Tag Archives: TSAT

This topic was addressed by Dr Carolyn Lam (National Heart Centre, Singapore) during a Vifor satellite symposium. Iron deficiency is frequently defined as a serum ferritin <100 μg/L (or 100–299 ng/ml, if transferrin saturation [TSAT] <20%); the usual iron deficit in a 35–70 kg heart failure patient with a haemoglobin 10–14 g/dl is 1,000 mg. Iron deficiency is common irrespective of haemoglobin, sex, ethnicity, and even ejection fraction. In heart failure patients it adversely affects: functional status, including exercise capacity quality of life outcome Iron deficiency (but not anaemia) is associated with adverse prognosis. My

Table 1. Origins of anaemia Haematinic deficiency The commonest single haematinic deficiency related to anaemia in patients with CHF is iron deficiency. Around half of all patients with anaemia have evidence of iron deficiency on the basis of abnormal results for serum iron, iron binding capacity and ferritin.1,2 Folate or vitamin B12 deficiency is relatively uncommon. Iron is used by the body not only for haemoglobin production but in a variety of enzyme systems, which may be affected by iron deficiency. There are many possible reasons for iron deficiency in patients with CHF. Dietary intake may be poor in the elderly population, and blood l

The situation in the anaemia of CHF is less advanced, but in recent years there has been increasing interest in the use of both of these treatment strategies. A few small clinical trials have suggested some potential benefits of stimulating erythropoiesis with ESA therapy in heart failure anaemia, whilst the administration of IV iron has shown similar benefits even in the absence of ESA therapy. Indeed, the recently published FAIR-HF (Ferinject® Assessment in patients with Iron deficiency and chronic Heart Failure) trial1 has opened the eyes of cardiologists to the potential for this latter treatment strategy to improve the symptoms and sig

Epidemiology of anaemia in CKD The likelihood of anaemia occurring in CKD increases as renal function declines. All patients receiving haemodialysis therapy will require treatment for anaemia, and so too will almost all of those receiving peritoneal dialysis (the difference accounted for by haemodialysis exposing the patient to a greater inflammatory state, and also regular minor blood losses). Below a glomerular filtration rate (GFR) of 45 ml/min, erythropoietin secretion by the kidney declines and when patients enter stage 4 CKD (eGFR < 30 ml/min), around 30–40% will be anaemic. Aetiology of anaemia in CKD Figure 1. Factors contributi