Patients with ESRF experience considerable morbidity and the burden of symptoms is similar in frequency and severity to that of cancer patients. Researchers have investigated symptoms found in patients with ESRF who have chosen not to dialyse.1

Figure 1 shows symptoms ranked by prevalence in a survey of these patients, while the prevalence of symptoms that caused the most distress to patients is listed in Box 1.

Consideration must be given to residual renal function. Conventionally, ESRF is considered to be when the glomerular filtration rate falls to less than 15ml/min. However, even below this level, there remains useful residual renal function, with partial removal of excess fluid and toxins. It is therefore prudent to consider how residual renal function will be affected by changes in treatment, such as NSAIDs or diuretics.

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Survival and quality of life
The survival of patients with ESRF who do not dialyse is in the order of six to 18 months.2 However, many patients whose renal function is declining only very slowly live several years with minimal renal function. It has been found that physical and mental quality of life is reasonably well maintained until the end-of-life phase, which lasts less than a week.3 Management for this period should be the same as for patients at the end-of-life phase from any other cause.4

In all cases, the underlying cause of the symptom should be addressed where possible. Causes and circumstances particular to, or common in, ESRF are outlined in Box 2.

Management of iron-deficiency anaemia
At the outset, it is important to exclude other causes of anaemia. In some cases, anaemia can be corrected with iron replacement alone. Where erythropoietin is used, iron requirements will be higher, owing to the increased bone marrow activity.

Functional iron deficiency can occur with normal ferritin levels and occurs when iron stores are not released sufficiently rapidly to meet the demands of erythropoiesis, despite adequate total body iron stores. Iron status should be assessed by measuring transferrin saturations and ferritin levels. In absolute iron deficiency, ferritin will be low, while in functional iron deficiency, it is usually above 100ng/ml, but transferrin saturations are usually below 20 per cent.5

In the treatment of iron deficiency anaemia, oral iron therapy can be used, but it is often inadequate in maintaining iron stores in patients with ESRF, especially those receiving erythropoietin. Uraemia and fluid overload reduce iron absorption from the gut. Sodium feredetate, a liquid formulation containing 100mg ferrous sulphate per 5ml, is sometimes effective. There are no universally agreed guidelines on the amount of iron required for a given patient with iron-deficiency anaemia.

Treatment is therefore tailored to achieve a ferritin level above 100ng/ml and transferrin saturations above 20 per cent by administering the iron in the most convenient form for the patient. This may mean using IV iron. There are two commonly used preparations, iron-hydroxide sucrose and iron-hydroxide dextran. The dose of iron given is limited by how quickly the compound releases iron and the method by which it is given. Small doses (100mg) can be given by bolus injection; larger doses should be given by infusing in combination with sodium chloride.2 Suggested regimens for the two IV preparations are given in box 3.

The usual practice is to administer five loading doses of iron to replenish stores, then either monthly or three-monthly maintenance doses can be given, or iron stores replenished when transferrin saturations and ferritin fall. Iron therapy should be discontinued if ferritin is >800ng/ml or transferrin saturation is >50 per cent. Iron-hydroxide dextran has a low but significant incidence of anaphylactic reactions and a test dose should be given on the first occasion. Most centres also give test doses of iron-hydroxide sucrose preparations before proceeding with larger infusions.