This study showed no difference in haemoglobin level increase between patients treated for 3 months with a high-flux biocompatible membrane in comparison with those treated with a standard membrane. When patients are highly selected, adequately dialysed, and have no iron or vitamin depletion, the effect of a high-flux membrane is much less than might be expected from the results of uncontrolled studies.

A 64-year-old Moroccan man was referred to our clinic for abdominal cystic echinococcosis (CE). He had undergone surgery for hepatic CE 29 years earlier, with no perioperative prophylaxis with albendazole. He presented with abdominal distension and abdominal pain. An ultrasound (US) showed multiple CE3b and CE4 cysts with calcifications and two echo-free collections 13 cm in diameter seen on paraumbilical scans (Figure 1a). The portal tract, pancreas, spleen, kidneys, and aorta were not visible on US. The bladder was compressed by a large cyst. Serology for Echinococcus granulosus was positive (indirect hemagglutination test titer 1/4096; Echinococcus IgG ELISA optical density 6.70).

We have previously shown that, assuming urea distribution volume (V) remains constant for 1 month, ionic dialysance (ID) allows the dialysis dose to be calculated without the need for blood sampling. The aim of this multicenter study was to verify whether the assumption of a constant V can be extended to 1 year. In clinically stable patients receiving thrice-weekly hemodialysis at 13 dialysis centers, V and Kt/V were assessed during three dialysis sessions at baseline and 1 year later using ID as dialyzer urea clearance and the single-pool urea kinetic model. Baseline albumin, hemoglobin, and C reactive protein were prespecified covariates for predicting the change in V over time. Of the 52 enrolled patients, 40 (25 males; age 63.0+/-13.5 years) completed the study. Baseline end-dialysis body weight (62.4+/-13.7 kg) showed a non-significant 1% reduction during follow-up (-0.6+/-2.8 kg; P=0.175), whereas V significantly decreased from 29.0+/-6.8 to 27.4+/-6.0 l (-1.6+/-3.0 l or 4.5%; P=0.002). The reduction in V was greater when baseline albumin was lower (P=0.001) and baseline V was higher (P=0.005). The single-pool K(t)/V calculated using baseline V underestimated the actual value by 0.07+/-0.16 (P=0.008). The slight underestimate of Kt/V during follow-up suggests that annual V evaluations may be sufficient for dialysis dose quantification as the only risk is underestimating the actually delivered dialysis dose. However, the relationship between baseline albumin and the reduction in V over time may have nutritional value, and suggests more frequent V evaluations.

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Introduction: Increased urinary albumin excretion in uncomplicated hypertension has been recently associated with impaired vascular reactivity (NO dependent and independent vasodilation) and increased levels of adhesion molecules (2), thereby suggesting that endothelial dysfunction is responsible for the increased cardiovascular (CV) risk associated with albuminuria (1,2). Methods: In light of this reports, we have used our human model of vascular tone control, Bartter's/ Gitelman's syndromes (BS/GS) patients, which have biochemical and hormonal characteristics typical of hypertension, yet normo/hypotension hyporesponsiveness to pressors and reduced vascular resistance (3-5), to assess the urinary albumin/creatinine ratio (UACR) as a potential marker of endothelial dysfunction. Results: We found that UACR in BS/GS did not differ from healthy subjects (12.07±8.3 mg/g Cr vs 11.5±9.2). Conclusions: These results are perfectly in keeping with the evidence in these patients of a markedly higher insulin sensitivity compared with healthy normotensive subjects and an Ang II signalling/ insulin-glucose metabolism relationships which points toward reduced insulin resistance, which are opposite of those typical of diabetes and hypertension, including the absence of microalbuminuria and endothelial dysfunction. This evidence in BS/GS is sustained by reduced oxidative stress and inflammatory status, up-regulation of NO system down-regulation of RhoA-Rho kinase pathway, activation of Akt pathway and blunted Ang II signalling which joined with the absence of albuminuria depict a biochemical and molecular picture of reduced CV risk and therefore indirectly support the association of endothelial dysfunction and albuminuria with increased CV risk.