understanding lab values when on dialysis-2[1]

8/13/2019 Understanding Lab Values When on Dialysis-2[1]

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Connie Gilet, ANP

UNC Kidney Center/ UNC Healthcare

September 2011


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Objectives Discuss lab values related to anemia management

>Interpret CBC results, including H/H, RDW (red cell

distribution width), MCV (mean corpuscularvolume) and MCHC (mean corpuscular hemoglobin

concentration)

>Examine iron study results, focusing on iron

saturation and ferritin


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Objectives Discuss the complex relationship between calcium,

phosphorus, vitamin D and PTH

>Review bone and mineral pathophysiology>Discuss why interventions involve thinking about all

four of the above lab values

>Outline when lab values are only abnormalvs when

they are alarming

>Discuss treatment of bone and mineral abnormalities

with medications and surgery


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Objectives Discuss how dialysis adequacy is determined and used

in a clinical setting

>Discuss URR, Kt/V and PET, how to calculate thesemeasures and how to interpret the results

>Discuss the advantages and disadvantages of URR

(Urea Reduction Ratio) vs Kt/V

>Examine when, why and how the dialysis prescription

should be adjusted


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Plan Briefly present basic information for each topic

Hopefully, present new information for each topic

Case studies will help to enhance understanding ofinformation presented


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Anemia Decrease in RBCs can be due to a variety of factors..

>Abnormal destruction of red blood cells (e.g.

hemolytic anemia, sickle cell disease)>Lack/decreased cell production from bone marrow

(e.g. aplastic anemia, myeloproliferative disorders)

>Blood loss (e.g. GI Bleed)

>Lack of substances needed to produced RBCs

>All of the above seen in people with CKD


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Anemia Management Current practice

>If Hgb less than 10 g/dl x 2, start Epogen/Aranesp>Hgb levels checked at least monthly (KDOQI)>Goal: maintain Hgb between 10 and 12 g/dl

>CREATE and CHOIR study>Do not know optimal Hgb for people with CKD

>If Hgb exceeds upper limit (12 g/dl) or increases more than 1 g/dl in2 wks:>Hold the dose (per FDA)

>No benefits to hemoglobin > 13 g/dl. In fact, increasesthe risk of clots, vascular events (heart attack and stroke) anddeath


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Anemia Management New?

>TREAT--Trial to Reduce Cardiovascular Events with

Aranesp Therapy (people not on dialysis)>Study completed in 2009

>Recommends Hgb >10 and Reduce risk of clots, heart attacks, stroke and death

>Several other studies currently underway

>Will guidelines for people on dialysis also change?


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Red Blood Cells and Hemoglobin Red blood cells (RBC)

>Normal life span 120 days/80-90 days if on dialysis>Decreased life span due to toxic, uremic environment*

>Composed of mostly water and hemoglobin Hemoglobin

>Hgb molecule made of iron and protein>The predominant

protein in RBC>Carries oxygen

*Ly, et al (200$)


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Hemoglobin CKD abnormal H/H; what are critical Hgb values? Hgb values below 5 g/dl can cause heart failure

Hgb values above 13 g/dl can cause CV events/death*

KDOQI Anemia Guidelines: 2007 Update


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Hematocrit Hematocrit

>% of RBC in plasma (liquid part of the blood)>Increase/decrease of plasma volume affects the

hematocrit values>Decrease occurs with over hydration (diluted)>Increase occurs with under hydration(concentrated blood volume)

>How would Hct change before/after dialysis?>What lab value used to dose epo? Why?

>If RBC and Hgb are normal, estimate Hct bymultiplying the Hgb times 3. (10 x 3 = 36)


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Reticulocyte Count Reticulocytes are immature forms of erythrocytes (also called

RBCs)

>Up to 1.5% normal in men

>Up to 2.5% normal in women>Low retic count seen with folic acid deficiency

>High retic count seen when the bone marrow is responding

to an increase need for RBCs. Bone marrow cant produce

enough mature RBCs fast enough, so it does the next

best thing, increases the production of immature RBCs

>What would you expect a retic count to be in a person with

ESRD on dialysis?


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RDW (RBC Distribution Width) RDW

>Indicator of variation in the size of red blood cells

>Values > 14.5% = RBC vary a lot in size

>Immature red cells usually larger

>RDW increased in those with ESRD

Why?

Bone marrow working hard to produce enoughred blood cells but cant produce enough mature

cells to keep up with demand.


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MCV and MCHC Results MCV (mean corpuscular volume)

>Measures average size of RBC

MCHC (mean corpuscular hemoglobin concentration)

>Measures % of hemoglobin in the RBC

>Hgb/Hct x 100

Why should I care about the MCV and MCHC values?


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Anemia Case study

>E.R. is a 39 y/o Hispanic female. Separated with 3

children, ages 12, 13 and 19 years old.>ESRD of unknown etiology; transplant in 2003.

Kidney was from her sister.

>Rejection (per renal biopsy) August 2010;

restarted dialysis in August 2010.

>Receives dialysis via ED every 4-5 days.

>Receives Aranesp every 2-3 weeks with dialysis.


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Putting It All Together Before looking at lab values, you should be asking.

>What are normal vs. abnormal values?

>What information does the abnormal lab values

tell you?

>Are there any alarming/critical lab values?


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CBC Results

Test Range Patient = E.R.RBC (red cell count) 4.00-5.20 2.99 million

HGB (hemoglobin) 12-16 g/dl 9.2 g/dl

HCT (hematocrit) 36-46 % 26.9 %

Retic count

(reticulocyte count)

0.5% - 1.5%/2.5% 3.0%

MCV (meancorpuscular volume)

80-100 90.0-------------75%

MCHC (meancorpuscular

hemoglobinconcentration)

31-37 34.0%-----------28%

RDW 12-15 % 18.0%

B12 193-900 pg/ml 843 pg/ml

Folic Acid 2.7 20.0 ng/ml > 20 ng/ml


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Anemia Case Study

>32 year old male, T.A., mentally challenge

>Lives with his mother>ESRD on hemodialysis 2/2 neurogenic bladder and

>Gout

>HTN

>Sickle cell trait


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CBC ResultsTest Range Patient = T.A.RBC (red cell count) 4.00-5.20 3.52

HGB (hemoglobin) 12-16 g/dl 10.8 g/dl

HCT (hematocrit) 36-46 % 32.2 %

Retic count (reticulocytecount)

0.5% - 1.5%/2.5% Not reported

MCV (mean corpuscular

volume)

80-100 FL 91 FL

MCHC (mean corpuscularhemoglobinconcentration)

31-37 g/dl 34 g/dl

RDW 12-15 % 16.4%


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Measuring Iron Where iron is found

Two tests used to estimate iron stores: Ferritin and Saturation>Ferritin>Is a protein that binds to iron; helps to transport iron in the body

>Most ferritin is found in the liver, spleen, muscle and bone marrowwith a small amount found in the blood>Normally, 1 ng of ferritin (in blood) = 10 ng of iron stores (in liver, spleen, muscle and bonemarrow)>Ferritin is a proxy measure for iron stores and has it s limitations.

Image retrieved August 11, 2011 from http://www.google.com/imgres?q=diagram+iron+stores+body&um...


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Ferritin Low ferritin levels usually indicates iron deficiency

High ferritin levels, however..>Does not necessarily indicate adequate iron stores

>Many factors can increase ferritin levels, e.g. recent iron infusion, infection,inflammation, e.g. autoimmune disorders, malignancy, blood transfusions(250 mg of iron/1 unit packed red cells)

>Wait two weeks before measuring iron stores after giving iron load (morethan 125 mg/week)

>Can become iron toxic (ferritin greater than 1000)>High levels can be due to inherited disorders or too much iron

administration>Toxic levels of iron can cause organ failure and death


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DRIVE STUDY Dialysis Patients Response to IV iron with elevated ferritin

Study (DRIVE)

>Provided some clarification for safe upper limits offerritin levels in hemodialysis patients.>Ferric gluconate (ferrlecit) administration is superiorto no iron therapy in anemic dialysis patientsreceiving epogen and ferritin levels of 500 to 1200

ng/ml and Tsats of


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Iron Saturation Complete name = transferrin iron saturation or Tsat

>Estimates ability to bind iron and

transport it to various sites in thebody

>Serum iron / total iron binding

capacity X 100

More sensitive than ferritin; not affected byinflammation/infection


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Goal for Iron Stores*HD-CKD ND-CKD/PD-CKD*

Ferritin > 200 ng/mlSats > 20% Ferritin > 100 ng/mlSats > 20%

From KDOQI Anemia Guidelines *No RCT to support recommendation


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Iron Deficiency Many causes

>Blood loss

>Celiac disease (decreases absorption of iron)>Hemolysis (RBC breaks apart)

>Gastric bypass (decreases absorption)

>Epogen administration, etc.

Must identify cause of iron deficiency before

treating


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Look at Entire Picture Decreasing ferritin/stable sats/decreasing Hgb = iron

deficit

>? external iron loss

>Need more iron Decreasing ferritin and increasing Hgb = iron moving

from storage to hemoglobin (e.g. in response toepogen administration)

Increasing ferritin and decreasing sats and decreasingHgb = inflammation

>Increase ESA dose


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Case Study Case Study

>F.L. 86 yo female who attends the anemia/CKD clinic.

History significant for.>HTN

>CKD IV

>Anemia

>Unable to tolerate po iron supplements due to GI

upset


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Case StudyTEST/INTERVENTION

DATE = 11/8/2010 DATE = 12/22/2010 DATE = 1/17/2011

Hemoglobin 8.8 (decreasing) 7.7 9.5

Hematocrit 28.4 25.3 30.9

Saturation none 10% none

Ferritin none 33 none

BUN 54 (increasing) 55 39

Creatinine 2.4 (increasing) 2.35 2.04

GFR 23 ml/min 24 ml/min 28 ml/min

Aranesp dose Increased to 200mcg

200 mcg 200 mcg


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Take Home Points for Anemia and Iron

Administration Look at hemoglobin trends

>If Hgb is decreasing

>Dont miss other causes of anemia>Increase epogen

Look at iron sats and ferritin

>If iron sats and ferritin both low, give iron

>Remember iron is stored in places we dont measure,

so look at the entire clinical picture


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Bone and Mineral Balance Briefly discuss the four primary players:

>Vitamin D

>Calcium>Phosphorus

>PTH

Discuss the complex interdependence amongstcalcium, phosphorus, vitamin D and PTH


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Vitamin D2-3 Vitamin D comes from

sun, food and our body

25-hydroxyvitamin D2produced in the liver

Normally kidneys producean enyzme that converts

D2 to D3 (1,25dihydroxyvitamin

= calcitriol)


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Vitamin D A complex group of fat-soluble substances (D1-D5)>D2 = ergocalfciferol>Sources

>Foodonly found in seafood, mushrooms, eggyolks and fortified foods>OTC: Generic Vitamin D>Prescription: Drisdoll

>Changed in the liver to 25-hydroxycholecalciferol (25-OH)

>Measured in those with CKD Stages 3-5>25-OH changed in normal kidneys to 1,25dihydroxycholecalciferol>Measured in those with CKD Stage 3-6


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Vitamin D3 D3 = cholecalciferol

>D3 = 1,25 dihydroxycholecalciferol

>Decreased amounts produced in CKD>Also referred to as active Vitamin D

>Sources: Calcitriol (Rocaltrol)

Hectoral (doxercalciferol)

Zemplar (paricalcitrol)

Sunlight (converted to Vitamin D3 in

the skin)


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Vitamin D Lab ranges

>25OH = < 30/32

>1,25 = 18-78

>Controversy on what level is normal & too high What does Vitamin D do?

>Helps maintain serum calcium and phosphorus

levels/regulates release of calcium and phosphorus

from the bone>Increases calcium absorption from the intestines

>Suppresses PTH synthesis


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Calcium Functions

>Maintains bone structure

>Plays a major role in nerve conduction

>Assists with muscle contraction/relaxation Most calcium found in bone

Serum calcium binds to albumin

>Serum calcium = 6.5 Albumin = 2.5

>0.8 x (4.0-2.5) + 6.5 = 7.7>Corrected serum calcium more accurate

>Corrected total calcium 8.4 to 9.5 mg/dl


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Hypercalcemia Long term consequences for those with CKD

>Increased risk CV calcifications (larger arteries)

>Calciphylaxis (soft tissue)

Serum calcium > 13.0 Causes

>Medications (calcium acetate, zemplar)

S/S of hypercalcemia

>Depression, anxiety, muscle weakness, cognitivedysfunction, fatigue, hypertension, constipation

>ECG changes/arrhythmias


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Hypocalcemia Serum calcium < 6.5

>Numbness/tingling in

perioral area, fingers,toes

>Muscle cramps or

tetany (muscle spasm

or tremors)

>Seizures

community.wegohealth.com

http://morningreporttgh.blogspot.com/2010/03/hypocalcemia.html


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Hypocalcemia Causes

>CKD (usually CKD Stages 5 & 6)

>Medications (e.g. Cinacalcet, Hectoral)>Rapid correction of acidemia (CO2 low) during

hemodialysis can trigger tetany and seizures

>Hungry Bone Syndrome after parathyroidectomy

>Severe decrease in serum calcium due to abrupt

decreased in PTH release; change upsets balance

of calcium moving to and from the bones


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Phosphorus 85% of phosphorus is found in bone and teeth

Has many functions

>Helps maintain health bone and teeth>Essential for storage of energy (ATP)

>Helps maintain tissues, cells, DNA, and RNA

Phosphate = 3.5 to 5.5 mg/dl


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Hyperphosphatemia Serum levels greater than 12

May be asymptomatic

Signs and symptoms, if present>Pruritus, rash, bone and joint pain


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Elevated PhosphorusWhat is the role of dietary restriction in decreasing

serum phosphorus levels?

>Much phosphorus is found in high quality protein

foods>Need high protein intake to prevent muscle wasting

but can limit dairy, some vegetables, processed foodsand colas

>Goal protein intake = 1 gm protein per kg of body

weight per day


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Phosphorus and Protein 70 kg person = 70 gms prot Breakfast

>Two eggs

>Two pieces toast Lunch

>Grilled chicken-4 oz>Garden salad-2 cups

Dinner

>Steak-4oz>Green beans-1cup>Apple-medium, fresh

*www.davita.com

FOOD PHOS* PROTEIN*

Eggs 170 mg 12 gms

Bread 60 mg 4 gms

Chicken 265 mg 36 gms

GardenSalad

340 mg 2 gms

Steak 265 mg 32 gms

Gr. Beans 25 mg 1 gms

Apple 40 mg 0 gms

1355 mg 88 gms


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Calculating Phosphorus Balance Intake = 1000 mg per day X 7 days = 7000 mg per week

GI tract absorbs 60% of what is consumed

>7000 mg X 0.6 = 4200 mg phosphorus/wk 800 mg eliminated/HD treatment = 2400 mg/wk

4200 2400 = 1800 mg

Net + phosphorus balance 1800 mg per week

>1 Renagel binds about 100 mg phosphorus

1 pill/meal X 100 = 300 x 7 days = 2100 mg/wk

1800 mg 2100 mg = 300 mg negative balance/wk


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Hypophosphatemia Serum levels less than 2.5

May be asymptomatic

Causes>Not eating =>> malnutrition

Symptoms, when present

>Muscle weakness (e.g. diplopia, dysphagia)

>Ventricular arrhythmias

>Neuro manifestions (e.g. confusion, coma, seizures)

>Poor oxygenation (phosphorus and ATP)


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Changes During Progression of CKD

Kidneys excretion of phosphorus decreases, causingthe serum phosphorus to increase

Kidney does not reabsorb calcium and vitamin D is notactivated, causing decreased serum calcium levels

Vitamin D is not activated, causing parathyroid gland

hypertrophy and hyperplasia>Decreased serum calcium and increased serum

phosphorus levels caused increased secretion of PTH


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Changes During Progression of CKD Kidney dysfunction results in>Calcitriol (Vitamin D) deficiency

>Hyperphosphatemia kidneys no longer excrete phosphate

>Decreased Vitamin D and increased phosphorus causes

hypocalcemia

Major factors responsible for stimulating PTH are

>Hypocalcemia (sensed by receptors on parathyroid gland =>

increased secretion of PTH)>Decreased vitamin D levels (1,25 dihydroxyvitamin D

= calcitriol)

>Hyperphosphatemia


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Bone and Mineral Balance


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http://www.medscape.com/viewarticle/518757_2
http://www.medscape.com/viewarticle/518757_2http://www.medscape.com/viewarticle/518757_2


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Treatment Goals

CKD VI Values Per KDOQI for CKD VI PTH = 150 to 300 pg/ml (PTH values vary with CKD stage)

>Optimal PTH levels in advanced kidney disease notknown

Phosphate = 3.5 to 5.5 mg/dl Corrected total calcium 8.4 to 9.5 mg/dl Calcium-phosphate product < 55 mg2/dl2

>Larger doses Vitamin D analogs associated with increasedcalcium and phosphorus

Outcomes>Manage secondary hyperparathyroidism>Manage calcium/phos/vitamin D abnormalities>Minimize vascular calcification


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Case Study S.M., an 89 yo with HTN, DM, CVA (residual left sided

weakness), MVR , CABG and CKD V

>Very knowledge about dietary content for potassium and

phosphorus

>Medications

>Coreg, Lotrel, Lasix, Mirtazapine, ASA, MVI,

Vitamin D 1000 u/day, calcium acetate 667 mg/meal

>Pleasant, alert and oriented

>BUN 107, Creatinine 7.48, GFR 6 ml/min, K 4.8, CO2

15-----Decision made to start dialysis


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Lab Values for S. M.LAB TEST/DATE RESULT LAB RANGECalcium/7.18.2011 8.7 Corrected total calcium

8.4 to 9.5 mg/dl

Albumin 3.5 Corrected = 9.1

Phosphorus/7.18.2011 6.2 3.5 to 5.5 mg/dl

Vitamin D/4.25.2011 25 OH 43.01,25 OH 17.0

25OH >30/321,23 = 18-78

PTH/4.25.2011 327 150 to 300 pg/ml


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Take Home Points for BMD Must look at all lab values-calcium, albumin,

phosphorus, vitamin D and PTH-to decide if anyactions are needed

While can shoot for stated lab values, getting all labs

values within stated goal range can be very difficult

Must always consider how the person feels/looks when

interpreting lab results


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Dialysis Adequacy Used to determine if enough dialysis is being delivered

or if blood being cleaned enough?

Adequate dialysis treatments replace less than 15%of normal kidney function/adequacy is relative term

>Intermittent dialysis (3x per week) inefficient, onlydialyzing out toxins about 7% of the time while the

body produces toxins 100% of the time


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More About Adequacy Urea is not the only toxin, yet it is the one we measure>Urea = being water soluble, it is easily measured

However, there are 90 different compounds that are toxins thatwe dont measure. Many of these compounds are more toxic

than urea.>No current measure of adequacy for these different toxins

Conventional dialysis has its limitations:>It removes urea (small, water soluble molecules)>Weekly clearance of urea = about 1/6thof normal physiologic

clearance (what would be cleared by healthy kidneys)>28% of toxins are protein bound and not easily removedby dialysis

Yavuz, et al (2005)


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Dialysis AdequacyAdequacy is important since under-dialysis can cause:

>Weakness and fatigue

>Weight (muscle) loss

> Nausea, decreased appetite

> Sleep disturbances


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How Is Adequacy Determine? Three methods used to calculate adequacy:

>URR = Urea Reduction Ratio (HD)

>Kt/V (HD and PD)

>PET = Peritoneal Equilibration Test (PD)


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URR (Urea Reduction Ratio) URR is one measure of how effectively a hemodialysis

treatment has removed urea from the blood

Formula: preBUN postBUN X 100 =

preBUN

94 (pre) 32 (post) / 94 (pre) x 100 = 65.9% URR


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URR (Urea Reduction Ratio) No one percentage (URR) represents adequate dialysis.

However, people usually live longer and have fewer

hospitalizations if URR >= 60%

>So, if no one number determines adequate dialysis,

how does one choose a URR goal?

Usually measured once per month


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Kt/V Also measures how much urea is removed during dialysis,but takes into account two additional factors:

>Urea made by the body during dialysis

>Urea removed during dialysis along with excess fluid Goals* (many different values found in literature)

>For CAPD, Kt/V = 2.0

>Kt/V = 1.7 is minimal dose

>For HD (adults and peds), Kt/V = 1.2 is minimal dose>As little as 3% residual renal function can increase the

Kt/V calculation from 1.2 to 1.65

*KDOQI


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Kt/VSYMBOL EXPLANATION

K Rate at which blood passes through thedialyzer in ml/min

t Time (expressed in minutes)

Kt Volume of blood cleared of urea during

one dialysis treatment

V Volume of water in a persons body


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Calculating Kt/V* Example>Dialyzers clearance = 400 ml/min

>Treatment time = 210 min (3.5 hours)

>Kt = 400 ml/min x 210 min = 84,000 ml (84 L)>V = volume

>Weight = 70 kg. 60% body water (average)

>70 kg. x .60 = 42

>Kt/V = 84/42 = 2.0>Would you/could you make any dialysis changes?

*http://kidney.niddk.nih.gov/kudiseases/pubs/hemodialys is dose


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Difference Between URR and Kt/V Kt/V is more accurate then URR

>URR measures urea removed during dialysis

>Kt/V adds the amount of urea removed with excess

fluid

More weight loss during dialysis will yield a higher

Kt/V for the same URR URR may be lower than usual if large volume removed

Kt/V of 1.2 ~ URR 63%


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How Can Clearance of Toxins Be Increased?

For both Kt/V and URR.

>Increased the blood flow (Qb)

>Increase treatment time

>Use a larger dialyzer

>Increased dialysis solution flow rate (Qd)

>600 ml/min to 800 ml/min>Assess access &/or needle placement for problems


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Nocturnal/Home Dialysis Nocturnal

>3x/week, decreased blood flows, longer treatment

times

Home Dialysis

>5-6 times per week, shorter treatment times

Since both treatment modalities lead to feeling

better/improved lab results; challenges currentconcepts of adequacy


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PET (Peritoneal Equilibrium Test) Transport of substances is a function of peritoneal

membrane area times permeability, so a test is useful to

determine the function of the peritoneal membrane>Assesses rate at which solutes (substance dissolved in

fluid) equilibrate between the peritoneal capillary

blood and dialysate

>Solutes = creatinine, urea, phosphate, proteins

commonly measured

>Dextrose concentration responsible for UF


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Diffusion


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PET Standardized 4-hour procedure>Measures dialysate creatinine and glucose levels at 0,

2 and 4 hours after dialysis solution is infused into the

abdomen and serum creatinine and glucose levels at

any time during the test.

>Performed several weeks after PD initiated and when

clinical problems arise, e.g. suspect alteredmembrane transport


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PET Transport rates assessed by calculating the rates whenequilibrium is reached between the peritoneal bloodand dialysate

>D/P ratio = solute concentration in dialysate/

solute concentration in plasma (blood)

>D/DO = Decrease in dialysate glucose concentration

over time Expressed as standard deviation (SD)SD tells you

how much variation from the average


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PET (Peritoneal Equilibration Test)

Dialysate Glucose Glucose D/D00 hour 1979 1.0002 hour 1004 0.5074 hour 732 0.370

Dialysate Creatinine Creat. D/P0 hour 0.5 0.0632 hour 4.5 0.5634 hour 6 0.750

Serum Creatinine @ 2 hrs = 8Serum Glucose 257


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PET (Peritoneal Equilibration Test)


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Rapid Transporters Those with high rates of diffusion/osmosis>Transport small molecules (e.g. urea, creatinine,

glucose) quickly

>Leads to equilibration between dialysate and bloodearly in the dwell>If fluid left in peritoneum, it will be continuouslyabsorbed by the lymphatics, potentially leading topoor UF and volume expansion

>Do best with short dwell times>May benefit from icodextrin dialysate solution

>Poorly absorbed so osmotic gradient maintained


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Decreased Clearance? Increasing BUN and creatinine could be due to:>Poor compliance

>High protein intake or metabolic acidosis

>Decreased peritoneal permeability

>Slow transporter

>UF continues through out the dwell; clearance

continues through out long dwell exchange>Increase inflow dialysate volumes to increase

clearance


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Interpreting PET Results If clearance unchanged but UF decreased>Could be due to increased lymph absorption

or catheter malfunction

If PET shows increased clearance

>? Peritonitis

>If UF inadequate ? membrane failure

If PET shows decreased clearance and decreased UF>? membrane failure


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PET Test can be used to:>Predict dialysis dose (# cycles and dwell duration)

>Help choose peritoneal dialysis regimen

>Classify peritoneal dialysis transport (rapid and slowtransporters)

>Calculate creatinine clearance

>CCL = (D/P) X V

Peritoneal characteristics change over time>Peritonitisproblems with UF common due to

increase glucose absorption that occurs during infection


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Take Home Points For Adequacy While we can measure urea, it is one of the less toxic wasteproducts. Currently there is no way to measure all the toxinsthat accumulate in the blood.

While Kt/V and URR help us to measure outcomes, they have

limitations. In the end, it is as important to look at the entire clinical picture

as it is to calculate Kt/V and URR.

>How does the person feel?

>Is his/her weight stable?

PET results can help

>Determine dwell times and # cycles needed to clear toxins.

>Confirm impending membrane failure.


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References Coyne, D.W., Kapoian, T., Suki, W., Singh, A.K., Moran, J.E., Dahl, N.V.,and Rizkala, A.R (2007). Ferric gluconate is highly efficacious inanemic hemodialysis patients with high serum and low transferrinsaturation: results of the Dialysis Patients Response to IV Iron withElevated Ferritin (DRIVE) Study. Journal of American Society of

Nephrology,(3), 975-984.

Http://kidney.niddk.nih.gov,kudiseases/pubs/hemodialysisdoseretrieved August 16, 2011.

KDOQI Clinical Practice Guidelines and Clinical PracticeRecommendations for Anemia in Chronic Kidney Disease. Retrieved

August 25, 2011 fromhttp://www.kidney.org/professional/kdoqi/guidelines_anemia/cpr32.htm
http://kidney.niddk.nih.gov%2Ckudiseases/pubs/hemodialysisdose%20retrieved%20August%2016http://kidney.niddk.nih.gov%2Ckudiseases/pubs/hemodialysisdose%20retrieved%20August%2016http://kidney.niddk.nih.gov%2Ckudiseases/pubs/hemodialysisdose%20retrieved%20August%2016http://kidney.niddk.nih.gov%2Ckudiseases/pubs/hemodialysisdose%20retrieved%20August%2016


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References KDOQI Clinical Practice Guidelines and Clinical PracticeRecommendations for Anemia in Chronic Kidney Disease:2007 Update of Hemoglobin Target. Retrieved August 25,2011 from

http://www.kidney.org/professional/kdoqi/guidelines_anemia/cpr21.htm

KDOQI Clinical Practice Guidelines and Clinical PracticeRecommendations 2006 Updates for Hemodialysis

Adequacy and Peritoneal Adequacy. Retrieved August 16,2011 fromhttp:/www.kidney.org/professional/kdoqi/guidelines/guideline_update HD_PD/pd_guide2.htm
http://www.kidney.org/professional/kdoqi/guidelines_anemia/cpr21.htmhttp://www.kidney.org/professional/kdoqi/guidelines_anemia/cpr21.htmhttp://www.kidney.org/professional/kdoqi/guidelines_anemia/cpr21.htmhttp://www.kidney.org/professional/kdoqi/guidelines_anemia/cpr21.htmhttp://www.kidney.org/professional/kdoqi/guidelines_anemia/cpr21.htmhttp://www.kidney.org/professional/kdoqi/guidelines_anemia/cpr21.htm


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Referrences Ly, J., Marticorean, R., Donnelly S., (2004). Red bloodcell survival in chronic renal failure. American Journalof Kidney Diseases, 44(4), 715-719.

National Kidney Foundation (2001). KDOQI clinicalpractice guidelines for hemodialysis adequacy.American Journal of Kidney Diseases, 37, supp 1, S7-64.


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