Background: Short frequent dialysis with NxStage System One cycler (NSO) has become increasingly popular as home hemodialysis prescription. Short dialysis sessions with NSO might not allow adequate phosphate (P) removal. Methods: Single-session and weekly balances of P and calcium (Ca) were compared in 14 patients treated with NSO (6 sessions/week) and in 14 patients on standard bicarbonate dialysis (BHD). Results: NSO and BHD showed similar plasma P fall, with end-dialysis plasma P slightly lower in BHD (2.2 ± 0.5 vs. 2.7 ± 0.8 mg/dL, p < 0.02). Single-session P removal was lower in NSO, but weekly removal was higher (3,488 ± 1,181 mg vs. 2,634 ± 878, p < 0.003). Plasma Ca increase was lower in NSO, with similar PTH fall. Ca balance varied according to start plasma Ca, dialysate to blood Ca gradient and net ultrafiltration. Conclusions: short, frequent home hemodialysis with NSO, on a 6/week-based prescription, allows higher weekly P removal than BHD. With the dialysate Ca concentration in use (6 mg/dL), total plasma Ca and iCa concentration increase is lower in NSO.

A case of acute hypercapnia occurring during a session of bicarbonate hemodialysis is reported. The 82-year old female patient was affected by cardiac insufficiency, pulmonary hypertension and chronic obstructive lung disease. She developed acute symptomatic respiratory acidosis immediately after the beginning of a bicarbonate hemodialysis session, with arterial pH of 7.25 and paCO 2 of 48.1 mmHg. This was related to the well known, but frequently forgotten, CO 2 load from bicarbonate-based dialysate. We treated her with acetate-free biofiltration, with stable paCO 2 throughout the session. Physiopathology of blood gas dynamics during hemodialysis is reviewed.

Çàïðîøåí³ ñòàòò³ Guest Articles Definition and epidemiology Gitelman syndrome (GS; OMIM # 263800) is a renal tubular disorder mechanistically linked to impaired function of the electroneutral Na +-Clcotransporter (NCC) expressed in the apical membrane of distal convoluted tubule (DCT) cells. NCC is the product of the member 3 of the solute carrier family 12 (SLC12A3, locus 16q13), and is the target of the thiazide diuretics. Autosomal recessive loss of function mutations of SLC12A3 are the cause of GS, though exceptional case reports describe acquired disease in adults, possibly secondary to selective (immunologic) damage of DCT (Kim et al., 2008). Genetic GS is a monogenic disorder, thus it might be more properly defined as Gitel-man disease. Patients with mutations of CLCNKB gene (a basolateral chloride channel) may present with a «Gitelman» phenotype (see below), but they represent a variant or subtype of Bartter syndrome (i.e. salt wasting tubulopathy secondary to Henle's loop defect). GS is widespread throughout human races; the prevalence of pathogenetic mutations in the general caucasian populations is estimated at 1 %, which results in about 25 affected patients p.m.p.