[On-line hemodiafiltration with endogenous reinfusion (HFR). Experience of a Centre]. / Emodiafiltrazione con reinfusato on-line di liquido endogeno: esperienza di un Centro.

PURPOSE: Hemodiafiltration reinfusion (HFR) treatment is a dialysis technique that uses the endogenous reinfusion fluid and performs, simultaneously and separately, the three mechanisms of extracorporal depuration: diffusion, convection and adsorption. This study aimed to evaluate clinical and biochemical data of a group of six patients submitted to a dialytic HFR method for >6 months. METHODS: Six patients with a mean age of 53.8 +/- 11 yrs (five males, one female), treated with standard bicarbonate dialysis for a mean of 79.2 months, underwent HFR for a mean period of 14.9 +/- 6 months. Filters used were: a) in all patients polysulfone with 0.7 m2 of surface for the convection; b) polysulfone with 1.7 m2 in one patient, and modified cellulose with 2.0 m2 in five patients for diffusion; c) hydrophobic interaction resin and uncovered mineral carbon 240 mL for the adsorption. For all patients dialysis duration was 240 min and the amount of reinfusion fluid was 2.5 L/h as a mean, calculated according to blood flow and hematocrit (Hct), keeping a filtration fraction <22%. We evaluated, at different times, the following parameters: a) patient weight; b) Hct and erythropoietin (EPO) doses; c) parathyroid hormone (PTH); d) phosphatemia and doses of administered vitamin D; e) homocysteine (Hcy) and Beta2-microglobulin (Beta2-m); f) and albuminemia and transferrinemia as nutritional parameters. RESULTS: We observed an increase in Hct, with a reduction in EPO dosage, and an increase in albumin and transferrin levels, an improvement in nutritional indexes and in patient well-being. The mild increase in Hct with the same EPO dose was present in spite of a switch to intravenous (i.v.) administration from subcutaneous administration. There was low morbidity and only one hospitalization due to an infectious episode. CONCLUSIONS: HFR allows an amino acid saving and pro-inflammatory middle molecule removal, resulting in a better clinical situation for progressively critical uremic patients.

Plasma ouabain-like factor during acute and chronic changes in sodium balance in essential hypertension.

An ouabain-like factor has been implicated repeatedly in salt-sensitive hypertension as a natriuretic agent. However, the response of plasma ouabain-like factor to acute and chronic variation of body sodium is unclear. We studied 138 patients with essential hypertension who underwent an acute volume expansion/contraction maneuver (2 days) and 20 patients who entered a blind randomized crossover design involving chronically controlled sodium intake and depletion (170 to 70 mmol/d; 2 weeks each period). In both studies, plasma levels of ouabain-like factor were higher during sodium depletion (acute: 338.8+/-17.4 and 402.7+/-22.8 pmol/L for baseline and low sodium, respectively, P<0.01; chronic: 320.4+/-32.0 versus 481.0+/-48.1 pmol/L, P=0.01). No significant change in plasma ouabain-like factor was observed after a 2-hour saline infusion (333.4+/-23.9 pmol/L) or controlled sodium (402.1+/-34.9 pmol/L). When patients were divided into salt-sensitive or salt-resistant groups, no differences in plasma ouabain-like factor were observed in the 2 groups at baseline or in response to the 2 protocols: salt resistant (n=69, 340.1+/-25.9 pmol/L) versus salt sensitive (n=69, 337.4+/-23.6 pmol/L) and chronic salt resistant (n=11, 336.0+/-53.2) versus salt sensitive (n=9, 301.1+/-331.4 pmol/L). However, circulating ouabain-like factor was increased by sodium depletion in both groups. These results demonstrate that circulating ouabain-like factor is raised specifically by maneuvers that promote the loss of body sodium. Acute expansion of body fluids with isotonic saline is not a stimulus to plasma ouabain-like factor. Moreover, basal levels of plasma ouabain-like factor do not differ among patients with salt-sensitive or salt-resistant hypertension. Taken together, these new results suggest that ouabain-like factor is involved in the adaptation of humans to sodium depletion and argue against the hypothesis that ouabain-like factor is a natriuretic hormone.