Calcification detection on upper extremity arteries: a comparison of ultrasonic and X-ray methods.

Background: Vascular calcification (VC) has been observed in patients with hemodialysis, whereas few studies have investigated calcification in the upper extremity vasculature. Both ultrasound and X-ray are used to investigate the calcification of arteries in patients. However, there is a lack of data on the consistency between these two methods. The aim of this study was to investigate the occurrence of VC in the radial and ulnar arteries of hemodialysis patients and investigate the detection consistency in VC between ultrasound and X-ray. Methods: Ultrasound and X-ray examinations were performed in the radial and ulnar arteries of both the left and right upper extremities of 40 patients on hemodialysis. The calcification status of arteries was evaluated by the calcification index from ultrasound and X-ray respectively. Clinical variables of patients were collected from all the involved patients. Results: Of the 40 patients, VC was detected in 31 patients by ultrasound, while X-ray detected VC in 22 patients. Compared to ultrasound assessment, X-ray assessment was 73.21% sensitive but only 66.35% specific with a positive predictive value of 53.95% for detecting calcifications in the radial or ulnar artery. The level of agreement between ultrasound and X-ray results was fair. In addition, our data showed that more ulnar arteries had VCs than the corresponding radial arteries. Conclusion: Ultrasound is more sensitive in detecting the presence of calcified atherosclerotic lesions. Ultrasound and X-ray exhibited fair consistency. Ultrasound screening for upper extremity radial and ulnar arteries in hemodialysis patients may deserve attention to explore its clinical significance.

Lower limb arterial thrombosis in an adult with membranous glomerulonephritis.

Massive proteinuria and hypoalbuminemia are potential risk factors in thromboembolic complications. Venous thrombosis is a frequent complication of thromboembolism in patients with membranous glomerulonephritis, while arterial thrombosis is much less reported. A 35-year-old man presented with nephrotic syndrome and osteofascial compartment syndrome in the right lower limb due to arterial thrombosis. The biopsy findings were consistent with those of stage 2 membranous nephropathy. After immunotherapy (steroids and cyclosporine), the massive proteinuria, renal function, and serum albumin improved markedly. This is the first case of adult membranous glomerulonephritis with unilateral lower extremity arterial thrombosis diagnosed by renal biopsy and arteriography. It further confirms the high incidence of thromboembolic complications with membranous nephropathy.

Alterations in Amygdala/Hippocampal Volume Ratios in Children with Obstructive Sleep Apnea Syndrome Caused by Adenotonsillar Hypertrophy.

BACKGROUND Intermittent hypoxemia can cause changes in certain brain structures. However, in pediatric patients with obstructive sleep apnea (OSA) caused by adenotonsillar hypertrophy (ATH), there is only limited information on the effect of ATH-induced OSA on brain structures. This study sought to investigate alterations in amygdala and hippocampal volumes in children with OSA by ATH. MATERIAL AND METHODS Magnetic resonance imaging scans were applied in children who had ATH-induced OSA (ATH/OSA) and in healthy children. Amygdala and hippocampus volumes and adenoid sizes were measured on MRI volumetric images. The ratio of adenoid size/nasopharyngeal depth was used to describe the severity of adenoid hypertrophy. The clinical variables of the involved subjects were investigated. RESULTS One hundred ATH/OSA children and 100 healthy children without ATH/OSA participated in the study. The ATH/OSA children had higher amygdala volumes and amygdala/hippocampus volume ratios but lower hippocampus volumes than healthy controls, and the amygdala/hippocampus volume ratios were correlated with disease duration and hypoxemia conditions. However, our data showed that amygdala/hippocampus volume ratios were not correlated with the ratios of adenoid size/nasopharyngeal depth in the ATH/OSA children. In addition, the ratio of adenoid size/nasopharyngeal depths in ATH/OSA children was higher than that in healthy children in each subgroup based on the age of participants. CONCLUSIONS Compared to healthy controls, amygdala/hippocampus volume ratios are increased in children with ATH/OSA.

Circ_0008529 Contributes to Renal Tubular Cell Dysfunction in High Glucose Stress via miR-185-5p/SMAD2 Pathway in Diabetic Nephropathy.

Circular RNA (circRNA) is key regulator of diabetic nephropathy (DN) progression. However, the role of circ_0008529 in DN progression remains to be better deciphered. Cell viability, cell cycle, apoptosis and inflammation were measured by MTS assay, flow cytometry and corresponding assay kits. RT-qPCR was used to assess the expression of circ_0008529, miR-185-5p and SMAD family member 2 (SMAD2). Also, western blotting was performed to measure protein expression. Target relationship was validated by RNA pull-down assay, dual-luciferase reporter assay and RNA immunoprecipitation assay. Urinary exosome was isolated using ultracentrifugation method and identified by transmission electron microscopy. Receiver operating characteristic curve was used to analyze the diagnostic value of circ_0008529 in DN patients. Circ_0008529 and SMAD2 were upregulated, while miR-185-5p was downregulated in high glucose (HG)-induced renal tubular HK-2 cells. Under HG treatment, cell viability and cell cycle process were suppressed, while apoptosis, inflammation and extracellular matrix accumulation were enhanced. However, interfering circ_0008529 could attenuate HG-induced effects, and this protection was abated by miR-185 inhibition or SMAD2 re-expression. Mechanically, circ_0008529 and SMAD2 were competing endogenous RNAs for miR-185-5p via target binding, and circ_0008529 regulated SMAD2 expression via miR-185-5p. Notably, circ_0008529 expression was upregulated in urinary exosomes of DN patients, and showed diagnostic value (Sensitivity: 70.21%; Specificity: 86.67%). Circ_0008529 might be a potential target for DN, which regulated DN progression via miR-185-5p/SMAD2 pathway.

Suppression of lncRNA GAS6-AS2 alleviates sepsis-related acute kidney injury through regulating the miR-136-5p/OXSR1 axis in vitro and in vivo.

Acute kidney injury (AKI) is a common complication of sepsis and increase morbidity and mortality. Long non-coding RNA (LncRNA) GAS6-AS2 was related to inflammation and apoptosis in different diseases by regulating miRNAs and downstream genes, but its role in AKI remains unclear. Thus, we speculated that GAS6-AS2 might function in sepsis-related AKI via regulating target genes. Here, LPS or CLP was used to establish in vitro or in vivo sepsis-related AKI model. The interactions between GAS6-AS2 and miR-136-5p, and miR-136-5p and OXSR1, were validated by luciferase reporter assay, RNA pull-down, or RIP assay. Cell apoptosis was determined by flow cytometry, Western blotting, or IHC. The kidney injury was evaluated by H&E staining. The expression of GAS6-AS2, miR-136-5p, and OXSR1 was determined by qRT-PCR or Western blotting. We found that GAS6-AS2 was up-regulated in LPS-treated HK2 cells and the CLP-induced rat model. In vitro, GAS6-AS2 knockdown decreased cleaved caspase-3 and bax expression and increased bcl-2 expression. The levels of TNF-α, IL-1ß, and IL-6 were reduced by GAS6-AS2 down-regulation. GAS6-AS2 knockdown ameliorated oxidative stress in the cells, as indicated by the reduced ROS and MDA levels and the elevated SOD level. In vivo, GAS6-AS2 down-regulation decreased urinary NGAL and Kim-1 levels and serum sCr and BUN levels, and H&E proved that the kidney injury was alleviated. GAS6-AS2 knockdown also reduced apoptosis, inflammation, and oxidation induced by CLP in vivo. Mechanically, GAS6-AS2 sponged miR-136-5p which targeted OXSR1. Overall, lncRNA GAS6-AS2 knockdown has the potential to ameliorate sepsis-related AKI, and the mechanism is related to miR-136-5p/OXSR1 axis.

CircSMAD4 alleviates high glucose-induced inflammation, extracellular matrix deposition and apoptosis in mouse glomerulus mesangial cells by relieving miR-377-3p-mediated BMP7 inhibition.

BACKGROUND: Diabetic nephropathy (DN) is a common complication of diabetes mellitus. Accumulating studies suggest that the deregulation of circular RNA (circRNA) is involved in DN pathogenesis. This study aimed to investigate the role of circSMAD4 in DN models. METHODS: Mice were treated with streptozotocin to establish DN models in vivo. Mouse glomerulus mesangial cells (SV40-MES13) were treated with high glucose to establish DN models in vitro. The expression of circSMAD4, miR-377-3p and bone morphogenetic protein 7 (BMP7) mRNA was measured by quantitative real-time PCR (qPCR). The releases of inflammatory factors were examined by ELISA. The protein levels of fibrosis-related markers, apoptosis-related markers and BMP7 were checked by western blot. Cell apoptosis was monitored by flow cytometry assay. The predicted relationship between miR-377-3p and circSMAD4 or BMP7 was validated by dual-luciferase reporter assay or pull-down assay. RESULTS: CircSMAD4 was poorly expressed in DN mice and HG-treated SV40-MES13 cells. HG induced SV40-MES13 cell inflammation, extracellular matrix (ECM) deposition and apoptosis. CircSMAD4 overexpression alleviated, while circSMAD4 knockdown aggravated HG-induced SV40-MES13 cell injuries. MiR-377-3p was targeted by circSMAD4, and miR-377-3p enrichment partly reversed the effects of circSMAD4 overexpression. BMP7 was a target of miR-377-3p, and circSMAD4 regulated BMP7 expression by targeting miR-377-3p. MiR-377-3p overexpression aggravated HG-induced injuries by suppressing BMP7. CONCLUSION: CircSMAD4 alleviates HG-induced SV40-MES13 cell inflammation, ECM deposition and apoptosis by relieving miR-377-3p-mediated inhibition on BMP7 in DN progression.

Pre-dialysis renal clinic visits and patients' outcomes on peritoneal dialysis.

PURPOSE: To investigate the effect of pre-dialysis renal care on peritoneal dialysis (PD) patients' outcomes in China. METHODS: In this retrospective cohort study, patients who started PD during January 1, 2006, to December 31, 2014, were included. Patients' medical charts were reviewed to extract the information. To explore the effect of pre-dialysis renal care on patients' outcomes, patient were divided into two groups according to whether or not they had frequent renal clinic visits: Group A (with frequent visits) and Group B (without frequent visits). RESULTS: A total of 668 patients were included. Patients who admitted to emergency room before PD initiations were significantly higher in Group B than in Group A (42.7 vs. 33 %, p = 0.01). However, there was no significant difference in the proportion of patients requiring emergency hemodialysis prior to PD commencement (20.5 vs. 24.6 %, p = 0.21), acute heart failure (30.2 vs. 35.4 %, p = 0.16) and pulmonary infection (15.4 vs. 12.1 %, p = 0.23) between groups. Both the mortality and technical failure rate in Group A were significantly lower as compared to Group B (p = 0.003 and p < 0.01, respectively). Multivariable Cox regression analysis showed frequent pre-dialysis renal clinic visits were associated with both lower mortality rate (HR 0.62, 95 % CI 0.46-0.85, p = 0.003) and technical failure on PD (HR 0.58, 95 % CI 0.36-0.92, p = 0.022). CONCLUSION: Pre-dialysis frequent clinic visits were associated with better PD outcomes. Pre-dialysis renal clinic management was suboptimal in the present cohort. More organized system to ensure people with established chronic kidney disease are well managed is necessary in China.