5 years. Intermediate risk predicted overall hazard ratio (HR) (2.157, P = 0.039) and cardiovascular mortality (HR= 5.023; P = 0.004) versus low risk, but ‘high’ risk did not. High risk (vs low risk) predicted cardiovascular events (HR = 2.458, P = 0.05). Besides, the addition of ABI < 0.9 (P = 0.021) and baPWV (P = 0.014) to a FRS model significantly improved the predictive ITF2357 mouse value for overall mortality. In hemodialysis patients, intermediate risk but not high risk categorization by FRS predicted overall and cardiovascular mortality, and high risk predicted cardiovascular events. ABI < 0.9 and baPWV provided additional

predictive values for overall mortality. Future study is needed to develop hemodialysis-specific equations and assess whether risk refinement using ABI < 0.9 and baPWV leads to a meaningful change in clinical outcomes.

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“All chronic kidney disease (CKD) patients (CKD Stage 3–5; CKD Stage 5D (both peritoneal dialysis (PD) and haemodialysis (HD)). a. That therapeutic B-Raf inhibition iron be used to correct diagnosed iron deficiency (1D). c. That to achieve target haemoglobin levels in patients with CKD (2C), HD (2B) and PD (2D) the following iron indices should be targeted by increasing or decreasing iron therapy: Regular monitoring helps to predict iron overload and the overshoot of target Hb. (Ungraded) Suggested frequency of testing iron indices (Ungraded) CKD Stage 1–2 CKD Stage 3–5 CKD Stage 5D PD HD As clinically indicated ∼3 monthly ∼3 monthly ∼1–3 monthly In recent

years, since the publication of adjusted Hb targets (refer to KHA-CARI guideline ‘Haemoglobin Thiamet G Levels in Patients using ESAs’) and the demonstration that higher dosing of ESAs to achieve Hb targets is associated with an excess of cardiovascular events,[1] more emphasis has been placed on reasons for renal anaemia and the subsequent ESA resistance that may occur. The use of iron as a means of treating renal anaemia has assumed greater importance and particularly in people who have a higher demand for iron when on ESAs. Ten per cent of patients receiving ESAs are unresponsive.[2] Pro-inflammatory cytokines antagonize the action of ESAs by exerting an inhibitory effect on erythroid progenitor cells and disrupting iron metabolism (a process where hepcidin has a central role). Iron deficiency is also common in pre-dialysis CKD. In the NHANES III study less than one-third of the CKD non-dialysis patients had TSAT% >20% and ferritin >100 μg/L,[3] suggesting that iron homeostasis disruption begins relatively early in CKD progression. In many patients with CKD, as with patients with other chronic inflammatory diseases, poor absorption of dietary iron and the inability to use iron stores contribute to the anaemia.[4] Detection is also complicated by the lack of sensitivity of peripheral indices.