Anaemia is one of common symptoms of chronic kidney disease.know let us learn more about anaemia in chronic kidney disease.
In patients with chronic kidney disease, normochromic normocytic anaemia
mainly develops from decreased renal synthesis of erythropoietin. The anaemia
becomes more severe as the GFR (glomerular filtration rate) progressively
decreases. No reticulocyte response occurs, red blood cell survival is
decreased, and there is an associatedincreased bleeding tendency due to
uraemia-induced platelet dysfunction.
Iron deficiency is also common in patients with chronic kidney disease. The
iron deficiency may be absolute, often due to poor dietary intake or sometimes
occult bleeding, or functional, when there is an imbalance between the iron
requirements of the erythroid marrow and the actual iron supply. Iron deficiency
leads to a reduction in formation of red cell haemoglobin, causing hypochromic
microcytic anaemia. Other causes for anaemia in chronic kidney disease include
the presence of uraemic inhibitors (eg parathyroid hormone, inflammatory
cytokines), reduced half-life of circulating blood cells, and deficiencies of
folate or vitamin B12.
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Aetiology
Studies of patients with chronic kidney disease (CKD) have shown that the
prevalence of anaemia (defined as a haemoglobin level less than 12 g/dL in men
and postmenopausal women and less than 11 g/dL in premenopausal women) is about
12%.
The National Health and Nutrition Examination Survey (NHANES) III study
showed that the prevalence of anaemia increases as eGFR falls (1% at eGFR 60, 9%
at 30 and 33% at eGFR 15 ml/min/1.73 m2).
In patients with chronic renal failure, patients withdiabetes are at a
greater risk of developing anaemia earlier in the course of their disease
(associated with inappropriately low levels of erythropoietin). Comparing
patients with similar eGFR and erythropoietin levels, those with type 2 diabetes
are generally more anaemic.
Presentation
Often diagnosed by routine review blood tests.
Renal anaemia may lead to the onset or aggravation of lethargy, cold
intolerance and loss of stamina.
Anaemia increases cardiac output, therefore contributing to the development
of left ventricular hypertrophy and dilatation.
Differential diagnosis
Causes of anaemia in patients with chronic kidney disease (CKD), other than
renal failure itself, include:
Chronic blood loss
Iron deficiency
Vitamin B12 or folate deficiency
Hypothyroidism
Chronic infection or inflammation
Hyperparathyroidism
Aluminium toxicity
Malignancy
Haemolysis
Bone marrow infiltration
Pure red cell aplasia
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Investigations
Investigate patients with chronic kidney disease (CKD) if their haemoglobin
falls to 11 g/dL or less, or they get symptoms due to anaemia, such as tiredness
or breathlessness.
This will involve ruling out other causes of anaemia, assessment of renal
function, assessment of any cardiovascular and other complications of anaemia or
chronic kidney disease.
Renal function, eGFR and electrolytes.
FBC, blood film, iron studies (ferritin, transferrin saturation, iron), B12
and folate. Where ferritin <100 μg/L there is iron-deficiency anaemia. If
ferritin is above this level, a functional iron deficiency (and hence a
requirement for iron supplementation) is defined by the percentage of
hypochromic red cells >6% (if test is available) or otherwise a transferrin
saturation <20%.
Other investigations will be determined by likely alternative diagnoses and
cardiovascular effects of anaemia, eg thyroid function tests, renal ultrasound,
echocardiography, investigations for gastrointestinal bleeding.
Management
Any patient with chronic kidney disease presenting with anaemia:
Should be referred to the local specialist renal department for full
assessment and management. Clinical assessment should include an assessment of
nutrition, general wellbeing and other possible causes for anaemia (eg occult
blood loss).
Blood pressure should also be checked and any other factor suggesting acute
on chronic renal failure, eg infection.
The basic blood test investigations as outlined above should be sent
(ensuring the results are available at the renal department).
Management of anaemia should be considered in people with anaemia of chronic
kidney disease (CKD) when the haemoglobin level is less than or equal to 11 g/dL
(or 10 g/dL if under 2 years of age).
In people with anaemia of CKD, treatment should aim to maintain stable
haemoglobin levels between 10 and 12 g/dL for adults and children aged over 2
years, and between 9.5 and 11.5 g/dL in children aged under 2 years.
Treatment with erythropoiesis-stimulating agents should be offered to
patients with anaemia of CKD who are likely to benefit in terms of quality of
life and physical function. There is no evidence to distinguish between
erythropoiesis-stimulating agents in terms of efficacy.
The time taken for erythropoetin treatment to be effective will depend on
individual patient factors, such as degree of anaemia, degree of renal failure
and presence of other adverse factors, eg iron deficiency.
Contra-indications for erythropoetin treatment include uncontrolled
hypertension.
Potential side-effects of erythropoetin include increase in blood pressure or
aggravation of hypertension, headache, increase in platelet count,
influenza-like symptoms (may be reduced if intravenous injection given over 5
minutes), thromboembolic events, pure red cell aplasia, hyperkalaemia, and skin
reactions.
There have been very rare reports of pure red cell aplasia in patients
treated with epoetin alfa. The Commission on Human Medicines has advised that in
patients developing epoetin alfa failure with a diagnosis of pure red cell
aplasia, treatment with epoetin alfa must be discontinued and testing for
erythropoietin antibodies considered. Patients who develop pure red cell aplasia
should not be switched to another erythropoietin.
Monitoring: in people with anaemia of CKD, haemoglobin should be
monitored:
Every 2-4 weeks in the induction phase of erythropoiesis-stimulating agent
therapy.
Every 1-3 months in the maintenance phase of erythropoiesis-stimulating agent
therapy.
More actively after dose adjustment of the erythropoiesis-stimulating
agent.
Epoetin alfa:
Epoetin (recombinant human erythropoietin) is used for the anaemia associated
with erythropoietin deficiency in chronic renal failure. The clinical efficacy
of epoetin alfa and epoetin beta is similar.
It is also used to increase the yield of autologous blood in normal
individuals and to shorten the period of anaemia in patients receiving cytotoxic
chemotherapy.
Epoetin beta is also used for the prevention of anaemia in preterm neonates
of low birthweight.
Darbepoetin:
Is a hyperglycosylated derivative of epoetin which has a longer half-life and
may be administered less frequently than epoetin.
Other factors which contribute to the anaemia of chronic renal failure, eg
iron or folate deficiency, should be corrected before treatment and monitored
during therapy.
Aluminium toxicity, concurrent infection or other inflammatory disease may
impair the response to erythropoietin.[3]
People receiving erythropoiesis-stimulating agent maintenance therapy should
be given iron supplements (often requires intravenous iron) to keep their:
Serum ferritin between 200 and 500 μg/L, and either:
The transferrin saturation level above 20% (unless ferritin >800 μg/L);
or
Percentage hypochromic red cells less than 6% (unless ferritin >800
μg/L).
Clinically relevant hyperparathyroidism should be treated in order to improve
anaemia management in patients with anaemia of CKD.
Where possible, blood transfusions should be avoided in patients in whom
kidney transplant is a treatment option.
Prognosis
Anaemia is an adverse indicator for the progression of chronic kidney
disease. Therefore, correcting anaemia is considered an important part of
slowing or even stopping the progression of chronic kidney disease.
Treatment with recombinant human erythropoietin in pre-dialysis patients
corrects anaemia, avoids the requirement for blood transfusions and also
improves quality of life and exercise capacity.
Prevention
Restricting the progression of chronic kidney disease, eg smoking cessation,
optimal control of diabetes.
Treatment
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