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Iron deficiency (ID) is the main cause of hyporesponsiveness to erythropoietin in haemodialysis patients and its detection is of value since it is easily corrected by intravenous iron. Markers of iron supply to the erythron, including erythrocyte zinc protoporphyrin (Er-ZPP), percentage of hypochromic erythrocytes (Hypo), reticulocyte haemoglobin content (CHr) and soluble transferrin receptor (sTfR), may be more accurate predictors of ID than ferritin (Fer) and transferrin saturation (TSat), but relative diagnostic power and best threshold values are not yet established.

To test the validity of the determination of protein catabolic rate (PCR) as a measure of protein intake in dialysis patients, we studied a selected population of 27 well-dialysed patients, free of catabolic illnesses, and in apparent clinical stability. Daily protein intake, obtained by controlled dietary records, and protein catabolic rate, measured by urea kinetic modelling, were 1.02±0.26 and 0.99±0.16 g/kg respectively. Although there was a good correspondence between protein intake and protein catabolic rate in many of our patients, in the six cases with dietary protein content less than 0.8 g/kg, protein catabolic rate was regularly greater than 0.8 g/kg; on the contrary, in four patients ingesting more than 1.2 g/kg of protein, protein catabolic rate values were significantly less than protein intake. Our results demonstrate that some degree of nitrogen imbalance may be present in about 25% of clinically stable dialysis patients, and suggest that current concepts of clinical stability do not imply a stable metabolic state in a substantial portion of dialysis patients. Therefore, protein catabolic rate determination does not provide a reliable index of protein intake in many dialysis patients.

Systemic hypertension may develop, or worsen, in 20–30% of haemodialysis patients treated with recombinant human erythropoietin (r-HuEPO). No particular group of patients, however, should be excluded from r-HuEPO treatment because of this increased risk. In the vast majority of cases, hypertension can be managed effectively by reducing dry weight, and by adding an antihypertensive agent if necessary. Only if these approaches are ineffective should the dose of r-HuEPO be reduced. Patients on dialysis are likely to be intolerant of cardiac ischaemia, as a result of coronary artery disease, microvascular occlusive disease, inadequate neo-vascularization in cardiac hypertrophy, or reduced glucose uptake (which impairs non-oxidative metabolism of the heart). Treatment with r-HuEPO can significantly reduce cardiac risk, as measured by surrogate endpoints such as left ventricular hypertrophy. More studies are urgently needed to investigate the potential beneficial effects of r-HuEPO on hard endpoints such as cardiac morbidity and mortality. In addition, dose-response data for target haematocrits in the range 30–40% are needed before an appropriate target haematocrit can be determined for patients with symptomatic vascular and cardiac disease.