Should we adjust erythropoiesis-stimulating agent dosage to postdialysis hemoglobin levels? A pilot study.

BACKGROUND: Predialysis hemoglobin (Hb) may overestimate the true erithropoiesis-stimulating agents (ESA) requirements. We tested whether predialysis Hb is a reliable predictor of the postdialysis level to better control ESA dosage, and evaluated the relation between ESA, Hb and cardiovascular events (CVE). METHODS: Cohort study including 67 stable hemodialysis patients. Pre- and post-dialysis Hb concentrations were measured, and ESA doses were calculated. A model to predict post-dialysis Hb is proposed. During 18 months follow-up, CVE, hospitalizations and mortality were collected. RESULTS: After dialysis, Hb concentration rise by 6.1 ± 5.6%. Using postdialysis Hb, the weight-adjusted ESA dosage would be lower respect to the prescription using predialysis Hb: 104 ± 120 vs 128 ± 124 U/kg/week (P < 0.001). Using predialysis Hb, 40.2% of subjects had a Hb level above 12 g/dL, whereas this percent increased to 70.1% using postdialysis Hb. During the follow-up, 15 patients had a CVE, without differences in Hb levels respect to subjects without CVE. However, patients with CVE had received higher ESA doses: 186 ± 180 vs 111 ± 98 U/Kg/week (P = 0.001). The prediction model is: Postdialysis Hb (g/dL) = 1.636 + 0.871 x predialysis Hb* (g/dL) + 0.099 x UF rate** (mL/kg/h) - 0.39 for women***. [R2 = 0.74; *P < 0,001; **P = 0.001; ***P = 0.03). CONCLUSIONS: Postdialysis Hb can be a better reflect of the real Hb level in hemodialysis patients. Using postdialysis Hb would avoid the use of inappropriately high ESA doses. The prediction of postdialysis Hb with an adjusted model would help us to identify those patients at risk for ESA overdosification.

In vitro interference of tigecycline at subinhibitory concentrations on biofilm development by Enterococcus faecalis.

OBJECTIVES: Since biofilm formation is the hallmark of Enterococcus faecalis isolates, the aim of this study was to quantify biofilm formation in the presence of subinhibitory concentrations of tigecycline. METHODS: Interference of tigecycline on biofilm formation was spectrophotometrically quantified using 20 biofilm-producing E. faecalis isolates with tigecycline MICs of 0.12 (8 strains) or 0.25 mg/L (12 strains). Biofilm production was measured in antibiotic-free tryptic soy broth supplemented with 1% glucose and compared with biofilm production in the same medium with tigecycline at subinhibitory concentrations (0.25× or 0.5× MIC, similar to trough concentrations in serum or concentrations in the colon after a standard dose) by reading the optical density at 450 nm (OD(450)) after staining with Crystal Violet. RESULTS: In the presence of subinhibitory tigecycline concentrations, pooled OD(450) values for the 20 strains [median (IQR)] were significantly lower than those for controls: 0.468 (0.379-0.516) for antibiotic-free controls versus 0.295 (0.200-0.395) for 0.25× MIC tigecycline (P < 0.001) and 0.287 (0.245-0.479) for 0.5× MIC tigecycline (P < 0.001), with significant differences between pooled OD(450) values obtained with each concentration of tigecycline (P = 0.022). In 17 out of 20 (85%) strains the OD(450) obtained with 0.25× MIC tigecycline was significantly (P < 0.05) lower than the basal OD(450), while this occurred in 12 out of 20 (60%) strains with 0.5× MIC. CONCLUSIONS: In vitro tigecycline subinhibitory concentrations were able to interfere with biofilm formation by E. faecalis.