Failure of maturation of native autologous arteriovenous fistulae (AVFs), fistula thrombosis and dialysis access dysfunction are most often caused by arteriovenous (AV) access stenosis. 1 The pathophysiology of AVF stenosis and mechanisms of restenosis are not yet fully understood.Venous neointimal hyperplasia is a recognised cause of vascular access stenosis and fistula failure. 2 Failure of fistula maturation and early fistula failure have been shown to be due to both neointimal hyperplasia and adverse adventitial remodelling or a failure of venous dilatation resulting in AVF stenosis. 2 Ultrasound is a non-invasive, readily available diagnostic tool used in the assessment of AVF dysfunction and failure of fistula maturation. Doppler ultrasound has a high sensitivity and specificity in the diagnosis of vascular access stenosis. 3,4 The technique, in the hands of an experienced operator, has high accuracy and reproducibility in detecting more than 90% of significant stenosis. 4 Ultrasound can also be used to assess neointimal hyperplasia by measuring intimal-medial thickness (IMT) at the site of a stenosis. 5 Carotid intima-media thickness (CIMT) measurements are made
Acute kidney injury (AKI) is a relatively frequent problem, occurring in approximately 20 % of hospitalized patients with cirrhosis. Although serum creatinine (S Cr) is the most commonly used method to determine AKI because of easy availability and low cost, practically it underestimates the extent of kidney injury in patients with chronic liver disease. AKI is defined as an abrupt rise in S Cr of 0.3 mg/dl or more (>26.4 mmol/l) or an increase of 150 % or more (1.5-fold) from baseline. The cause of AKI in cirrhosis is multifactorial and is unique in terms of pathogenesis. The most common causes of AKI in cirrhosis can be subdivided into either functional or structural. The functional group includes volume-responsive (prerenal azotemia) and volume-unresponsive states (hepatorenal syndrome). Volume responsive is the most common type of AKI due to frequent use of diuretics, large volume abdominal paracentesis and gastrointestinal bleeding in patients with liver disease. The structural causes include acute tubular necrosis, tubulointerstitial and glomerular diseases. Patients with decompensated cirrhosis are in a vasodilatory state leading to a decrease in effective arterial blood volume, predisposing to AKI. Therefore, management of AKI depends on the underlying cause, and therapy should be directed toward removal of the cause. The outcome in cirrhosis when patients are on dialysis is very dismal. Every effort should be made to prevent AKI.
Background Physical activity (PA) levels are low in patients with advanced chronic kidney disease (CKD), and associate with increased morbidity and mortality. Reliable tools to assess PA in CKD are scarce. We aimed to develop and validate a novel PA questionnaire for use in CKD (CKD-PAQ). Methods In phase 1, a prototype questionnaire was developed based on the validated Recent Physical Activity Questionnaire (RPAQ). Structured feedback on item relevance and clarity was obtained from 40 CKD patients. In phase 2, the questionnaire was refined in 3 iterations in a total of 226 CKD patients against 7-day accelerometer and RPAQ measurements. In phase 3, the definitive CKD-PAQ was compared with RPAQ in 523 CKD patients. Results In the final iteration of phase 2, CKD-PAQ data were compared to accelerometer-derived and RPAQ data in 60 patients. Mean daily Metabolic Equivalent of Task (MET) and Total Energy Expenditure (TEE) levels were similar by all methods. Intraclass correlation coefficients showed fair agreement (MET) and good (TEE) between accelerometry and both CKD-PAQ and RPAQ. Agreement between questionnaires was excellent. For mean daily MET bias was 0.035 (SD 0.312) for CKD-PAQ and 0.018 (SD 0.326) for RPAQ. For TEE bias was 91 (SD 518) for CKD-PAQ and 44 (SD 548) kcal for RPAQ. Limits of agreement were wide for both parameters, with less dispersion of CKD-PAQ values. In phase 3, agreement between questionnaires was good (MET) and excellent (TEE). Bias of CKD-PAQ-derived mean daily MET from RPAQ-derived values was 0.031 (SD 0.193) with 95% limits of agreement -0.346 to 0.409. Corresponding values for TEE were 48 (SD 325) and -588 to 685 kcal/day. CKD-PAQ appeared to improve discrimination between low activity groups. Conclusions CKD-PAQ performs comparably to RPAQ though is shorter, easier to complete, may better capture low level activity and improve discrimination between low-activity groups.
Background/aims: (1-3)-β-D glucans (BG) are cellular components of yeasts and fungi. Elevated blood levels may be an adjunct in diagnosing invasive fungal infection, though can be high in dialysis patients without fungaemia. BG can also induce false positive signals in endotoxin detection assays (Limulus Amoebocyte Lysate [LAL] assay). We explored the relationship between BG levels, renal impairment, endotoxaemia and inflammation. Methods: We measured serum BG levels, markers of inflammation and blood endotoxin levels in 20 controls, 20 with stages 1-3 chronic kidney disease (CKD), 20 with stages 4-5 CKD, 15 on peritoneal dialysis (PD) and 60 on haemodialysis (HD). Another 30 patients were studied before and after HD initiation. Results: BG levels increased with advancing CKD, being highest in HD patients, 22% of whom had elevated levels (> 80 pg/ml). Levels increased significantly following HD initiation. Levels also correlated positively with CRP, TNFα, IL-6 levels, independently of CKD stage. Blood endotoxin was detectable by LAL assays in 10-53% of the CKD cohort, being most prevalent in the HD group, and correlating positively with BG levels. Adding BG blocking agent to the assay reduced endotoxin detection confining it to only 5% of HD patients. Levels of inflammatory markers were higher in those with detectable endotoxin-whether false-or true positives. Conclusion: BG levels increased with decreasing renal function, being highest in dialysis patients. High BG levels were associated with false positive blood endotoxin signals, and with markers of inflammation, independently of CKD stage. The cause for high BG levels is unknown but could reflect increased gut permeability and altered mononuclear phagocytic system function.
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