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Anaemia of chronic kidney
disease
“GUIDELINES TO PRACTICE ”
Dr Ayman SEDDIK , Msc , MD
ASS. PROF. NEPHROLOGY, AIN SHAMS UNIVERSITY
CONSULTANT NEPHROLOGIST DUBAI HEALTH
AUTHORITY
objectives
 ANAEMIA OF CKD CAUSES & CONSEQUENCES
 K-DIGO GUIDELINES 2012 , Eurpean best practice
guidelines statement 2013 , data from DOPS 2013
I) Diagnosis and evaluation of anemia in CKD
2) Use of iron
3) Use of Erythrocyte stimulating agents ESAs and other
agents
4) evaluation and correction of persistent failure to reach or
maintain intended haemoglobin concentration
5) evaluation of pure red blood cell aplasia
6) Red cell transfusion to treat anemia in CKD
ANAEMIAOF CKD, CAUSES& CONSEQUENCES
Causes of anaemia in CKD
 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.
Anemia Worsens as Kidney Function
Declines
14
20
43
62
8
8
15
9
17
15
10
5
0
10
20
30
40
50
60
70
80
90
100
<2 2.0-2.9 3.0-3.9 >4
Serum Creatinine Level (mg/dL)
PrevalenceofAnemia(%)
Reference: Adapted from Kausz et al. Dis Manage Health Outcomes. 2002;10:505-513.
Hb Levels
Hb=11-12 g/dL (n=181)
Hb=10-11 g/dL (n=105)
Hb=<10 g/dL (n=315)
 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
 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
 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.
KDOQI
2006
Anemia
Guidelines
 rHuEPO was genetically modified proteins that
were very similar to the nascent EPO.
 Contained the 165AA backbone with one O-
linked and three N-linked gycosylated chains.
 There gycosailylated chains contain variable
amounts of sialic acid residues.
 Many forms of rHuEPO are available: Alfa,
 Methoxy polyethylene glycol-epoetin beta is
made from erythropoietin by chemically linking
the N-terminal amino group or the Є-amino
group of any lysine present in the protein with
methoxy polyethylene glycol butanoic acid.
 The average molecular weight is approximately
60kDa
 Marketed as Mircera (Roche)
KDOQI 2006
Anemia
Guidelines
 The use of darbepoetin alfa (to achieve a higher Hb
target) in patients with diabetes, chronic kidney disease,
and moderate anemia who were not undergoing dialysis
did not reduce the risk of either of the two primary
composite outcomes (either death or a cardiovascular
event or death or a renal event) and was associated with
an increased risk of stroke.
 This risk may outweigh the potential benefits.
 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.
Diagnosis of anaemia of CKD in adults
eGFR < 60ml/min/1.73m2
AND Hb ≤ 11 g/dl
No
Consider
other causes
Yes
Non renal and
haematinic
deficiency excluded?
No
Treat and repeat
Hb
Yes
Patient on
haemodialysis?
No
See sections
1.2 & 1.3
Yes
See initial
management
algorithm
Hb maintenance algorithm
(assumes ESA therapy and maintenance i.v. iron)
Measure Hb
Hb < 11 g/dl Hb 11–12 g/dl Hb 12–15 g/dl Hb > 15 g/dl
↑ ESA dose/
frequency as
per schedule
unless Hb
rising by
1/g/dl/month.
Check Hb
as per
Schedule.
No change
unless Hb
rising by
1g/dl/month
in which case
consider
ESA dose
adjustment
Consider
stopping i.v.
iron. ↓ ESA
dose/frequency
as per schedule
unless Hb
falling by more
than 1g/dl/month.
Check Hb as
per schedule.
Stop i.v. iron.
Consider
stopping
ESA or halve
dose/frequency.
Check Hb in
2 weeks.
If Hb is
persistently low
see poor
response
algorithm
Ferritin < 200 µg/l?
Iron dosage schedule
Hb monitoring
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE  2013

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Anaemia of chronic kidney disease GUIDELINES TO PRACTICE 2013

  • 1. Anaemia of chronic kidney disease “GUIDELINES TO PRACTICE ” Dr Ayman SEDDIK , Msc , MD ASS. PROF. NEPHROLOGY, AIN SHAMS UNIVERSITY CONSULTANT NEPHROLOGIST DUBAI HEALTH AUTHORITY
  • 2. objectives  ANAEMIA OF CKD CAUSES & CONSEQUENCES  K-DIGO GUIDELINES 2012 , Eurpean best practice guidelines statement 2013 , data from DOPS 2013 I) Diagnosis and evaluation of anemia in CKD 2) Use of iron 3) Use of Erythrocyte stimulating agents ESAs and other agents 4) evaluation and correction of persistent failure to reach or maintain intended haemoglobin concentration 5) evaluation of pure red blood cell aplasia 6) Red cell transfusion to treat anemia in CKD
  • 3. ANAEMIAOF CKD, CAUSES& CONSEQUENCES
  • 5.
  • 6.
  • 7.
  • 8.
  • 9.
  • 10.
  • 11.  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.
  • 12. Anemia Worsens as Kidney Function Declines 14 20 43 62 8 8 15 9 17 15 10 5 0 10 20 30 40 50 60 70 80 90 100 <2 2.0-2.9 3.0-3.9 >4 Serum Creatinine Level (mg/dL) PrevalenceofAnemia(%) Reference: Adapted from Kausz et al. Dis Manage Health Outcomes. 2002;10:505-513. Hb Levels Hb=11-12 g/dL (n=181) Hb=10-11 g/dL (n=105) Hb=<10 g/dL (n=315)
  • 13.  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
  • 14.  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
  • 15.  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
  • 16.  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.
  • 17.
  • 19.
  • 20.  rHuEPO was genetically modified proteins that were very similar to the nascent EPO.  Contained the 165AA backbone with one O- linked and three N-linked gycosylated chains.  There gycosailylated chains contain variable amounts of sialic acid residues.  Many forms of rHuEPO are available: Alfa,
  • 21.  Methoxy polyethylene glycol-epoetin beta is made from erythropoietin by chemically linking the N-terminal amino group or the Є-amino group of any lysine present in the protein with methoxy polyethylene glycol butanoic acid.  The average molecular weight is approximately 60kDa  Marketed as Mircera (Roche)
  • 22.
  • 23.
  • 24.
  • 25.
  • 27.  The use of darbepoetin alfa (to achieve a higher Hb target) in patients with diabetes, chronic kidney disease, and moderate anemia who were not undergoing dialysis did not reduce the risk of either of the two primary composite outcomes (either death or a cardiovascular event or death or a renal event) and was associated with an increased risk of stroke.  This risk may outweigh the potential benefits.
  • 28.  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.
  • 29. Diagnosis of anaemia of CKD in adults eGFR < 60ml/min/1.73m2 AND Hb ≤ 11 g/dl No Consider other causes Yes Non renal and haematinic deficiency excluded? No Treat and repeat Hb Yes Patient on haemodialysis? No See sections 1.2 & 1.3 Yes See initial management algorithm
  • 30. Hb maintenance algorithm (assumes ESA therapy and maintenance i.v. iron) Measure Hb Hb < 11 g/dl Hb 11–12 g/dl Hb 12–15 g/dl Hb > 15 g/dl ↑ ESA dose/ frequency as per schedule unless Hb rising by 1/g/dl/month. Check Hb as per Schedule. No change unless Hb rising by 1g/dl/month in which case consider ESA dose adjustment Consider stopping i.v. iron. ↓ ESA dose/frequency as per schedule unless Hb falling by more than 1g/dl/month. Check Hb as per schedule. Stop i.v. iron. Consider stopping ESA or halve dose/frequency. Check Hb in 2 weeks. If Hb is persistently low see poor response algorithm Ferritin < 200 µg/l?