Pamela Lopez-Vargas

Barriers to Timely Arteriovenous Fistula Creation: A Study of Providers and Patients

BACKGROUND Current clinical practice guidelines recommend a native arteriovenous fistula (AVF) as the vascular access of first choice. Despite this, most patients in western countries start hemodialysis therapy using a catheter. Little is known regarding specific physician and system characteristics that may be responsible for delays in permanent access creation. STUDY DESIGN Multicenter cohort study using mixed methods; qualitative and quantitative analysis. SETTING & PARTICIPANTS 9 nephrology centers in Australia and New Zealand, including 319 adult incident hemodialysis patients. PREDICTOR Identification of barriers and enablers to AVF placement. OUTCOMES Type of vascular access used at the start of hemodialysis therapy. MEASUREMENTS Prospective data collection included data concerning predialysis education, interviews of center staff, referral times, and estimated glomerular filtration rate (eGFR) at AVF creation and dialysis therapy start. RESULTS 319 patients started hemodialysis therapy during the 6-month period, 39% with an AVF and 59% with a catheter. Perceived barriers to access creation included lack of formal policies for patient referral, long wait times for surgical review and access placement, and lack of a patient database for management purposes. eGFR thresholds at referral for and creation of vascular accesses were considerably lower than appreciated (in both cases, median eGFR of 7 mL/min/1.73 m(2)), with median wait times for access creation of only 3.7 weeks. First assessment by a nephrologist less than 12 months before dialysis therapy start was an independent predictor of catheter use (OR, 8.71; P < 0.001). Characteristics of the best performing centers included the presence of a formalized predialysis pathway with a centralized patient database and low nephrologist and surgeon to patient ratios. LIMITATIONS A limited number of patient-based barriers was assessed. Cross-sectional data only. CONCLUSIONS A formalized predialysis pathway including patient education and eGFR thresholds for access placement is associated with improved permanent vascular access placement.

KHA‐CARI Guideline: Vascular access – central venous catheters, arteriovenous fistulae and arteriovenous grafts

Department of Nephrology, Monash Medical Centre, Department of Medicine, Monash University, Department of Radiology, Austin Health, Melbourne, Victoria, Department of Renal Medicine, Fremantle Hospital, Fremantle, Western Australia, Department of Nephrology, Royal Adelaide Hospital, Adelaide, South Australia, Department of Renal Medicine, The Canberra Hospital, Canberra, Australian Capital Territory, and Centre for Kidney Research, The Children’s Hospital at Westmead, Sydney, New South Wales, Australia

Knowledge deficit of patients with stage 1-4 CKD: A focus group study

Patients with early‐stage chronic kidney disease (CKD) must make lifestyle modifications and adhere to treatment regimens to prevent their progression to end‐stage kidney disease. The aim of this study was to elicit the perspectives of patients with stage 1–4 CKD about their disease, with a specific focus on their information needs in managing and living with CKD and its sequelae.

Consumer involvement in topic and outcome selection in the development of clinical practice guidelines.

Background  Consumer involvement in guideline development is advocated, but minimal participation, such as a nominated consumer representative on a guideline working group, can inhibit their decision‐making power and contribution. Little is known about how to involve consumers more effectively in guideline development.

Prevention, detection and management of early chronic kidney disease: a systematic review of clinical practice guidelines.

In response to the increase in Chronic Kidney Disease (CKD) worldwide, several professional organizations have developed clinical practice guidelines to manage and prevent its progression. This study aims to compare the scope, content and consistency of published guidelines on CKD stages I–III.

Cardiovascular risk factors in Australian indigenous and non-indigenous children: a population-based study.

Aim:  Indigenous people have a two‐ to tenfold increased risk of premature death from cardiovascular disease. We aimed to determine whether some key risk factors for cardiovascular disease occur more commonly in Aboriginal than non‐Aboriginal Australian children.

Risk of CKD in Australian Indigenous and Nonindigenous Children: A Population-Based Cohort Study

BACKGROUND Aboriginal Australians have a 9-fold increased risk of end-stage renal disease. There is no information about the natural history and risk of chronic kidney disease (CKD) in Aboriginal and non-Aboriginal children. STUDY DESIGN Using a prospective study design, we aimed to determine the prevalence of persistent markers and risk factors for CKD in Australian Aboriginal and non-Aboriginal children and whether Aboriginal children are at increased risk of persistent markers of CKD after accounting for sociodemographic differences. SETTING & PARTICIPANTS Children were enrolled from elementary schools throughout New South Wales. PREDICTOR Aboriginal (Aboriginal and Torres Strait Islander Australians) versus non-Aboriginal ethnicity. OUTCOMES & MEASUREMENTS Urine analysis, height, weight, blood pressure, birth weight, and sociodemographic status were measured at baseline and 2-year follow-up. Albuminuria was defined as albumin-creatinine ratio of 3.4 mg/mmol or greater, hematuria as 25 or greater red blood cells/microL (>or=1+), obesity as body mass index of 2 SDs or greater, and systolic and diastolic hypertension as blood pressure greater than the 90th percentile. RESULTS 2,266 children (55.1% Aboriginal; 51.0% boys; mean age, 8.9 +/- 2.0 years [SD] years) were enrolled at baseline. Early markers and predictors of CKD at baseline were frequent: hematuria (5.5%), albuminuria (7.3%), obesity (7.1%), systolic hypertension (7.2%), and diastolic hypertension (5.8%). 1,432 children (63%) were available for retesting at 2-year follow-up (54.0% Aboriginal; 50.5% boys; mean age, 10.5 +/- 2.0 years). Persistent obesity (5.3%) was frequent, but persistent markers of CKD were infrequent (systolic hypertension, 1.1%; diastolic hypertension, 0.2%; hematuria, 1.1%; and albuminuria, 1.5%). Although there were more Aboriginal than non-Aboriginal children with baseline hematuria (7.1% versus 3.6%; P = 0.001), after adjustment for age, sex, birth weight, and sociodemographic status, there was no increased risk of persistent hematuria, albuminuria, obesity, or hypertension in Aboriginal children. LIMITATIONS Persistent markers of CKD were much less frequent than anticipated, which may have affected study power. The group lost at follow-up was older children, which may have biased results. CONCLUSIONS Overall, only 20% of children found to have markers of early CKD had persistent abnormalities (diastolic and systolic hypertension, albuminuria, and hematuria) 2 years later, equivalent to a population point prevalence of 1% to 2% in children with a mean age of 10 years. Aboriginal children had greater rates of baseline and transient hematuria, but no increased risk of persistent markers of CKD, suggesting that adolescence and young adulthood is a critical time for preventative strategies.

Autosomal Dominant Polycystic Kidney Disease: A Path Forward

Autosomal dominant polycystic kidney disease (ADPKD) is the commonest inherited cause of renal failure in adults, and is due to loss-of-function mutations in either the PKD1 or PKD2 genes, which encode polycystin-1 and polycystin-2, respectively. These proteins have an essential role in maintaining the geometric structure of the distal collecting duct in the kidney in adult life, and their dysfunction predisposes to renal cyst formation. The typical renal phenotype of ADPKD is the insidious development of hundreds of renal cysts, which form in childhood and grow progressively through life, causing end-stage kidney failure in the fifth decade in about half affected by the mutation. Over the past 2 decades, major advances in genetics and disease pathogenesis have led to well-conducted randomized controlled trials, and observational studies that have resulted in an accumulation of evidence-based data, and raise hope that the lifetime risk of kidney failure due to ADPKD will be progressively curtailed during this century. This review will provide a contemporary summary of the current state of the field in disease pathogenesis and therapeutics, and also briefly highlights the importance of clinical practice guidelines, patient perspectives, patient-reported outcomes, uniform trial reporting, and health-economics in ADPKD.

Identifying and integrating consumer perspectives in clinical practice guidelines on autosomal-dominant polycystic kidney disease

This study aimed to identify consumer perspectives on topics and outcomes to integrate in the Kidney Health Australia Caring for Australasians with Renal Impairment (KHA‐CARI) clinical practice guidelines on autosomal‐dominant polycystic kidney disease (ADPKD).

KHA-CARI Autosomal Dominant Polycystic Kidney Disease Guideline: Management of Intracranial Aneurysms.

a. We suggest screening for intracranial aneurysms in high-risk individuals with autosomal dominant polycystic kidney disease (ie, those with a positive family history of subarachnoid hemorrhage, intracerebral hemorrhage, and/or unruptured intracranial aneurysm in at least one affected first-degree relative) (2B). b. We suggest performing the screening of individuals at high risk of intracranial aneurysms at the time of diagnosis of autosomal dominant polycystic kidney disease and preferably prior to the development of end-stage kidney disease (2C). c. We recommend intracranial imaging be performed urgently in patients with autosomal dominant polycystic kidney disease who experience a sudden onset of severe headache or neurological symptoms of concern (1D). d. We recommend that magnetic resonance angiography or computed tomography (circle of Willis angiography) be used for the screening and detection of intracranial aneurysms in individuals with autosomal dominant polycystic kidney disease (1B). e. We recommend referral to a neurosurgeon if an intracranial aneurysm is detected (1D). f. We suggest treatment of intracranial aneurysms in patients with autosomal dominant polycystic kidney disease in centers that have expertise in endovascular coiling and microsurgery (2B).