The sonographic features of lymph node venous networks and flow patterns in patients with primary chronic venous disease.

BACKGROUND: Our study aims to enhance the understanding of lymph node venous networks (LNVNs) by summarising their anatomical, sonographic features, and reflux patterns. METHOD: We examined 241 legs from 141 patients with primary chronic venous disease (CVD) using duplex ultrasound. RESULTS: The findings indicated variations in the shape, size, vascularity, and echogenicity of LNVN. The superficial inguinal lymph node with reflux appeared slightly larger, exhibiting higher velocities in the hilar artery. Regarding connections, venous flow within LNVN was predominantly drained through the saphenofemoral junction (SFJ), anterior accessory great saphenous vein (AAGSV), and great saphenous vein (GSV). A significant number of LNVNs were observed to be associated with anterolateral thigh tributaries. The study also identified valve cusps within LNVN. CONCLUSION: This study revealed a 12% prevalence of primary LNVN. Understanding the anatomical and haemodynamic features of LNVN informs treatment strategies and potentially helps prevent the recurrence of varicose veins.

A snapshot of venous ultrasound examinations in Australia and New Zealand: Implications for diagnosis and management of chronic venous disease interventions.

Objective: Chronic venous disease is a common vascular condition, affecting up to 60% of the population worldwide. In Australia and New Zealand, chronic venous insufficiency ultrasound examinations are primarily performed by sonographers. This research aimed to explore how ultrasound examinations are being performed, providing insights into current practices and recommendations for quality improvement. Method: A questionnaire was distributed to capture demographics, practices of ultrasound, examination techniques, the use of nomenclature and experience of the respondents. Results: The analysis of 97 responses showed a heterogeneity in the clinical application of ultrasound. Most sonographers performed less than two scans per day within 30-45 minutes. Deep venous incompetence was routinely excluded by all respondents. The majority used standing, sitting and reverse Trendelenburg position except for a few using supine position. Manual augmentation was the preferred provocation manoeuvre. Anatomical variations at the junctional level were not adequately evaluated. Although Giacomini's vein was assessed by 80%, 57% of those did not evaluate paradoxical reflux. Seventy-five per cent routinely assessed non-saphenous reflux; however, over 50% were unfamiliar with lymph node venous networks. A significant number of out-dated venous terms were still being used. A low participation rate in continuing professional development was identified, which might be attributable to limited education and training programs. Conclusion: The study is a multi-faceted exploration that identified a need for standardized diagnostic and reporting guidelines. Our results could explain discrepancies in diagnostic findings and inconsistencies in the use of medical terminology, with implications for clinical decision making and assessment of surgical outcome.

miR-103a-3p Silencing Ameliorates Calcium Oxalate Deposition in Rat Kidney by Activating the UMOD/TRPV5 Axis.

Maintaining the balance of calcium (Ca2+) metabolism in the kidney is crucial in preventing the formation of kidney stones. Functionally, the microRNA (miRNA) participating in this process needs to be unveiled. We induced NRK-52E cell injury by oxalate treatment. The role of transient receptor potential cation channel subfamily V member 5 (TRPV5) in oxalate-induced cells was studied by TRPV5 overexpression transfection, qRT-PCR, Western blot, MTT, and crystal adhesion detection. After identifying uromodulin (UMOD) expression in injured cells, we confirmed the interaction between TRPV5 and UMOD by coimmunoprecipitation (CoIP) and cell-surface biotinylation assays. The validation of UMOD-regulating TRPV5 in viability, crystal adhesion, and Ca2+ concentration of oxalate-induced cells was performed. Bioinformatics analysis and luciferase assay were used to identify the miRNA-targeting UMOD. The role of the miR-103a-3p-regulating UMOD/TRPV5 axis was detected by rescue experiments. We constructed a rat model with treatment of ethylene glycol (EG) to investigate the miR-103a-3p/UMOD/TRPV5 axis in vivo by hematoxylin-eosin (H&E) staining, Western blot, and immunohistochemistry (IHC). Upregulation of TRPV5 protected NRK-52E cells from oxalate-induced injury by enhancing cell viability and inhibiting CaOx adhesion. UMOD was depleted in oxalate-induced cells and positively interacted with TRPV5. UMOD silencing reversed the effect of TRPV overexpression on oxalate-induced cells. miR-103a-3p targeted UMOD and was mediated in the regulation of the UMOD/TRPV5 axis in oxalate-induced cells. Downregulating miR-103a-3p mitigated EG-induced CaOx deposition in kidney tissues in vivo by activating the UMOD/TRPV5 axis. miR-103a-3p silencing ameliorated CaOx deposition in the rat kidney by activating the UMOD/TRPV5 axis.