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29 April 2017Nabieh Alhilali 1
Dr. Nabieh Alhilali
Consultant Nephrologist and Physcian
Therapeutic landscape
for anemia in CKD

1836 Anemia in CKD
1977 Purified EPO
1985 1st use of EPO in human
29 April 2017 2Nabieh Alhilali

Definition and prevalence in
CKD

 Kidney Disease Improving Global Outcomes
(KDIGO) guidelines define CKD
AND
 Kidney Disease Outcomes Quality Initiative
(KDOQI)
1.GFR <60 ml/min/1.73 m2 (less than
half of the normal level in young
adults)
OR
2.kidney damage for >3 months,
irrespective of cause of disease.
4/29/2017 4Al-Hilali N

AGE / GENDER Hb BELOW
gm/dl
Children 6 months to 5 years 11
Children 5 to11 years 11.5
Children to 14 years 12
Non-pregnant ladies more than 15 years 12
Men more than 15 years 13

Based upon these criteria,
nearly 90 % of patients with a glomerular
filtration rate (GFR) <25 to 30 mL/min
have anemia, many with Hb levels <10
g/dL.

CAUSES OF anemia in CKD

CAUSES OF ANEMIA IN CKD

29 April 2017
Nabieh Alhilali 11

Effects of anemia in CKD

 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 studies have positively
demonstrated that the QOL scores improved in
patients who were given ESA and iron to
increase their Hb

 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 with anemia.
 Also, other data show that CKD with anemia
increases the mortality rate by 2.7 times than
without.
 Interventional studies show that for an increase
of 1g/dL of Hb results in 4% decline in
mortality.

 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

 Acceleration of progression of kidney
disease by oxygen deprivation.
 Increased risk of bacteremia (11% increased
risk for every 1g/dl fall in Hb)
 Detrimental effects on brain and cognitive
functions.

PRELMENARY INVESTIGATIONS

THERAPEUTIC OPTIONS
IRON THERPY
ERYTHROPOITIN STIMULATIG AGENTS
BLOOD TRANSFUSION
OTHERS

1. IRON THERPY

In the opinion of the Work Group, sufficient iron
should be administered to generally maintain the
following indices of iron status during ESA
treatment:
Hemodialysis:
•Serum ferritin >200 ng/mL
• TSAT >25%
Non- dialysis and peritoneal dialysis:
• Serum ferritin >100 ng/mL
• TSAT >25%.
Targets of iron therapy

 Allergic reaction.
 Hypotension. Dizziness.
 Dyspnea.
 Headache.
 Low back pain.
 Arthralgia.
 Syncope.
 Arthritis.
 Some side effects can be reduced by decreasing the
dose or rate of infusion.
 Sodium ferric gluconate or iron sucrose has better
safety profile than iron dextran.

2. ERTHROPOIESIS STIMULATING
AGENT
(ERTHROPOITEN)

 Also known as EPO, hematopoietin, or hemopoietin,
It is a GLYCOPROTEIN HORMONE that
controls ERTHROPOISIS.
Human EPO has a molecular weight of 34 kDa.
It is produced by interstitial fibroblasts in the
kidney in close association with pretubular capillry
and proximal convoluted tubule. 90%
It is also produced in perisinusoidal cells in
the liver.10%
While liver production predominates in the fetal and
perinatal period, renal production is predominant
during adulthood.
2.ERYTHROPOIETIN

 They are used in treating anemia resulting
from chronic kidney disease,
 chemotherapy induced anemia in patients
with cancer,
 inflammatory bowel disease (Crohnes
disease and ulcerative colitis)[20] and
 myelodysplasia from the treatment
of cancer (chemotherapy and radiation).

1. Occult blood loss and/or iron deficiency
2. Vitamin B12 or folate deficiency
3. Infection and inflammation
4. Inadequate dialysis
5. Hyperparathyroidism
6. Aluminum toxicity
7. Patient adherence
8. Hypothyroidism
9. Primary disease activity
10. Transplant rejection
11. Malignancy
12. Pure red cell aplasia

when ESAs were given to maintain
hemoglobin levels of more than 12
grams per deciliter
Higher chance of
1. deaths were reported.
2. blood clots.
3. Strokes.
4. heart failure, and heart attacks.
.

5. increased rate of tumor growth were
reported in
a) patients with advanced head and neck
cancer receiving radiation therapy
and in
b) patients with metastatic breast
cancer receiving chemotherapy.
c) Patients with cancer and anemia not
receiving chemotherapy.

6. Higher chance of death was reported
and no fewer blood transfusions were
received when ESAs were given
7.Higher chance of blood clots was
reported in patients who were scheduled
for major surgery and given ESAs.

 ESA therapy is ineffective
 The risks of ESA therapy may outweigh its
benefits (e.g., previous or current malignancy,
previous stroke).
 When rapid correction of anemia is required to
stabilize the patient’s condition (e.g., acute
hemorrhage, unstable coronary artery disease).
 When rapid pre-operative Hb correction is
required.
 Transfusion should be directed toward
reduction of anemia sign and symptoms rather
than achieving specific target.

 Longer half life
 Absent immunogenicity
 Oral
 Simple manufacturing
 Not costly
1. Hematide
2. HIF stablizer
3. CATA Inhibitors

Take home message

Anemia is a significant contributor to mortality
and morbidity in CKD.
ESA and iron supplementation forms the core of
anemia management and has to be understood
in detail.
The data on the upper limit of target Hb is
conflicting but there is a trend towards a
lower value.

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