Anemia in CKD

case

36 y.o
ESRF
on CAPD since 2011

Hep B+ve
Hypertension
 in CAPD clinic patient result
WBC 4.5 Hb 8.7 plt 140
MCV 73 MCHc 32.5

Renal profile
Na 141 K 4.1 Urea13.8 creat 959
 How we going to approach for his anemia ??
Introduction

Anemia is a condition in which the number of RBCs or

their oxygen-carrying capacity is insufficient to meet
physiologic needs, which vary by age, sex, altitude,
smoking, and pregnancy status (WHO).

For diagnosis and further evaluation Hb values according

to NKF guidelines:
<13.5 g/dL in adult males. (WHO-13g/dL)
<12.0 g/dL in adult females.
Effects of anemia (QOL)
QUALITY OF LIFE:

Anemia results in poorer quality of life in patients with

renal failure.

This correlation can be proven by the poor quality of

life scores in patients with lower Hb values.

Many observational as well as RCT have positively

demonstrated that the QOL scores improved in
patients who were given ESA and iron to increase
their Hb
 Effects of anemia(mortality)
Generation of hypoxia due to anemia is poorly tolerated in
patients with preexisting cardiac and vascular diseases.
Compensatory mechanisms leads to development of LVH.
Observational studies do show an increase in mortality in
patients with CKD but not direct casualty.
Interventional studies (DOPPS) show that for an increase
of 1g/dL of Hb results in 4% decline in mortality.
Also, Medicare data show that CKD=100% and
CKD+Anemia=270% in 2-yr mortality risk.
EFFECTS of anemia on CV health

CV disease related mortality is 15 times more in

patients with CKD.
50% of deaths in patients with CKD are due to
CV disease.
LVH is the most common abnormality seen in
patients with CKD and there is a strong
correlation between anemia and LVH.
Tissue hypoxia due to anemia is the principal
stimuli triggering the compensatory changes that
stresses the CV system
cause of anemia in CKD

erythropoietin deficency
iron deficiency
blood loss
shorten red cell surival
effect of uremic inhibitor on bone marrow
severe hyperparathyroidism leading to myelofibrosis
aluminium overload
nutrional deficeincy
hypothyroidism
infection
haemoglobinopathy
KDIGO

In patients with CKD and anemia (regardless of age and

CKD stage), include the following tests in initial evaluation
of the anemia (Not Graded):
Complete blood count (CBC), which should include Hb
concentration, red cell indices, white blood cell count and
differential, and platelet count
Absolute reticulocyte count
Serum ferritin level
Serum transferrin saturation (TSAT)
Serum vitamin B12 and folate levels
Iron
Serum ferritin
reflects iron stores
should not be measured within 1-2 weeks after intravenous
iron or blood transfusion
serum ferritin should be interpreted with care in the
presence of infection, inflammation or hepatitis

Transferrin saturation (TSAT)

reflects availability of iron
ratio of serum iron to total
 absolute iron deficiency :
serum ferritin < 100 ng/ml
functional iron deficiency :
serum ferritin > 100 ng/ml
and TSAT < 20% or %
hypochromic rbc >10%
 Oral iron should
be taken 2 hours
before or
1 hour after
phosphate
binders
Administration of intravenous iron
Resuscitation equipment should be available during
administration of iv iron
Patients receiving iv iron for the first time should receive a
25mg test dose

Method of administration
Iron dextran should be given by iv infusion over 1hour
Iron sucrose may be given by iv slow bolus (20mg/min) or
by infusion
Haemodialysis patients:

Absolute iron deficiency : iv iron sucrose or iron dextran

100mg every HD session for 10 sessions then check iron
status no earlier than 7 days

Functional iron defi ciency : iv iron sucrose or iron

dextran 100mg every week for 10 weeks

Maintenance: 25mg to 100mg per week

CAPD patient

200mg to 500mg of iron dextran infused in 250mls saline

over 1-2 hours or
iron sucrose 200 to 500 mg in 100 to 500 ml saline over 1
to 4 hours

The manufacturers recommended maximum single dose

is 1000mg of iron dextran and 500mg of iron sucrose
Case

Tsat =67%
serum iron =27
transferin =1.6

Thalassemia screening : negative

Administration of Epoetin
Indication
Persistent Hb concentration < 11g/dl after evaluation for
other causes of anaemia (Level A)

Pre-treatment evaluation
Clinical evaluation to exclude other causes of anaemia
Hypertension should be controlled
Assessment of iron status and treatment of iron deficiency
prior to initiation of Epoetin to achieve target iron levels
Ensure dialysis is adequate (Level C)
 Starting dose: iv 4000 units weekly in one or two divided doses (or 50-
150 IU/kg/week)

Monitoring during Epoetin therapy

BP
Hb response
Hb should be checked every 2 weeks at initiation or following a change in
Epoetin dosage until Hb stabilises after which it should be checked every 3
months (Level C)
Iron status
Serum ferritin, transferrin saturation (serum iron and TIBC) and % hypochromic
red cells should be monitored every 3 months.
 Target Hb should be 11 to 12 g/dL13-21 (Level A)
Target rise in Hb is 1 2 g/dl per month and target should
be reached within 2 to 4 months
Titrate dosage

If Hb rise is < 0.5g/dl over 2-4 weeks, Epoetin dose

should be increased by 2000 units to 4000 units every 2
to 4 weeks
If Hb rise is > 2.5 g/dl per month or Hb exceeds the target,
reduce dose of Epoetin by 25 50% (Level C)
Resistance to Epoetin

Resistance to Epo is arbitrarily defined as failure to

achieve or maintain target haemoglobin with > 300
units/kg/week (20,000 units/week) subcutaneously
cause of resistence
iron deficiency (absolute or functional) is hyperparathyroidism
the most common reason for resistance
to Epoetin haemoglobinopathies e.g.
chronic blood loss thalassemias
inflammation e.g. chronic allograft
rejection, folate or Vit B12 defi ciency
SLE bone marrow disorders e.g.
infections e.g. tuberculosis, access mutiple
infection,
AIDS myeloma, myelofibrosis,
malignancies myelodysplastic syndrome,
inadequate dialysis pure red cell aplasia (PRCA).
drugs e.g. ACE inhibitors
haemolysis
aluminium toxicity
hypothyroidism
pure red blood cell aplasia
PRCA should be suspected in patients on Epoietin for > 4
weeks:
(a) develop a sudden and rapid decline in Hb (decline in Hb
>05-1g/dl per week or requirement for blood transfusion
every 1-2 weeks); AND
(b) absolute count reticulocyte count of < 10,000/ul; AND
(c) normal white count and platelet count.

Diagnosis is confirmed by the presence of < 5%

erythroblasts on bone
marrow examination and anti-epoietin antibodies (if
available).
KDIGO
In general, we suggest that ESAs not be used to maintain
Hb concentration above 11.5 g/dl (115 g/l) in adult
patients with CKD. (2C)
Individualization of therapy will be necessary as some
patients may have improvements in quality of life at Hb
concentration above 11.5 g/dl (115 g/l) and will be
prepared to accept the risks. (Not Graded)
In all adult patients, we recommend that ESAs not be
used to intentionally increase the Hb concentration above
13 g/dl (130 g/l). (1A)
 Blood transfusion
When managing chronic anemia, we recommend avoiding, when
possible, red cell transfusions to minimize the general risks related to
their use. (1B)
In patients eligible for organ transplantation, we specifically
recommend avoiding, when possible, red cell transfusions to minimize
the risk of allosensitization. (1C)
When managing chronic anemia, we suggest that the benefits of red
cell transfusions may outweigh the risks in patients in whom (2C):
ESA therapy is ineffective (e.g., hemoglobinopathies, bone marrow failure, ESA
resistance)
The risks of ESA therapy may outweigh its benefits (e.g., previous or current
malignancy, previous stroke)
We suggest that the decision to transfuse a CKD patient with non-
acute anemia should not be based on any arbitrary Hb threshold, but
should be determined by the occurrence of symptoms caused by
 Thank You