Pathy's Principles and Practice of Geriatric Medicine. Группа авторов

Pathy's Principles and Practice of Geriatric Medicine - Группа авторов


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historically difficult to treat because the crux of the treatment relies on the elimination of the chronic disease and inflammation. In some cases, erythropoietic‐stimulating agents will improve haemoglobin levels, but care must be taken to diagnose and treat any concomitant iron deficiency for these agents to be effective.

      Anaemia of chronic kidney disease

      Anaemia of chronic kidney disease (CKD) is quite prevalent in older adults because of the high prevalence of CKD in the older population. In a report released by the National Kidney Foundation, 45–70% of adults over 75 meet the diagnostic criteria for CKD (i.e. glomerular filtration rate of less than 90 mL/min).61 In another study focused specifically on nursing home residents with a diagnosis of CKD, 51–60% were also found to have anaemia.62 Although anaemia is deleterious in any individual, it is thought to be particularly onerous in those with CKD who are receiving haemodialysis. In a large retrospective study of CKD patients on dialysis, haemoglobin levels of less than 8 g/dL were associated with a twofold risk of death when compared to the risk associated with haemoglobin levels of 10–11 g/dL.63 Correction of anaemia in individuals with CKD has been positively associated with an improvement in quality of life as well as decreased mortality.64

      The pathophysiology of anaemia of CKD and anaemia of chronic disease share many overlapping features because of the underlying inflammation present in both conditions. Inflammation leads to functional iron deficiency from deranged iron homeostasis and a limited amount of free iron available to use in the production of new RBCs. In anaemia of CKD, hepcidin levels are more elevated than in anaemia of chronic disease, which is presumably because of reduced renal clearance of the peptide, resulting in even greater functional iron deficiency. An even more pronounced deficit of renally produced erythropoietin occurs due to the intrinsic renal dysfunction, leading to reduced bone marrow stimulation and impaired RBC production. Additionally, uraemia and elevated levels of unfiltered toxins in the blood can cause uraemia‐associated platelet dysfunction, leading to increased bleeding and worsening anaemia. Toxins also shorten RBC lifespan from the typical 120 days to 30 or 40 days.65 Individuals with CKD who are on dialysis have increased blood losses through frequent phlebotomy and haemodialysis. The cumulative effect of these mechanisms can produce severe anaemia (haemoglobin levels less than 8 ng/dL) that is frequently refractory to treatment.

      The National Kidney Foundation recommends a workup of anaemia of CKD when haemoglobin levels fall below 12 g/dL in men and 11 g/dL in women.66 Anaemia of CKD is routinely diagnosed by laboratory studies. Typically manifesting as a normocytic, normochromic anaemia, the diagnosis requires impaired renal function as determined by glomerular filtration rate (GFR), low haemoglobin, low to normal serum iron, normal to high ferritin, low to normal transferrin saturation, and normal to high TIBC. The reticulocyte count is low in proportion to degree of anaemia (Figure 22.3). Erythropoietin production is most severely depressed once the creatinine clearance falls below 30 mL/min but also progressively decreases with a decline in creatinine clearance under the normal range (under 90 mL/min).67 It is unclear how diagnostically useful erythropoietin levels are in anaemia of CKD, as they may be normal or even slightly increased above normal ranges but are low in proportion to the degree of anaemia present.68 Additionally, the currently available commercial assays are unable to specifically measure biologically active erythropoietin, making their usefulness controversial.69 Concurrent iron deficiency and anaemia of CKD is quite common, as RBC turnover is increased and bleeding losses through phlebotomy, uraemia‐associated platelet dysfunction, and haemodialysis are prominent.

      In summary, anaemia of chronic kidney disease and anaemia of chronic disease share many similar features, although anaemia of chronic kidney disease is often more pronounced because of the renal dysfunction. The laboratory diagnosis is also similar in that haemoglobin is low, iron levels are normal to low, and ferritin is elevated. It can be managed with erythropoietin‐stimulating agents and frequently concurrent IV iron administration. In anaemia of chronic kidney disease, the ideal upper limit of ferritin when treating with IV iron is unknown, but it is suggested that iron not be supplemented if the ferritin level reaches 500 ng/mL.

      A full discussion of clonal disorders is beyond the scope of this chapter. In general, the term clonal disorders refers to genetic aberrations in hematopoietic progenitor cells, which are typically in the bone marrow. These conditions include clonal haematopoiesis of indeterminate potential (CHIP), myelodysplastic syndrome (MDS), monoclonal gammopathy of undetermined significance (MGUS), aplastic anaemia, and acute myeloid dysplasia (MDS). A defining feature in anaemia of clonal disorders is stem cell mutations that lead to abnormal blood cell proliferation and progressive bone marrow failure. Diagnostic clues include the presence of macrocytic anaemia, anaemia with concurrent leukopenia, thrombocytopenia, and low to normal reticulocyte count. If suspected, a prompt referral to a haematology specialist should be made. Diagnostic confirmation is made by a bone marrow biopsy and requires cytogenetic and molecular studies.

      Key points

       Anaemia is defined as a haemoglobin of less than 13 g/dL in men and 12 g/dL in women and occurs in 10–25% of older adults.

       Iron deficiency anaemia is diagnosed by low serum iron, low ferritin,


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