The high prevalence of unrecognized anaemia in patients with diabetes and chronic kidney disease: a population-based study.

BACKGROUND: Anaemia occurs early in the course of diabetes-related chronic kidney disease (CKD). There is little evidence about the prevalence of anaemia in people with diabetes. The aim of this study was to assess the prevalence of anaemia, by stage of CKD, in the general diabetic population. METHODS: Haemoglobin (Hb) was measured on all glycated haemoglobin (HbA1c) samples and the most recent (< 4 months) estimated glomerular filtration rate (eGFR) was obtained. Anaemia (at treatment level) was defined as Hb < 110 g/l or the use of erythropoetic stimulating agents (ESA). RESULTS: Twelve per cent (10-14%) of people had Hb < 110 g/l. The prevalence of anaemia increased progressively with worsening CKD. People with CKD stage 3 accounted for the largest number of people with anaemia; 18% (95% CI 13-24%) had Hb < 110 g/l. Those with eGFR < 60 ml/min/1.73 m2 and not on ESA or dialysis were four (2-7) times more likely than patients with better renal function to have Hb < 110 g/l. The relation between Hb and eGFR became approximately linear below an eGFR of 83 ml/min/1.73 m2, where, for every 1 ml/min/1.73 m2 fall in eGFR, there was a 0.4 (0.3-0.5) g/l fall in haemoglobin. CONCLUSIONS: This study demonstrates that anaemia, at levels where treatment is indicated, occurs commonly in people with diabetes and CKD stage 3 or worse. The screening for anaemia in current diabetes management should be extended.

Inhibition of normal human granulopoiesis in vitro by amiloride: evidence for the involvement of facilitated sodium influx in the induction of differentiation.

The formation of colonies by normal human bone marrow granulopoietic progenitor cells in vitro in soft agar was inhibited in a simple, dose-dependent manner by amiloride (50% inhibitory concentration 26.4 +/- 3.4 microM, n = 9). Such inhibition was reversible and is evidence for the involvement of amiloride-sensitive sodium influx in granulopoietic cell proliferation. Colony-forming cells were capable of some proliferation at concentrations of amiloride 3-fold in excess of that required to inhibit full colony formation. A two-stage model is invoked to explain this observation: an early amiloride-insensitive stage and a late amiloride-sensitive stage which includes terminal differentiation. We conclude that the cellular mechanism by which differentiation is induced includes activation of the amiloride-sensitive sodium influx channel, which would indicate a new approach to the therapeutic induction of differentiation in vivo.