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

ANAEMIA OF 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

1420

43

628

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)

Pre

vale

nce o

f A

nem

ia (

%)

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

CKD+Anemia=270% in 2-yr mortality risk.

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, beta(NeoRecormon, Roche), omega, delta(Dynepo), pegylated forms

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