SDMA exhibits some properties of a reliable marker of renal function. Future studies have to clarify whether SDMA is indeed suited to improve diagnosis and eventually optimize care of patients.

Changes in extracellular phosphorus concentrations may directly modulate vascular function and thereby modulate the vascular smooth muscle response to physiological or pathological stimuli in normal and CKD mice. Whether serum phosphorus lowering and/or dietary phosphate restriction can improve arterial function in humans remains to be established.

Our data suggest that patients treated with ED using a high-flux dialyzer (polysulphone, 1.3 m(2); blood and dialysate flow, 160 ml/min; ED time, 480 min) and employing current dosing regimen, 6 mg/kg daptomycin every 48 h, run the risk of becoming significantly under dosed if one adheres to a twice daily dosing schedule that is recommended for patients on maintenance haemodialysis. Our data suggest that a daily dose of 6 mg/kg daptomycin is necessary in this special patient population to avoid under dosing, which may have detrimental effects in critically ill patients suffering from life-threatening infections.

Background The pleiotropic cytokine osteopontin (OPN) is thought to be involved in the pathogenesis of atherosclerosis. However, the relationship between OPN and renal function, a cardiovascular risk factor itself, is not known. Therefore, we assessed the relationship between OPN plasma levels and renal function in patients at different stages of chronic kidney disease (CKD).

We examined structure, composition, and endothelial function in cerebral arterioles after 4 wk of chronic renal failure (CRF) in a well-defined murine model (C57BL/6J and apolipoprotein E knockout female mice). We also determined quantitative expression of endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (on serine 1177 and threonine 495), and caveolin-1; quantitative expression of markers of vascular inflammation or oxidative stress [Rock-1, Rock-2, VCAM-1, and peroxisome proliferator-activated receptor-␥ (PPAR␥)]; and the plasma concentration of L-arginine and asymmetric dimethylarginine (ADMA). Our hypothesis was that endothelial function would be impaired in cerebral arterioles during CRF following either a decrease in NO production (through alteration of eNOS expression or regulation) or an increase in NO degradation (due to oxidative stress or vascular inflammation). Endothelium-dependent relaxation was impaired during CRF, but endothelium-independent relaxation was not. CRF had no effect on cerebral arteriolar structure and composition. Quantitative expressions of eNOS, eNOS phosphorylated on serine 1177, caveolin-1, Rock-1, Rock-2, and VCAM-1 were similar in CRF and non-CRF mice. In contrast, quantitative expression of PPAR␥ (which exercises a protective role on blood vessels) was significantly lower in CRF mice, whereas quantitative expression of eNOS phosphorylated on the threonine 495 (the inactive form of eNOS) was significantly higher. Lastly, the plasma concentration of ADMA (a uremic toxin and an endogenous inhibitor of eNOS) was elevated and plasma concentration of L-arginine was low in CRF. In conclusion, endothelial function is impaired in a mouse model of early stage CRF. These alterations may be related (at least in part) to a decrease in NO production. pial vessels; endothelium-dependent relaxation; endogenous endothelial nitric oxide synthase inhibitors; inflammatory markers; ApoE Ϫ/Ϫ mice CARDIOVASCULAR DISEASE IS highly prevalent in patients with chronic renal failure (CRF) and may account for 50% of all deaths in this population (39). Stroke is the third most common cause of cardiovascular death in CRF sufferers. Patients with end-stage renal disease (ESRD) have a 4-to 10-fold greater risk of hospitalized ischemic and hemorrhagic stroke (35), an increased risk of cognitive impairment and dementia (28, 36), and a poor long-term poststroke prognosis (13) compared with non-ESRD individuals. Furthermore, the prevalence of asymptomatic, silent, cerebral infarction is four to five times higher in dialysis patients than in age-and gender-matched controls (29). Moreover, patients on dialysis with cognitive impairment appear to have a high number of cortical defects that are reminiscent of multiple infarct-related damage (20).The higher frequency of stroke and cognitive impairment in ESRD patients cannot be solely explained by their higher prevalence of traditional (27) and nontraditional risk factors (17). Other CRF-related factors (such as the accumulation of uremic toxins or arter...

This study shows for the first time that plasma levels of ADMA can be effectively lowered by an artificial liver support system (Prometheus). Effective elimination of ADMA might explain some of the beneficial clinical effects of these systems in patients with liver failure.

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