Arteriovenous Access Dysfunction Research Articles

Risk Factors for Internal Jugular Vein Thrombosis 1 Month After Non-Cuffed Hemodialysis Catheter Removal.

Background: Complications, namely, catheter-related thrombosis (CRT) and venous stenosis, are associated with non-cuffed hemodialysis catheters used for emergency vascular access. However, only a few reports have demonstrated changes in the venous lumen and intravenous thrombosis after catheter removal. In this study, we comprehensively investigated the risk factors for residual thrombus 1 month after hemodialysis catheter removal. Methods: This prospective observational study was conducted from June 2021 to October 2022. We included patients with end-stage kidney disease who underwent hemodialysis catheter placement in the internal jugular vein (IJV). After catheter removal, we observed the IJV using vascular ultrasound and evaluated the thrombus and vein properties. Furthermore, we observed thrombosis 1 month after catheter removal, and investigated the risk factors for residual thrombus 1 month after catheter removal. Results: A thrombus was observed at the site of catheter removal in all the cases. Of the 37 patients who were followed up, 11 exhibited a residual thrombus 1 month after catheter removal. Patients with arteriovenous (AV) access dysfunction and enlarged lymph nodes during catheter removal were significantly more likely to have a residual thrombus 1 month after catheter removal. These associations remained significant even after adjusting for age, sex, and diabetes status. Conclusions: In 29.7% of the patients, CRT persisted even 1 month after the removal of the non-cuffed hemodialysis catheter. The provision of early intervention in patients with AV access dysfunction and enlarged lymph nodes during catheter removal may prevent CRT persistence.

Contrast Venography Versus Intravenous Ultrasound in Hemodialysis Arteriovenous Access Dysfunction

Contrast Venography Versus Intravenous Ultrasound in Hemodialysis Arteriovenous Access Dysfunction

Is fetuin-A a biomarker of dialysis access dysfunction?

The arteriovenous (AV) access function of hemodialysis (HD) patients can be impaired by afferent artery stiffness due to preexisting microcalcification and by venous stenosis secondary to neointimal hyperplasia in whose development participates an upregulated local inflammatory process. Fetuin-A is a circulating potent inhibitor of vascular calcification and plays an important anti-inflammatory role. The aims of this prospective study were to investigate the relationship between baseline serum fetuin-A levels and: blood flow (QA) values at baseline, AV access failure (thrombosis or intervention for stenosis) during follow-up and primary unassisted AV access patency. We measured baseline serum fetuin-A levels and QA values of the AV access in 64 HD patients under routine QA surveillance for stenosis. Patients were classified into tertiles according to their baseline fetuin-A levels (g/L): <0.5 (tertile-1), 0.5-1.20 (tertile-2), and >1.20 (tertile-3). Fetuin-A was positively correlated with QA (Spearman coefficient = 0.311, p = 0.012). Fourteen patients (21.9%) underwent AV access failure and they had lower fetuin-A (0.59 ± 0.32 g/L) and lower QA (739.4 ± 438.8 mL/min) values at baseline compared with the remaining patients (1.05 ± 0.65 g/L and 1273.0 ± 596.3 mL/min, respectively) (p = 0.027 and p < 0.001, respectively). The AV access failure rate was highest (34.8%) in tertile-1 (lowest fetuin-A level). Unadjusted Cox regression analysis showed a decrease in the risk of AV access patency loss by increasing fetuin-A concentration (hazard ratio 0.395 (95% confidence interval: 1.42-1.69), p = 0.044) but it was not confirmed in the adjusted model, although the hazard ratio was low (0.523). Kaplan-Meier analysis showed that patients in tertile-3 (highest fetuin-A concentration) had the highest primary unassisted AV access patency (λ2 = 4.68, p = 0.030, log-rank test). If our results are confirmed in further studies, fetuin-A could be used as a circulating biomarker to identify HD patients at greater risk for AV access dysfunction, who would benefit from much closer dialysis access surveillance.

A comparison of stenting versus hemodialysis reliable outflow graft for hemodialysis patients with recurrent central venous obstructions

BackgroundCentral venous occlusive disease is a common cause of upper extremity arteriovenous access dysfunction in hemodialysis patients. When refractory to balloon angioplasty, the treatment options include central venous stenting and hemodialysis reliable outflow (HeRO; Merit Medical, South Jordan, Utah) graft. The purpose of the present study was to evaluate the outcomes of these options. MethodsA retrospective review was performed of patients who had undergone central venous stenting or HeRO placement for central venous obstruction from December 2008 to March 2018. The primary outcomes were the reintervention rates, patency, and mortality. ResultsA total of 75 hemodialysis patients were identified after failed balloon angioplasty for central venous obstruction. Of the 75 patients, 44 underwent central venous stenting comprising coverage of the subclavian vein (n = 27), innominate vein (n = 18), and/or superior vena cava (n = 5). Six stent patients later underwent HeRO placement. The stents used were stent grafts in 65% (Viabahn, n = 9; Fluency/Flair, n = 19; iCast, n = 2; and other, n = 1) and bare metal stents in 35% (Wall-stent, n = 6; Protégé, n = 1; Cobalt, n = 1; and other, n = 9). The remaining 31 patients underwent HeRO graft placement. The venous outflow component insertion sites were the internal jugular (n = 20), external jugular (n = 1), subclavian (n = 6), axillary (n = 2), and other (n = 2). The stent and HeRO groups were similar in the previous central venous intervention rates (median, 0.6 [interquartile range (IQR), 0-3.0]; vs median, 3.5 [IQR, 0-10.1] annually; P = .679). After the index procedure, no difference was found between the two groups in the frequency of dialysis circuit interventions annually (median, 2.0 [IQR, 0-6.0]; vs median, 2.0 [IQR, 0-7.0]; P = .291) nor central venous interventions (ie, angioplasty of the central veins or within the portion of the HeRO inside the central veins) annually (median, 2.0 [IQR, 0-4.1]; vs median, 0 [IQR, 0-2.4]; P = .419). The 1-year access circuit primary patency was 8.1% for stenting and 22.2% for HeRO (P = .109). The 2-year access circuit secondary patency was 40.0% for stenting and 52.4% for HeRO (P = .401). The all-cause mortality was similar at 1 year (3.7% vs 4.8%; P = .856) and 2 years (11.8% vs 23.5%; P = .368). ConclusionsCentral venous stenting and HeRO were shown to have similar rates of reintervention and patency. The results from the present study suggest that the multiple treatment options available for this problematic disease process can yield similar results when careful patient selection is applied.

Thoracic Central Venous Occlusive Disease and Haemodialysis Access

Benign central venous thoracic occlusion is a frequent issue in haemodialysis patients. Symptomatic stenosis affects quality of life and can cause dysfunction of arteriovenous access or make it impossible to implant a haemodialysis catheter. Common risk factors for the development of the occlusions are central venous catheters and cardiac rhythm devices. The gold standard for diagnosis is venous angiography. Treatment of asymptomatic lesions can lead to clinical deterioration and should be avoided. The primary method of treatment for symptomatic patients is endovascular therapy. Repeat balloon angioplasty is a standard therapy. In case of elastic recoiling or early recurrence, placement of bare metal stent or stent graft could be considered. Surgical options should be preserved only for refractory cases. Further randomised trials are needed to prove the efficacy of new devices, such as dedicated venous stents and drug coated balloons.

Orphan designation: Recombinant human type I pancreatic elastase for the prevention of arteriovenous access dysfunction in haemodialysis patients (vonapanitase), Prevention of arteriovenous access dysfunction in haemodialysis patients

Orphan designation: Recombinant human type I pancreatic elastase for the prevention of arteriovenous access dysfunction in haemodialysis patients (vonapanitase), Prevention of arteriovenous access dysfunction in haemodialysis patients

Orphan designation: Recombinant human type I pancreatic elastase for the prevention of arteriovenous access dysfunction in haemodialysis patients (vonapanitase), Prevention of arteriovenous access dysfunction in haemodialysis patients

Orphan designation: Recombinant human type I pancreatic elastase for the prevention of arteriovenous access dysfunction in haemodialysis patients (vonapanitase), Prevention of arteriovenous access dysfunction in haemodialysis patients

Orphan designation: Sirolimus, Prevention of arteriovenous access dysfunction...

Orphan designation: Sirolimus, Prevention of arteriovenous access dysfunction...

Orphan designation: Sirolimus, Prevention of arteriovenous access dysfunction...

Orphan designation: Sirolimus, Prevention of arteriovenous access dysfunction...

The association of genotype polymorphisms with vascular access patency in hemodialysis patients.

Some hemodialysis patients suffer from repeat dysfunction of dialysis vascular access and need procedures of angioplasty, thrombectomy, and even temporary catheter use. Why these patients are vulnerable to vascular access dysfunction and how to improve its patency are imperative to be discovered. Traditional risk factors for vascular access function had been widely investigated but could not fully explain this question. Several genotype polymorphisms were demonstrated to increase the incidence of cardiovascular disease and might also be linked to higher risk of vascular access dysfunction. As the major causes of arteriovenous access thrombosis are hypercoagulable status and arteriovenous access stenosis, the investigated genes mainly focus on the mediators of the coagulation cascade, inflammatory process, and endothelial dysfunction. The reported polymorphisms of genes significantly associated with arteriovenous access dysfunction included genes encoding methylene tetrahydrofolate reductase, coagulation factors, heme oxygenase-1, matrix metalloproteinase, transforming growth factor-β1, tumor necrosis factor-α, vascular endothelial growth factor-A, renin-angiotensin-aldosterone system, and protein methyl transferase. However, further prospective study is indispensable to elucidate the association between the genotype polymorphisms and the outcome of vascular access. More and more therapeutic options that focus on genotype polymorphisms may generate a great benefit to the patency of vascular access of uremic patients.

Deficiency of TLR4 homologue RP105 aggravates outward remodeling in a murine model of arteriovenous fistula failure

Arteriovenous access dysfunction is a major cause of morbidity for hemodialysis patients. The pathophysiology of arteriovenous fistula (AVF) maturation failure is associated with inflammation, impaired outward remodeling (OR) and intimal hyperplasia. RP105 is a critical physiologic regulator of TLR4 signaling in numerous cell types. In the present study, we investigated the impact of RP105 on AVF maturation, and defined cell-specific effects of RP105 on macrophages and vascular smooth muscle cells (VSMCs). Overall, RP105−/− mice displayed a 26% decrease in venous OR. The inflammatory response in RP105−/− mice was characterized by accumulation of anti-inflammatory macrophages, a 76% decrease in pro- inflammatory macrophages, a 70% reduction in T-cells and a 50% decrease in MMP-activity. In vitro, anti-inflammatory macrophages from RP105−/− mice displayed increased IL10 production, while MCP1 and IL6 levels secreted by pro-inflammatory macrophages were elevated. VSMC content in RP105−/− AVFs was markedly decreased. In vitro, RP105−/− venous VSMCs proliferation was 50% lower, whereas arterial VSMCs displayed a 50% decrease in migration, relative to WT. In conclusion, the impaired venous OR in RP105−/− mice could result from of a shift in both macrophages and VSMCs towards a regenerative phenotype, identifying a novel relationship between inflammation and VSMC function in AVF maturation.

Using Medical-Device Wearable to Improve Hemodialysis Patient’s Live and Access the Holistic Health

The increasing incidence of end-stage renal disease (ESRD) is the major burden to health budgets and a threat to public health worldwide. For many years, Taiwan has been ranked the first in the world for the number of hemodialysis patients. For solving the above-mentioned circumstance, we demonstrate the project, here, which goal is to construct the holistic health for hemodialysis patient. The project is to design a wearable medicine-device which can simultaneously measure and monitor the vital sign, including heart rate (HR), pulse oximetry (SPO2), continuous non-invasive blood pressure (c-NIBP), and total body water (TBW), of hemodialysis patient. By aid of the device we design, hemodialysis patients will get better health care than before. This device comprises three techniques. The first is named “Using phonoangiography technique to early detect the dysfunction of arteriovenous access by arteriovenous access (AVA) stenosis detector”. The stenosis detector based on autoregressive model was employed to simultaneously estimate the status of AVA life cycle and to tract changes in frequency spectra. It helps hemodialysis patients to early detect the dysfunction of AVA and alarms them to make a return visit. The second technique is named “Physiological detecting device for wearable medical device and encoding algorithm development”. The feature of the second technique is to optimize the prognosis by analyzing physiological signals, including water content index, pulse oximetry, and blood pressure in the meanwhile. The third technique is named “Intelligent and smart tourniquet”. This technique aims to preclude AVA dysfunction caused by inappropriate hemostasis.

Postoperative Pain Management following Thoracic Outlet Decompression

Thoracic outlet decompression (TOD) is associated with significant postoperative pain often leading to hospital length of stay out of proportion to the risk profile of the operation. We seek to describe the improvement in hospital length of stay and patient pain control with an improved multiagent pain management regimen. We retrospectively reviewed the hospital length of stay, medication regimen/usage, operative details, and operative indications for all patients undergoing TOD from January 2012 through June 2015. During early experience, single-agent narcotic therapy was the mainstay of postoperatively pain control. Since 2014, we have adopted a regimen consisting of narcotic patient controlled analgesia, oral narcotics, and scheduled ibuprofen and valium, which is transitioned to oral narcotics/valium upon discharge. Operative approach (supraclavicular, infraclavicular, transaxial, or paraclavicular) was determined by patient anatomy and indication for procedure (neurogenic/arterial thoracic outlet syndrome or arteriovenous access dysfunction). Seventy-four patients were treated with TOD over the study period: 36 (49.3%) for neurogenic thoracic outlet syndrome, 23 (31.5%) for venous thoracic outlet syndrome, and 15 (19.2%) for arteriovenous access dysfunction. Prior to 2014, the mean length of stay was 4days with a median pain score of 6. Since 2014, the mean length of stay was 2.6 (P=0.04) with a median pain score of 4 (P=0.005). There was no statistically significant difference in the indication for operation or operative approach between the two periods. Since adoption of a multiagent pain management regimen to include scheduled NSAIDs and benzodiazepines, we have reduced the mean pain score experienced by our patients as well as the hospital length of stay.

Postintervention Patency: A Comparison of Stenting versus Patch Angioplasty for Dysfunctional Hemodialysis Access Sites

Arteriovenous access dysfunction is commonly caused by venous outflow stenosis, leading to thrombosis of the conduit. Given that there are limited lifetime hemodialysis access sites, the preservation of existing sites through novel means is of high priority. This study compares the efficacy of balloon angioplasty and stent placement to surgical patch angioplasty for upper arm (brachium) thrombosed or dysfunctional hemodialysis access sites in a group of patients at a single institution. Using the operating room log and electronic medical record system, we retrospectively examined the outcomes of 52 consecutive patients (3 were lost to follow-up), who had either stent placement (34 patients) or patch angioplasty (15 patients) for hemodialysis access salvage to calculate postintervention patency. Initial postinterventional patency (PIP1) for patch angioplasty compared with stentplacement was not statistically significant at any time during a mean 6-month follow-up (60% vs. 67.65% at 1month, 33.33% vs. 41.18% at 3months, and 13.33% vs. 17.65% at 6months, respectively; P=0.75). Patency after secondary reintervention (PIP2) was longer for patients who had stent placement as the initial intervention (n=15) than patientswho had patch angioplasty (n=5; 100% vs. 80% at 1month, 66.68% vs. 80% at 3months, and 46.67% vs. 40% at 6months, respectively), but again there was no statistically significant difference between the 2 groups (P=0.84). At last, the initial PIP1 of arteriovenous fistula (AVF) and arteriovenous graft (AVG) salvaged before occlusion was significantly different from that of occluded access sites (40% vs. 10% at 6months, P=0.024). Our data suggest that AVF had a longer postinterventional primary patency than AVG though the difference did not reach statistical significance. Stents extended PIP1 for the thrombosed or failing arteriovenous access longer than patch angioplasty, but the difference was not statistically significant. Patency is longer if intervention is made before graft thrombosis. Our data also indicate better prolongation of patency with a second reintervention (PIP2) if the first intervention was a stent placement. Patch angioplasty appears to be a less attractive alternative for correction of venous outflow stenosis given the more invasive and occasionally technically difficult procedure.

Abstract 347: Chronic Kidney Disease Modulates Vascular Smooth Muscle Cell Phenotype and Increases de Novo Venous Intimal Hyperplasia

Background: Vascular access dysfunction associated with arteriovenous grafts and fistulas contributes significantly to the morbidity and mortality of end-stage renal disease (ESRD) patients receiving hemodialysis. The mechanism involved in the development of peri-anastomotic intimal hyperplasia, a major cause of the arteriovenous access dysfunction, is poorly elucidated. We hypothesized that the uremic condition associated with ESRD promotes a pathophysiological vascular smooth muscle cell (VSMC) phenotype that contributes to accelerated development of intimal hyperplasia in blood vessels, both de novo and following the arteriovenous anastomosis. Methods and Results: We examined the effect of culturing human VSMC with human uremic serum on its phenotype. We utilized quantitative real-time PCR to measure the expression of the VSMC-specific contractile marker genes, and found that these genes were reduced 50-80% in VSMC exposed to serum from hemodialysis patients as compared to serum from patients with normal renal function. Chromatin immunoprecipitation assays demonstrated that there were also significant changes in epigenetic markers associated with contractile gene promoters in VSMC cultured in uremic conditions. Moreover, there was a 60% increase in proliferation rate in cells exposed to uremic conditions, with no change in the levels of apoptosis as compared to cells exposed to non-uremic conditions. Interestingly, uremic serum from ESRD patients inhibited PDGF-induced migration of VSMC. We also examined the histopathology of veins from patients with normal kidney function and chronic kidney disease (CKD). Indeed, we found significant de novo venous intimal hyperplasia exists in CKD and ESRD patients prior to any surgical manipulation as compared to veins from patients with normal kidney function. Conclusion: CKD alters VSMC phenotype in vitro and contributes to intimal hyperplasia formation in vivo resulting in the pathogenesis of vascular access dysfunction in ESRD patients.

Thrombocytopenia in ESRD Patients: Epidemiology, Mechanisms and Interventional Nephrology Perspective

A well-functioning vascular access is essential for provision of life-sustaining dialysis treatment in patients with end-stage renal disease. Arteriovenous accesses are preferred form of vascular access. Although significant advances have been made in the field of dialysis access, arteriovenous access dysfunction remains the single most important cause of morbidity in ESRD patients. While thrombosis and stenosis of AV access are more frequently seen, hemorrhage from AV access can be life threatening with or without risk of permanent access loss. Aside from anticoagulation for comorbidities, qualitative and/or quantitative platelet abnormalities are often the predisposing factors. We describe an ESRD patient who developed new onset but severe thrombocytopenia due to metastatic small cell neuroendocrine carcinoma of lung. Given her persistent thrombocytopenia and presence of prolonged bleeding from the cannulation sites, a right internal jugular tunneled dialysis catheter was placed for continuation of maintenance dialysis. This review discusses the definition of thrombocytopenia, mechanisms of thrombocytopenia in patients with ESRD and with a special focus on implications of thrombocytopenia on dialysis access interventions. The review underscores the need for consensus with regard to cannulating AV access as well as guidelines specific to dialysis access-related endovascular intervention in the setting of thrombocytopenia and other coagulation abnormalities.

ASDIN Clinical Case Focus: Optimal Timing for Secondary Arteriovenous Fistula Creation: Devastating Effects of Delaying Conversion

AbstractA chronic hemodialysis patient was referred to interventional nephrology for evaluation of arteriovenous access dysfunction. The patient had been receiving hemodialysis using a left forearm brachiobasilic loop graft for the past 3 years. Physical examination revealed a hyperpulsatile graft. Angiography documented a critical stenosis at the vein–graft anastomosis and a well‐developed basilic vein from the elbow to the axillary region. Central veins were patent all the way to the right atrium. All attempts to navigate the wire across the stenosis failed. The patient was educated and counseled regarding the possibility of surgical creation of a secondary arteriovenous fistula (AVF). The images obtained were shared and discussed with the surgeon. A plan to create a secondary AVF using the basilic vein in the arm was made. A few months later the patient was referred to interventional nephrology, this time for thrombectomy of the same left arm loop graft. Thrombectomy could not be performed and a right internal jugular tunneled catheter was inserted. The patient again was referred to the surgeon for AVF creation. Six weeks later the patient was seen in the interventional laboratory for removal of the right internal jugular tunneled catheter. It was noted that instead of a fistula, the patient had received a right forearm brachiocephalic loop graft. Devastating consequences, such as the lost opportunity to create a fistula, insertion of a tunneled dialysis catheter, arteriovenous graft placement, exhaustion of available sites for fistula creation, and exposure to increased morbidity and mortality associated with grafts and catheters, can result if the opportunity to create a secondary AVF is not availed in a timely manner. This concept must be understood by every member of the vascular access team.

Interventional Nephrology in Puerto Rico

Vascular access is emerging as a critical issue for hemodialysis patients in Puerto Rico. In more than 50% of the hemodialysis patients, tunneled hemodialysis catheters are the sole access for providing dialysis therapy. Most disturbing is the fact that a significant number of these catheters are nontunneled temporary catheters, sometimes placed in the subclavian vein. These facts have contributed significantly to the morbidity and mortality seen in chronic dialysis patients. In addition, many cases of early or late dysfunction of arteriovenous access are not detected and treated in a timely manner due to the lack of a comprehensive vascular access program for end-stage renal disease (ESRD) patients. In fact, monitoring programs to identify and detect vascular access dysfunction are virtually nonexistent in many chronic dialysis units. Even when diagnosed, it is not treated in a timely fashion. Recently literature has shown that procedure-related delays in the treatment of patients with renal disease can be minimized and nephrology care more efficiently delivered by a nephrologist trained in nephrology-related procedures. In an effort to optimize the care of our ESRD patients, we took the initiative to develop an interventional nephrology program that effectively deals with vascular access-related procedures in a timely manner. This approach has minimized delays, decreased hospitalizations and the use of temporary catheters, and improved the medical care of our chronic dialysis patients. So far we have performed more than 400 procedures in the 6 months since the initiation of the program. In this article we describe our initial experience with interventional nephrology in Puerto Rico.