 0.043). However, no clinical factor was found to have correlation with visual function improvement. CONCLUSION: In sellar/suprasellar germinoma patients with VA decline, 3.4 Gy/2f of emergency irradiation was effective in improving visual function.

Smad7 inhibits AngII-mediated hypertensive nephropathy in a mouse model of hypertension.

The TGFß (transforming growth factor ß)/SMAD and NF-κB (nuclear factor κB) signalling pathways play a key role in hypertensive nephropathy. The present study examined whether targeting these pathways by SMAD7, a downstream inhibitor of both pathways, blocks AngII (angiotensin II)-induced hypertensive kidney disease in mice. A doxycycline-inducible SMAD7-expressing plasmid was delivered into the kidney by a non-invasive ultrasound-microbubble technique before and after AngII infusion. Results showed that pre-treatment with SMAD7 prevented AngII-induced progressive renal injury by inhibiting an increase in proteinuria and serum creatinine while improving the glomerular filtration rate. Similarly, treatment with SMAD7 in the established hypertensive nephropathy at day 14 after AngII infusion halted the progressive renal injury. These preventive and therapeutic effects of SMAD7 on hypertensive kidney injury were associated with inhibition of AngII-induced up-regulation of SMURF2 (SMAD-specific E3 ubiquitin protein ligase 2) and Sp1 (specificity protein 1), blockade of TGFß/Smad3-mediated renal fibrosis and suppression of NF-κB-driven renal inflammation. Moreover, overexpression of SMAD7 also prevented AngII-induced loss of renal miR-29b, an miRNA with an inhibitory role in both TGFß/Smad3 and NF-κB pathways. In conclusion, SMAD7 may be a therapeutic agent for AngII-mediated hypertensive nephropathy. Inhibition of the Sp1/SMAD3/NF-κB/miR-29b regulatory network may be a mechanism by which SMAD7 inhibits hypertensive nephropathy.