Hyperuricemia is particularly common in patients with arterial hypertension, metabolic syndrome, or kidney disease. Its role, however, as a risk factor for both renal and cardiovascular outcomes and in the context of the well-established interrelationship between cardiovascular disease and chronic kidney disease (CKD) is debated. For decades high serum uric acid levels were mainly considered the result of renal dysfunction and not a true mediator of renal disease development and progression. However, recent epidemiological studies suggest an independent association between asymptomatic hyperuricemia and increased risk of arterial hypertension, CKD, cardiovascular events, and mortality. Furthermore, data from experimental models of hyperuricemia have provided robust evidence in this direction. Hyperuricemia causes increased arterial pressure, proteinuria, renal dysfunction, and progressive renal and vascular disease in rats. The main pathophysiological mechanisms of these deleterious effects caused by uric acid are endothelial dysfunction, activation of local renin-angiotensin system, increased oxidative stress, and proinflammatory and proliferative actions. A small number of short-term, single-center clinical studies support the beneficial influence of pharmaceutical reduction of serum uric acid on total cardiovascular risk, as well as on renal disease development and progression. Hyperuricemia is probably related to the incidence of primary hypertension in children and adolescents, as serum uric acid lowering by allopurinol has an antihypertensive action in this group of patients. Finally, it is clear that adequately powered randomized controlled trials are urgently required to elucidate the role of uric acid in cardiovascular events and outcomes, as well as in the development and progression of CKD.

Vitamin E supplementation by vitamin E-coated CAE dialysis membrane suppresses oxidative stress and inflammation.

Purpose The impact of different dialysis modalities on oxidative stress and inflammation and the factors implicated in this interrelationship have not been adequately studied. This study was designed to comparatively evaluate the effect of hemodialysis (HD) and peritoneal dialysis (PD) on oxidative stress and inflammatory biomarkers and to search for associated factors. Methods We studied 20 HD, 11 PD patients and 11 healthy controls. Calculations were based on total antioxidant capacity (TAC) and superoxide dismutase (SOD), by spectrophotometry, as oxidative stress biomarkers; and high sensitivity CRP (hs-CRP), lnterleukin-6 (IL-6) and Tumor Necrosis Factor-α (TNF-α), by ELISA, as inflammation biomarkers. Results HD and PD patients showed significantly increased levels of TAC, SOD and hs-CRP compared to healthy controls. No significant difference was observed in TNF-α and IL-6. Compared to HD patients, PD patients showed TNF-α levels that were increased, although non-significantly and significantly higher homocysteine (Hcy). No differences were observed for IL-6, hs-CRP, TAC and SOD. In HD patients, significant positive correlations were found between intact parathyroid hormone (iPTH) and TNF-α, and between uric acid (UA) and TAC. β2-microglobulin (β2M) was negatively correlated with TAC, total cholesterol (TC) positively with TNF-α and negatively with SOD, and triglycerides (TG) correlated positively with TNF-α. In PD patients, TG correlated positively with TNF-α, HDL-cholesterol negatively with TNF-α, LDL-cholesterol negatively with SOD, and β2M negatively with SOD. Conclusions HD and PD patients show similar degrees of inflammation and oxidative stress activation. Factors such as UA, iPTH, β2M and lipid profile correlate to oxidative stress and inflammatory biomarkers in both HD and PD patients.

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Background: Use of uncuffed catheters (UCs) in hemodialysis patients is common practice. An antibiotic lock has been recommended to prevent catheter-related bacteremia (CRB), although insufficient data are available about the appropriate antimicrobial agent and dose with prolonged use of UCs. Methods: This open-label randomized study was conducted to compare gentamicin/heparin (group A) and taurolidine/citrate (group B), as catheter-lock solutions, in 119 chronic hemodialysis patients in whom a total of 150 UCs were placed. A well-matched historical control group (heparin) included 67 UCs in 58 patients (group C). Results: CRB episodes developed in 6 and 8 patients in groups A and B, respectively, significantly fewer than in group C (20 patients). Cumulative CRB-free catheter survival at 90 days was 82% for A and 78% for B, which is significantly higher than the 26% for C. Similar Gram-positive infection rates were found in all groups. The Gram-negative infection rate was significantly lower in B compared to C. No significant differences in thrombosis rates were observed between the groups. Conclusions: Gentamicin/heparin and taurolidine/citrate, used for locking UC, were similarly effective at preventing CRB and catheter thrombosis for up to 3 months, until a functional permanent vascular access became available. Both antimicrobial lock solutions were superior to heparin in CRB prevention with similar thrombosis rates.