Slide 1

Connie Gilet, ANP UNC Kidney Center/ UNC Healthcare September 2011 Slide 2 Objectives Discuss lab values related to anemia management >Interpret CBC results, including H/H, RDW (red cell distribution width), MCV (mean corpuscular volume) and MCHC (mean corpuscular hemoglobin concentration) >Examine iron study results, focusing on iron saturation and ferritin Slide 3 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 abnormal vs when they are alarming >Discuss treatment of bone and mineral abnormalities with medications and surgery Slide 4 Objectives Discuss how dialysis adequacy is determined and used in a clinical setting >Discuss URR, Kt/V and PET, how to calculate these measures 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 Slide 5 Plan Briefly present basic information for each topic Hopefully, present new information for each topic Case studies will help to enhance understanding of information presented Slide 6 Anemia Anemia is defined as a decrease in red blood cells (RBCs) Slide 7 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 Slide 8 Substances Needed for RBC Formation NECESSARY SUBSTANCE/STRUCTURE RELATED INFORMATION Erythropoietin (hormone)Stimulates bone marrow to produce RBCs Need adequate nutrientse.g. Iron, Vitamin B12, Folic acid To produce hemoglobin DNAChronic inflammation 2/2 infection and/or autoimmune disorders (e.g. Lupus) impairs DNA synthesis => anemia Bone marrow Images from www.google.com/bonemarrow Reticulocyte count reflects ability of bone marrow to produce RBCs. Retic ulocyte = immature RBCs Anemia in ESRD, can see decreased RBC production (lack of substances to make cells) and increased retic count. A very elevated retic count points to increase RBC destruction or hemolysis as a potential cause of anemia. Slide 9 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 in 2 wks: >Hold the dose (per FDA) >No benefits to hemoglobin > 13 g/dl. In fact, increases the risk of clots, vascular events (heart attack and stroke) and death Slide 10 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? Slide 11 Anemia Lets define lab values reported in a CBC results: >Red blood cells >Hemoglobin >Hematocrit >Reticulocyte count >MCV (mean corpuscular volume) >MCHC (mean corpuscular hemoglobin concentration) >RDW (red cell distribution width) Slide 12 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$) Slide 13 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 Slide 14 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 by multiplying the Hgb times 3. (10 x 3 = 36) Slide 15 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? Slide 16 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 enough red blood cells but cant produce enough mature cells to keep up with demand. Slide 17 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? Slide 18 What the MCV and MCHC Tells You TestNormal RangeValue Below Range (Microcytic = small than normal) Value Above Range (Macrocytic = larger than normal) Value Within Range MCV (mean corpuscular volume) (size of RBC) 80-100 femoliters< 80 = Iron deficiency anemia, congenital anemias > 100 = Folic acid deficiency, B12 deficiency, myelodysplastic, leukemias 80-100 = Anemia due to blood loss or a chronic disease MCHC (mean corpuscular hemoglobin concentration) (% RBC in fluid) 32-35%< 32% = Iron deficiency anemia > 35% = same as above 32-35% = Anemia due to blood loss or a chronic disease Slide 19 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. Slide 20 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? Slide 21 CBC Results TestRangePatient = E.R. RBC (red cell count)4.00-5.202.99 million HGB (hemoglobin)12-16 g/dl9.2 g/dl HCT (hematocrit)36-46 %26.9 % Retic count (reticulocyte count) 0.5% - 1.5%/2.5%3.0% MCV (mean corpuscular volume) 80-10090.0-------------75% MCHC (mean corpuscular hemoglobin concentration) 31-3734.0%-----------28% RDW12-15 %18.0% B12193-900 pg/ml843 pg/ml Folic Acid2.7 20.0 ng/ml> 20 ng/ml Slide 22 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 Slide 23 CBC Results TestRangePatient = T.A. RBC (red cell count)4.00-5.203.52 HGB (hemoglobin)12-16 g/dl10.8 g/dl HCT (hematocrit)36-46 %32.2 % Retic count (reticulocyte count) 0.5% - 1.5%/2.5%Not reported MCV (mean corpuscular volume) 80-100 FL91 FL MCHC (mean corpuscular hemoglobin concentration) 31-37 g/dl34 g/dl RDW12-15 %16.4% Slide 24 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 marrow with a small amount found in the blood >Normally, 1 ng of ferritin (in blood) = 10 ng of iron stores (in liver, spleen, muscle and bone marrow) >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... Slide 25 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 (more than 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 Slide 26 DRIVE STUDY Dialysis Patients Response to IV iron with elevated ferritin Study (DRIVE) >Provided some clarification for safe upper limits of ferritin levels in hemodialysis patients. >Ferric gluconate (ferrlecit) administration is superior to no iron therapy in anemic dialysis patients receiving epogen and ferritin levels of 500 to 1200 ng/ml and Tsats of Iron Saturation Complete name = transferrin iron saturation or Tsat >Estimates ability to bind iron and transport it to various sites in the body >Serum iron / total iron binding capacity X 100 More sensitive than ferritin; not affected by inflammation/infection Slide 28 Goal for Iron Stores* HD-CKDND-CKD/PD-CKD* Ferritin > 200 ng/ml Sats > 20% Ferritin > 100 ng/ml Sats > 20% From KDOQI Anemia Guidelines*No RCT to support recommendation Slide 29 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 Slide 30 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 to epogen administration) Increasing ferritin and decreasing sats and decreasing Hgb = inflammation >Increase ESA dose Slide 31 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 Slide 32 Case Study TEST/ INTERVENTION DATE = 11/8/2010DATE = 12/22/2010DATE = 1/17/2011 Hemoglobin8.8 (decreasing)7.79.5 Hematocrit28.425.330.9 Saturationnone10%none Ferritinnone33none BUN54 (increasing)5539 Creatinine2.4 (increasing)2.352.04 GFR23 ml/min24 ml/min28 ml/min Aranesp doseIncreased to 200 mcg 200 mcg Slide 33 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 Slide 34 Bone and Mineral Balance Briefly discuss the four primary players: >Vitamin D >Calcium >Phosphorus >PTH Discuss the complex interdependence amongst calcium, phosphorus, vitamin D and PTH Slide 35 Vitamin D2-3 Vitamin D comes from sun, food and our body 25-hydroxyvitamin D2 produced in the liver Normally kidneys produce an enyzme that converts D2 to D3 (1,25 dihydroxyvitamin = calcitriol) Slide 36 Vitamin D A complex group of fat-soluble substances (D1-D5) >D2 = ergocalfciferol >Sources >Foodonly found in seafood, mushrooms, egg yolks 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 1,25 dihydroxycholecalciferol >Measured in those with CKD Stage 3-6 Slide 37 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) Slide 38 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 Slide 39 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 Slide 40 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, cognitive dysfunction, fatigue, hypertension, constipation >ECG changes/arrhythmias Slide 41 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/h ypocalcemia.html Slide 42 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 Slide 43 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 Slide 44 Hyperphosphatemia Serum levels greater than 12 May be asymptomatic Signs and symptoms, if present >Pruritus, rash, bone and joint pain Slide 45 Elevated Phosphorus What 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 foods and colas >Goal protein intake = 1 gm protein per kg of body weight per day Slide 46 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 FOODPHOS*PROTEIN* Eggs170 mg12 gms Bread60 mg4 gms Chicken265 mg36 gms Garden Salad 340 mg2 gms Steak265 mg32 gms Gr. Beans25 mg1 gms Apple40 mg0 gms 1355 mg88 gms Slide 47 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 Slide 48 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) Slide 49 Changes During Progression of CKD Kidneys excretion of phosphorus decreases, causing the serum phosphorus to increase Kidney does not reabsorb calcium and vitamin D is not activated, 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 Slide 50 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 Slide 51 Bone and Mineral Balance Slide 52 http://www.medscape.com/viewarticle/518757_2 Slide 53 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 not known 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 increased calcium and phosphorus Outcomes >Manage secondary hyperparathyroidism >Manage calcium/phos/vitamin D abnormalities >Minimize vascular calcification Slide 54 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 Slide 55 Lab Values for S. M. LAB TEST/DATERESULTLAB RANGE Calcium/7.18.20118.7Corrected total calcium 8.4 to 9.5 mg/dl Albumin3.5Corrected = 9.1 Phosphorus/7.18.20116.23.5 to 5.5 mg/dl Vitamin D/4.25.201125 OH 43.0 1,25 OH 17.0 25OH >30/32 1,23 = 18-78 PTH/4.25.2011327150 to 300 pg/ml Slide 56 Take Home Points for BMD Must look at all lab values-calcium, albumin, phosphorus, vitamin D and PTH-to decide if any actions 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 Slide 57 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, only dialyzing out toxins about 7% of the time while the body produces toxins 100% of the time Slide 58 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 that we 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 1/6 th of normal physiologic clearance (what would be cleared by healthy kidneys) >28% of toxins are protein bound and not easily removed by dialysis Yavuz, et al (2005) Slide 59 Dialysis Adequacy Adequacy is important since under-dialysis can cause: >Weakness and fatigue >Weight (muscle) loss > Nausea, decreased appetite > Sleep disturbances Slide 60 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) Slide 61 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 Slide 62 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 Slide 63 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 Slide 64 Kt/V SYMBOLEXPLANATION KRate at which blood passes through the dialyzer in ml/min tTime (expressed in minutes) KtVolume of blood cleared of urea during one dialysis treatment VVolume of water in a persons body Slide 65 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 Slide 66 Changing the Kt/V Kt/V of 2.0 is too much >1.2 (goal)/2.0 (achieved) = 0.6 >3.5 -.6 = 2.9 hours (decrease from 3.5 hours) Increasing the t (time) >if the Kt/V is 0.9 but the goal is 1.2: 1.2/0.9 = 1.33 or 1.33 times more Kt needed 3 hours (current) x 1.33 = 4 hours Slide 67 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% Slide 68 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 Slide 69 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 current concepts of adequacy Slide 70 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 Slide 71 Diffusion Slide 72 Slide 73 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 altered membrane transport Slide 74 PET Transport rates assessed by calculating the rates when equilibrium is reached between the peritoneal blood and 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 Slide 75 PET (Peritoneal Equilibration Test) Dialysate Glucose Glucose D/D0 0 hour1979 1.000 2 hour1004 0.507 4 hour732 0.370 Dialysate Creatinine Creat. D/P 0 hour0.5 0.063 2 hour4.5 0.563 4 hour6 0.750 Serum Creatinine @ 2 hrs = 8 Serum Glucose257 Slide 76 PET (Peritoneal Equilibration Test) Slide 77 Rapid Transporters Those with high rates of diffusion/osmosis >Transport small molecules (e.g. urea, creatinine, glucose) quickly >Leads to equilibration between dialysate and blood early in the dwell >If fluid left in peritoneum, it will be continuously absorbed by the lymphatics, potentially leading to poor UF and volume expansion >Do best with short dwell times >May benefit from icodextrin dialysate solution >Poorly absorbed so osmotic gradient maintained Slide 78 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 Slide 79 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 Slide 80 PET Test can be used to: >Predict dialysis dose (# cycles and dwell duration) >Help choose peritoneal dialysis regimen >Classify peritoneal dialysis transport (rapid and slow transporters) >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 Slide 81 Take Home Points For Adequacy While we can measure urea, it is one of the less toxic waste products. Currently there is no way to measure all the toxins that 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. Slide 82 Slide 83 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 in anemic hemodialysis patients with high serum and low transferrin saturation: results of the Dialysis Patients Response to IV Iron with Elevated Ferritin (DRIVE) Study. Journal of American Society of Nephrology,(3), 975-984. Http://kidney.niddk.nih.gov,kudiseases/pubs/hemodialysisdose retrieved August 16, 2011. Http://kidney.niddk.nih.gov,kudiseases/pubs/hemodialysisdose retrieved August 16 KDOQI Clinical Practice Guidelines and Clinical Practice Recommendations for Anemia in Chronic Kidney Disease. Retrieved August 25, 2011 from http://www.kidney.org/professional/kdoqi/guidelines_anemia/cpr32.h tm Slide 84 References KDOQI Clinical Practice Guidelines and Clinical Practice Recommendations for Anemia in Chronic Kidney Disease: 2007 Update of Hemoglobin Target. Retrieved August 25, 2011 from http://www.kidney.org/professional/kdoqi/guidelines_ane mia/cpr21.htm http://www.kidney.org/professional/kdoqi/guidelines_ane mia/cpr21.htm KDOQI Clinical Practice Guidelines and Clinical Practice Recommendations 2006 Updates for Hemodialysis Adequacy and Peritoneal Adequacy. Retrieved August 16, 2011 from http:/www.kidney.org/professional/kdoqi/guidelines/guid eline_update HD_PD/pd_guide2.htmwww.kidney.org/professional/kdoqi/guidelines Slide 85 Referrences Ly, J., Marticorean, R., Donnelly S., (2004). Red blood cell survival in chronic renal failure. American Journal of Kidney Diseases, 44(4), 715-719. National Kidney Foundation (2001). KDOQI clinical practice guidelines for hemodialysis adequacy. American Journal of Kidney Diseases, 37, supp 1, S7-64. Slide 86 References Yavuz, A., Tetta, C., Ersoy, F., Dinitin, V., Ratanaret, R., De Cal, M., Borello, M., Bordoni, V., Savatori, G., Andrikes, E., Yakapoglu, E., Levin, N., & Ronco, C., (2005) Uremic toxins: A new focus on an old subject. Seminars in Dialysis, 18 (3), 203-212.