Anemia of chronic kidney disese Sepideh hajian,md Assistant professor Ghazvin university of medical science

Anemia of chronic

kidney disese

Sepideh hajian,MD Assistant professor

Anemia

Decrease Hb level in patients with

CKD

Etiology

The anemia of chronic kidney disease (CKD) is primarily due to insufficient

production of the glycoprotein hormone

PRODUCTION OF EPO

Although EPO can be produced in many of the body’s tissues, EPO required for

erythropoiesis

proximity to the renal tubules

As renal excretory function is lost, there is a relative decline in the production of EPO .

OTHER CAUSES OF ANEMIA

-Vitamin B12 deficiency -Folate deficiency -bleeding -comorbidity -hyperparathyroidism -ACEi

-Pure red cell aplasia -Hb pathy

Symptoms

The manifestations of anemia may be due both to the effects of

decreased oxygen

delivery to tissues

compensatory changes. The most prominent

Other symptoms : difficulty concentrating, dizziness,

sleep disorders, cold intolerance, and headaches.

The heart responds to diminished

oxygen-carrying capacity of blood by attempting

to maintain systemic oxygen delivery

with increased

cardiac output and left ventricular

hypertrophy

Severe anemia

deranged hemostatic function,

impaired immune function, and diminished cognitive and

sexual function. Exacerbations of angina,

claudication

transient ischemic attacks

Physical examination

pallor

the palms of the hands, the nail beds, and the oral mucosa.

Tx of decrease EPO production

agents that

replace erythropoietin

Epoetin alfa

that is indistinguishable from native erythropoietin. It is manufactured by

recombinant DNA

When we start treatment with

eprex?

plan

•Maintenance ob Hb between

10.5-11

gr/dl

•Decrease mortalitiy •Increas quality of life •Well being

Risks of EPO therapy

Hb level over 13 gr/dl has risks of:

•cardiovascular risk

•risk of death

•CVA

•Canser

The mechanism of harm for an ESA treatment with a Hgb target >13 g/dL is unknown

Route of administration

Subcutaneous versus intravenous

The

subcutaneous

efficiency of therapy, resulting in a reduced dosing requirement (of about 25%) for

shortacting ESAs, specifically epoetin alfa and non dialysis patients with ckd & PD patients

dosing

•2000-3000 unit 3 times/week for HD •6000 unit/week for PD

2 Weeks LATER Hb

reevaluation & during

maintenance phase of

therapy every 4 weeks

Max dose

the 2012 KDIGO guidelines recommend

not generally exceeding

four times

usual baseline weight-adjusted dose

Hypertension after treatment

•Vasoconstriction

•Increase cytosolic Ca

•Increase endothelin level •Activation of renin-Ag-Ald

OTHER COMPLICATIONS

•Graft thrombosis

•Stroke

•ESA Treatment and Cancer:

EPO may decrease survival ( head

and neck cancer)

For symptomatic, urgent

anemia correction, blood

transfusion should be

employed.

Iron deficiency

The second common cause of anemia in CKD

it develops during

EPO therapy

erythropoiesis

Blood loss

Hemodialysis patients develop iron deficiency

primarily because of chronic blood loss. Between retention of blood in the dialysis

lines and filter

surgical

blood loss, accidental bleeding

from the access

blood sampling for laboratory testing, and occult

Functional iron deficiency

After the injection of ESA, there is

an increase in the rate of erythropoiesis that leads to a greater immediate need for iron. In this setting, iron

deficiency may occur even in the face of normal body iron Stores.

This phenomenon has been termed functional iron deficiency.

Inflammation

(reticuloendothelial blockade)

Occult inflammationis often present in

ESKD patients. It causes an increase in

serum

hepcidin

concentrations, which

causes reduced

intestinal

iron

absorption

and

diminished

availability

of iron in

storage

tissues.

Poor absorption of dietary iron

Iron deficiency among patients on dialysis may be

exacerbated by poor absorption of dietary or medicinal iron.

1.Phosphate binders inhibit iron absorption

2. Histamine-2 blockers, proton-pump blockers impair iron absorption

Diagnosis of Iron deficiency anemia

iron status (TSAT and serum ferritin) at least every 3

months during ESA therapy.

intensification of iron therapy for

hemodialysis patients should be considered at a serum

ferritin of <200 ng/mL or TSAT of <20% and

TSAT <20% and serum ferritin <100 ng/mL in peritoneal

dialysis patients.

Iron testing should usually be delayed for 1 week after treatment with intravenous iron

Dosage and administration

Oral iron usually is given as ferrous sulfate, fumarate, or gluconate, in a dosage of 200 mg of elemental iron per day,

USUALLY FOR NON hemodialysis PATIENTS

There are two commonly

used intravenous iron dosing strategies. One is to treat

established iron deficiency with a repletive 1,000-mg dose administered over 8–10 consecutive hemodialysis

treatments.

Alternatively, since iron deficiency occurs so frequently in hemodialysis patients, a weekly maintenance

First sterategy is our

choice

complications

1-anaphylaxis

2-infection

Type of intravenous Iron

1-dextran

2-

sucrose

3-Na ferric gluconate

4-Triferic

Other causes of ESA resistance

Bleeding:

Occult or obvious:bleeding from access

RBC lifespan:

is 20%–30% shorter on average in hemodialysis

Other causes of ESA resistance

Infection &inflammation:

Occult:old AVF

CRP

is diagnostic

Rx:increase dose of

erythropoetin

Hyperparathyroidism

There is a clear relationship between elevated iPTH levels and diminished ESA response.

It

does not appear

inhibits erythropoiesis

pathogenesis is incompletely understood

Rx:intensification of the treatment of

hyperparathyroidism

Vitamin D

Data suggest that Hgb levels are lower in

dialysis patients with

low serum levels of

25-hydroxyvitaminD

, and

vitamin D

is a

potent

suppressor of hepcidin

in humans,

suggesting that treatment with vitamin

Relative vitamin B12 deficiency

Vitamin B12 and folic acid levels should be checked when unexplained ESA resistance is present.

Etiology:

taking proton-pump inhibitors

intensive high-flux hemodialysis

hemodiafiltration

Rx

B12 levels below 300 pmol/L

Hydroxycobalamin is ok(IM or SQ)

Cyanocobalamin does not

Aluminum intoxication

The effect on erythropoiesis is a

microcytic anemia associated with

impaired iron utilization.

Angiotensin-converting enzyme (ACE)

inhibitors

ACE inhibitors may

reduce EPO production

chronic renal failure or

following renal transplant.

Among patients on dialysis, a reduction in ESA responsiveness has not been uniformly

Pure red cell aplasia

The cause is the development of

antierythropoietin antibodies

that

neutralize both therapeutic and endogenous

erythropoietin.

Certain biosimilar forms of ESAs have been

associated with a greater risk for

Rx

Stop Eprex

Hemolysis

Dialysis solution Contaminants Chloramine

Copper, zinc,Nitrates, nitrites Overheated

Hypo-osmolar

Reuse of sterilants (formaldehyde)

•Needle trauma to RBCs

•Subclavian catheter (helmet cells, schistocytes) •Malfunctioning cardiac valve prosthesis

•Insufficient dialysis •Hypersplenism

•Associated diseases

• Sickle cell anemia

• Other hemoglobinopathies

• Connective tissue diseases with vasculitis

• Drug-induced

Rx

Stop hemodialysis

Stabilization of hemodynamic

Hyperkalemia evaluation

Ascorbic acid

Intravenous vitamin C given three times weekly with the hemodialysis treatment.