Conduit vessel stiffness in British south Asians of Indian descent relates to 25-hydroxyvitamin D status.

BACKGROUND: South Asians migrating to Northern latitudes are more susceptible to premature cardiovascular disease (CVD) than expected for given levels of blood pressure. Vitamin D deficiency is common in this group and may play an important role mediating vascular wall senescence in response to central pressure effects. METHODS: A cross-sectional association study. South Asian and White European participants were randomly recruited from a population-based diabetes-screening programme. Carotid-femoral pulse wave velocity (cfPWV), biochemistry (25-hydroxyvitamin D, fasting glucose), anthropometrics, resting blood pressure and a physical activity measure (International Physical Activity Questionnaire) were measured under controlled conditions. PARTICIPANTS: One hundred and thirty-two and 125 age-matched South Asians and White Europeans not taking vitamin D supplementation with a risk factor for diabetes but no overt CVD. RESULTS: Age (mean south Asian: 55.7 vs. White European: 56.0 years), mean arterial pressure (MAP) and calculated CVD risk were similar in both groups. Unadjusted (cf)PWV (m/s) was higher (9.32 vs. 8.68 P = 0.001) and 25-hydroxyvitamin D (nmol/l) lower in (21.29 vs. 52.5 P < 0.001) south Asians. 25-Hydroxyvitamin D independently associated with cfPWV in multivariate modelling adjusted for age, MAP, sex, glucose, heart rate, vasoactive medication and south Asian ethnicity (R = 0.73, P = 0.004). 25-Hydroxyvitamin D but not physical activity was negatively correlated with cfPWV independent of south Asian ethnicity. CONCLUSION: Aortic stiffness is increased in British Indo-Asians without vascular disease despite conventional risk profiles, which are comparable to age-matched white Europeans. This effect may be mediated by a greater pressure-dependent increase in stiffness in individuals with vitamin D insufficiency.

Intravenous iron in chronic kidney disease: haemoglobin change shortly after treatment of patients neither on dialysis nor on erythropoietin.

Anaemia is a common in chronic kidney disease. Although erythropoietin and iron supplementation are established treatments, knowledge on the use of IV iron alone in patients not on dialysis or erythropoietin is incomplete. The responses of 82 patients referred to the renal anaemia service with haemoglobin of 11.5 g/dl or less were assessed 1 week after completing four once weekly doses of 200 mg of venofer. No patients were on dialysis or erythropoietin. The haemoglobin rise 1 week after treatment was 0.53 g/dl. Ferritin levels improved from 110.8 to 410.2 ng/l and transferrin saturation from 17.7 to 27.3%. Ferritin levels remained below our target range (200-500 ng/l) in 7.7% while 25.6% had levels above this. Ferritin levels remained less than 800 ng/l in nearly all patients. Intravenous iron is cost effective and should be considered for use in patients with renal anaemia. Patients with CKD stage 5 appeared to respond less well.