Access surveillance using invasive or noninvasive methods with an objective to improve access patency and decrease hospital admissions for access dysfunction in dialysis population has been promoted, but its success to predict incipient thrombosis and subsequent access failure is a controversial topic. Some studies have shown improvement in access outcomes, while others have failed to demonstrate an ideal method to diagnose access problems. Furthermore, the use of endovascular interventions such as percutaneous transluminal angioplasty to timely correct access problem might itself be a promoter of neointimal hyperplasia and restenosis during balloon angioplasty. There are significant costs and efforts associated with routine dialysis surveillance; therefore, it is necessary to understand whether such programs will help improve access-related problems and guarantee adequate dialysis care. It is generally agreed upon that despite the lack of guaranteed success of surveillance, such strategies have helped improve dialysis management, resulted in decreased costs and hospitalizations, and represented clinically relevant indications of failure prior to planning any radiological or surgical intervention. In this study, the authors review monitoring and surveillance measures in place, and their associated merits and limitations to detect stenosis and prevent incidences of vascular access thrombosis.

In the United States, hemodialysis remains the most common treatment modality for kidney failure, chosen by almost 90% of incident patients. A functioning vascular access is key to providing adequate hemodialysis therapy. Recently, major innovations in devices and technology for hemodialysis vascular access care have rapidly changed the landscape. Novel endovascular devices for creation of arteriovenous fistulas may offer a solution to the barriers encountered in initiating maintenance hemodialysis with a permanent vascular access rather than a central venous catheter (CVC). Furthermore, in the prevalent hemodialysis population, the minimally invasive endovascular arteriovenous fistula procedure should help improve long wait times for vascular access creation, which remains a major barrier to reducing CVC dependence. Bioengineered grafts are being developed and may offer another option to polytetrafluoroethylene grafts. Early studies with these biocompatible grafts are promising, as additional studies continue to evaluate their clinical outcomes in comparison to cryopreserved or synthetic options. Prolonging the vascular access patency with appropriate use of devices such as drug-coated balloons and stent grafts may complement the novel techniques of creating arteriovenous access. Finally, innovative solutions to treat stenosed and occluded thoracic central veins can provide an approach to creating a vascular access and allow patients with exhausted vasculature to remain on hemodialysis. The robust developments in hemodialysis vascular access are likely to change practice patterns in the near future.Complete author and article information provided before references.

Introduction Magnesium disorders are commonly encountered in chronic kidney disease (CKD) and are typically a consequence of decreased kidney function or frequently prescribed medications such as diuretics and proton pump inhibitors. While hypomagnesemia has been linked with increased mortality, the association between elevated magnesium levels and mortality is not clearly defined. Additionally, associations between magnesium disorders, type of death, and CKD progression have not been reported. Therefore, we studied the associations between magnesium levels, CKD progression, mortality, and cause specific deaths in patients with CKD. Methods Using the Cleveland Clinic CKD registry, we identified 10,568 patients with estimated Glomerular Filtration Rate (eGFR) between 15 and 59 ml/min/1.73 m2 in this range for a minimum of 3 months with a measured magnesium level. We categorized subjects into 3 groups based on these magnesium levels (≤ 1.7, 1.7–2.6 and > 2.6 mg/dl) and applied cox regression modeling and competing risk models to identify associations with overall and cause-specific mortality. We also evaluated the association between magnesium level and slope of eGFR using mixed models. Results During a median follow-up of 3.7 years, 4656 (44%) patients died. After adjusting for relevant covariates, a magnesium level < 1.7 mg/dl (vs. 1.7–2.6 mg/dl) was associated with higher overall mortality (HR = 1.14, 95% CI: 1.04, 1.24), and with higher sub-distribution hazards for non-cardiovascular non-malignancy mortality (HR = 1.29, 95% CI: 1.12, 1.49). Magnesium levels > 2.6 mg/dl (vs. 1.7–2.6 mg/dl) was associated with a higher risk of all-cause death only (HR = 1.23, 95% CI: 1.03, 1.48). We found similar results when evaluating magnesium as a continuous measure. There were no significant differences in the slope of eGFR across all three magnesium groups (p = 0.10). Conclusions In patients with CKD stage 3 and 4, hypomagnesemia was associated with higher all-cause and non-cardiovascular non-malignancy mortality. Hypermagnesemia was associated with higher all-cause mortality. Neither hypo nor hypermagnesemia were associated with an increased risk of CKD progression.