CKD 101: Nutrition Intervention

CKD 101: Nutrition Intervention

Chronic Kidney Disease 101 Nutrition Intervention Objectives (be able to): 1. 2. 3. 4. Identify chronic kidney disease (CKD). Identify common co-morbidities and interventions to slow CKD progression. Associate CKD complications with lab data, nutrition interventions and basic medications.

Use nutrition education materials from the National Kidney Disease Education (NKDEP). You may find this useful as you go through the slides Reference: The kidneys maintain homeostasis 1. Regulatory function Control composition and volume of blood Maintain stable concentrations of inorganic anions such as sodium (Na), potassium (K), and calcium (Ca) Maintain acid-base balance

2. Excretory function Produce urine Remove metabolic wastes Including nitrogenous waste The kidneys have other functions 3. Hormone function Produce renin for blood pressure control Produce erythropoietin which stimulates marrow production of red blood cells Activate 25(OH)D to 1,25 (OH)2D (active vitamin D) 4. Metabolic function Gluconeogenesis

Metabolize drugs and endogenous substances (e.g., insulin) The nephron functions to maintain balance The functions include: Filtration Glomeruli generate ultrafiltrate of the plasma. Reabsorption Tubules selectively reabsorb substances from the ultrafiltrate. Secretion

Tubules secrete substances into the urine. Ultrafiltration of plasma is the main function of the glomeruli Filtration is based on size and charge. Small solutes cross readily. Larger substances are generally restricted. Negatively charged molecules are restricted. Volume of ultrafiltrate = 135180 liters(L)/day 99% water reabsorbed 11.5 L urine excreted

The ultrafiltrate is modified by the tubules Reabsorption and secretion of substances occurs within the tubules. Examples: Potassium is reabsorbed from and secreted into the urine by the tubules. Sodium is generally reabsorbed by the tubules. Organic acids are secreted into the urine. Albumin is generally reabsorbed within the tubules. Damaged kidneys allow albumin to cross the filtration barrier into the urine Increased glomerular permeability allows albumin (and other proteins) to cross the glomerulus into the

urine. Higher levels of protein within the tubule may exacerbate kidney damage by exceeding tubules ability to reabsorb the proteins. An elevated urine albumin-to-creatinine ratio (UACR) is used to identify damaged kidneys. Fewer nephrons disrupt the balance Urine volume may not change Composition of the urine changes Reduced waste excretion May not be apparent until CKD is advanced Altered hormone production

Anemia (erythropoietin) and mineral & bone disorders (vitamin D) Medication changes Reduced catabolism and clearance CKD is reduced kidney function and/or kidney damage Chronic kidney disease Kidney function Glomerular filtration rate (GFR) < 60 mL/min/1.73 m2 for > 3 months with or without kidney damage AND/OR

Kidney damage > 3 months, with or without decreased GFR, manifested by either Pathological abnormalities Markers of kidney damage, e.g., albuminuria Urine albumin-to-creatinine ratio (UACR) > 30 mg/g This definition does not account for age-related GFR decline. Reference: National Kidney Foundation, 2002 Use eGFR to assess and monitor kidney function The eGFR provides an estimate of how much blood is filtered by the kidneys each minute. The formula used to estimate GFR uses serum creatinine, age, gender, and race.

An eGFR greater than 60 may be reported as > 60. eGFR (mL/min/1.73m2) = 175 x (Scr)1.154 x (Age)0.203 x (0.742 if female) x (1.212 if African American) Reference: Stevens et al. J Am Soc Nephrol 2007; 18:2749-2757 Kidney failure is an eGFR < 15 Kidneys cannot maintain homeostasis. Kidney failure is associated with fluid, electrolyte, and hormonal imbalances and metabolic abnormalities. ESRD means the patient is on dialysis or has a kidney transplant.

Kidney function and eGFR decline with age Reference Table for Population Mean eGFR from NHANES III Age (years) Mean eGFR (mL/min/1.73 m2) 2029 116 3039 107 4049

99 5059 93 6069 85 70+ 75

Reference: Use eGFR to assess kidney function* Age, Race, Gender of Patient Serum Creatinine eGFR 35-year-old African American male 1.2 60

35-year-old White female 1.2 51 58-year-old Asian American female 1.2 46 58-year-old White male 2.4

28 58-year-old African American male 2.4 34 58-year-old African American female 2.4 25

80-year-old Hispanic female 2.4 19 *eGFR is not reliable for patients with rapidly changing creatinine levels, extremes in muscle mass and body size, or altered diet patterns. Explaining GFR Urine albumin (UACR) results are used for screening, diagnosing, and treating CKD

Standard of diabetes care (annual screen) Diagnosis Forty percent of people are identified with CKD on the basis of urine albumin alone. Prognosis Important prognostic marker, especially in diabetes mellitus (DM) Used to monitor and guide therapy Tool for patient education and self-management (such as A1C or eGFR)

Albuminuria is associated with mortality NHANES 19881994 participants Reference: USRDS Annual Data Report (NIDDK, 2010) Elevated UACR is associated with risk of renal events; lowering UACR may lower risk of progression References: NIH, February 2010; De Zeeuw et al. Kidney Int 2004; 65(6):23092320. Explaining urine albumin

Summary: Identify and monitor CKD Medicare beneficiaries may be referred for Medical Nutrition Therapy for CKD when the eGFR is between 13 and 50. Reference: The case study: a 35-year-old woman with type 2 diabetes, hypertension, and dyslipidemia (Abnormal values are shown in red.) Significant albuminuria may be associated with rapid decline in eGFR Slow CKD progression

MANAGE CO-MORBIDITIES Diabetes and hypertension are the leading causes of kidney failure in the United States Reference: NIH Publication No. 10-3895 Energy needs are not higher in CKD Individualized

Need 2335 kilocalories (kcal)/kg to maintain nutritional status. Current weight Weight-loss goals

Age and gender Physical activity Metabolic stressors May see spontaneous decrease in intake as CKD progresses. References: Byham-Gray, J Renal Nutr 2006; 16(1):1726.; Afshinnia et al., Nephrol Dial Transplant 2010; 25:1173-1183.

Blood pressure control is key to slowing progression Systolic BP 140 may be beneficial for many Multiple medications Intervention: Limit sodium to 2,400 mg/ day Assessment: Avoid salt substitutes Foodmedication interaction

Limit potassium when Hyperkalemia ACEi (____pril) ARBs (___sartan) serum level is elevated 2,400 Goal 201 0

Di e ta r y Gui deli nes U.S. adults sodium intake exceeds the UL Reference: (2009), IOM (2006), FDA (2009) As eGFR declined, blood pressure was harder to control

Marias potassium increased when her eGFR was quite low Tight control of diabetes of long duration may not be indicated for CKD Good control of newly diagnosed diabetes may delay onset of CKD and slow progression. A1C goal is individualized. Spontaneous improvement in glycemic control may indicate CKD progression and medications may change. Risk for hypoglycemia occurs with CKD; risk for hyperkalemia increases with ACEi and ARBs. Diabetes medications may be

discontinued or adjusted in CKD Glyburide Repaglinide Metformin Insulin (dose decrease) Alpha-glucosidase Glipizide inhibitors Exenatide

Pioglitazone Fluid retention Glimepiride Nateglinide Sitagliptin Pramlintide Reference: Reilly & Berns Seminars in Dialysis 2010; 23(2):163168. Maria needed less insulin to control

her blood glucose levels December 2007 Discontinue metformin Increase 70/30 insulin to 45 units BID (from 40 units) July 2008 Decrease 70/30 insulin to

35 units BID November 2008 Decrease 70/30 insulin to 30 units BID Treat hypoglycemia without adding potassium or phosphorus The risk for hyperkalemia is increased in diabetic kidney disease. Review medication list for ACEi or ARB. If prescribed, discuss use of glucose tablets or low-potassium juice to treat hypoglycemia.

Use light-colored soda pop, not dark-colored colas, if using to treat hypoglycemia. Colas have phosphoric acid. Avoid using milk which is rich in potassium and phosphorus. Any juice can treat hypoglycemia, even those low in potassium mg Interventions for reducing urine albumin Control blood pressure Reduce sodium intake Achieve good control of diabetes early; may help prevent albuminuria Reduce weight (if obese) Reduce protein intake, if excessive

Achieve tobacco cessation Animal protein intake may be associated with higher urine albumin Two or more servings of red meat per week may increase risk of microalbuminuria. Nurses Health Study (Lin J et al., 2010) Nondairy animal foods are associated with albuminuria. Multiethnic Study of Atherosclerosis (Nettleton et al., 2008) High protein intake is associated with urine albumin with both hypertension and diabetes. NHANES III (Wrone et al., 2003) Most U.S. adults eat more protein

than recommended Reference: (IOM, 2005; FDA, 2009) Which type of protein is best in CKD? Animal or vegetable? Data is limited in regard to CKD. If kidney function is normal: In short-term studies, increased animal protein intake may be associated with an increased GFR. If CKD is present: In obese rats, soy protein may result in a slower rate of glomerulosclerosis compared to casein. Excessive animal and vegetable protein intake may

accelerate progression in humans. References: Maddox et al. Kidney Int 2002; 61(1):96104; Bernstein et al. J Am Diet Assoc 2007; 107(4):644650. Eating less protein may mean fewer leftovers for urinary excretion Protein has nitrogen, potassium, other elements. Intake should be adequate, not excessive. In early CKD, reduce portions toward one serving per meal. In advanced CKD, a spontaneous reduction in protein intake may occur. In advanced CKD, encourage intake of protein-rich foods that are tolerated and accepted by the patient.

Lipid abnormalities increase as eGFR declines Reference: Astor et al. Am J Epidemiol 2008; 167(10):12261234. CVD is the leading cause of mortality; higher than lipids and blood pressure in CKD Nontraditional risk factors include: Albuminuria Anemia Abnormal calcium and phosphorus metabolism Statins are used in CKD patients with some caution. Some foods rich in soluble fiber may be higher in K and

P than recommended for CKD patients. Phosphorus in food additives is absorbed much more readily. Nutrition recommendations addressing CVD in persons with CKD may be similar to those for the general population Evidence is scarce for trials with CKD patients Dietary Guidelines 2010 Keep trans fats as low as possible Limit foods with synthetic sources of trans fats Partially hydrogenated oils Other solid fats Reference:

Soluble fiber may help reduce heart disease in the general population 2530 grams total fiber suggested per day. 713 grams soluble fiber/day may reduce LDL. Effectiveness in CKD is unknown. Foods high in soluble fiber may be too rich in potassium and phosphorus for CKD patients. Foods high in bran may be too rich in potassium, phosphorus, and/or sodium for CKD patients. References: Van Horn et al. J Am Diet Assoc 2008; 108(2):287331; Beto & Bansal. Advances Chronic Kidney Dis 2004; 11(4):391397. Legumes are rich in potassium and phosphorus; counsel appropriately

Serving of cup Soluble fiber (grams) K (mg) P (mg) Na (mg) Barley

1 73 42 2 Oatmeal 1 82

90 5 Oat bran 1 101 130 1 Black beans

2 305 120 1 Kidney beans 3 358

122 1 Pinto beans 2 373 126 1 Pinto beans, canned

5.5 (total fiber) 292 110 353 Lentils 1 365

178 2 Chick peas 1 239 138 6 Chick peas, canned

5.3 (total fiber) 206 108 359 References:; Some fruits with soluble fiber are rich in potassium; counsel appropriately Food

Soluble fiber (grams) K (mg) P (mg) Na (mg) Apple (3 diametermedium)

1 195 20 2 Apple, peeled 2.1 (total fiber) 145 18

0 Banana (77 7/8 long) 1 422 26 1 Blackberries (1/2 c.)

1 117 16 1 Orange (3 1/16 diameter large) 2 333 26

0 Peach (2 2/3 diameter medium) 1 285 30 0 Peach, canned (2 halves)

1.3 (total fiber) 194 20 3 Pear (1 medium) 2 212 20

2 Broccoli (1/2 c. cooked) 1 229 52 32 Carrots (1/2 c. cooked)

1 183 23 45 References:; Statins are used with caution in patients with CKD Statins reduce hepatic cholesterol synthesis. Statins significantly reduce all-cause and CVD

mortality in persons with CKD. Their use does not appear to slow CKD progression but may reduce proteinuria. Monitor for potential side effects. Muscle toxicity or elevated liver function tests may be seen with statin use. Reference: Navaneethan et al. Cochrane Database Syst Rev 2009. Inflammation may play a role in CVD in CKD Inflammation may modify risk relationship between cholesterol and CVD in this population. In patients with normal C-reactive protein (CRP), elevating cholesterol levels may be associated with increasing risk of CVD events.

In patients with elevated CRP, elevating cholesterol levels may not be not associated with increased risk of CVD events; inflammation may be associated with increased risk. African-American Study of Kidney Disease and Hypertension (AASK) Reference: Contreras et al. J Am Soc Nephrol 2010; 21(12):21312142. An educational handout you can use to get started Reference: Reference: Complications may increase as kidney function declines.

COMPLICATIONS Complications increase as kidney function declines Fewer functioning nephrons may mean: Inadequate erythropoietin (anemia) Accumulation of potassium (K) Accumulation of hydrogen ion (metabolic acidosis) Inadequate activation of vitamin D (bone disease) Accumulation of phosphorus (P) Accumulation of pro-inflammatory cytokines Toxins build up in the blood.

Low serum albumin in CKD is associated with inflammation and acidemia Reference: Eustace et al. Kidney Int 2004; 65(3):10311040. Nutrition alone may not improve hypoalbuminemia Reduce inflammation, treat infections Control blood pressure to slow progression Provide adequate protein and calories

Treat metabolic acidosis Serum albumin 4.0 g/dL at initiation of dialysis associated with lower risk of mortality Chronic metabolic acidosis is a concern Accelerates muscle degradation Reduces albumin synthesis Exacerbates pre-existing bone disease May impair glucose tolerance due to interference with insulin actions May increase risk of hyperkalemia May accelerate CKD progression May stimulate inflammation

Reference: Kraut & Madias, Nat Rev Nephrol 2010; 6(5):274285 Treating metabolic acidosis may improve serum albumin levels Serum bicarbonate (HCO3) level < 22 mEq/L may indicate metabolic acidosis. Animal protein may increase acid load. Reducing protein may increase serum HCO3. Supplemental base may be prescribed to treat. Sodium bicarbonate will increase sodium intake. Review salt restriction, if prescribed. Treatment may improve serum albumin levels. Marias bicarbonate level decreased,

medication was added, and dietary protein was restricted Correcting calcium for hypoalbuminemia is worthwhile when assessing calcium levels Lower serum calcium, higher serum phosphorus may be seen as eGFR declines Reference: Adapted from USRDS Annual Data Report (NIDDK, 2009) Abnormal mineral metabolism and bone disease may develop Mineral and bone disorders Inadequate activation of Vitamin D

Check 25(OH)D May be treated with supplemental vitamin D Increases both calcium and phosphorus absorption May be discontinued with hypercalcemia, hyperphosphatemia Accumulation of phosphorus iPTH and FGF-23 enhance excretion May need phosphorus restriction May need phosphate binders with meals CKD-MBD: Complex interactions involving numerous systems Interventions for bone disease in CKD Phosphorus restriction

Adequate, not excessive protein Phosphorus-binding medication Usually calcium-based salts in CKD Vitamin D (CKD) and vitamin D analogs Complex interactions between vitamin D and iPTH affect P and Ca Most U.S. adults exceed the RDA for phosphorus Reference: (2009), FDA (2009), IOM (1997) Phosphorus absorption varies by

source: organic < inorganic Organic phosphorus 4060% absorbed Inorganic phosphorus 90% absorbed Phytates absorption Dairy products Food additives Meat, poultry, fish Dietary supplements

Soy (soy milk, tofu) Calcium fortification Nuts and seeds Dried beans and peas Whole grains Reference: Kalantar-Zadeh et al. Clin J Am Soc Nephrol 2010; 5(3):519530. Phosphorus content by food group (organic sources) Reference: Marcoe et al. J Nutr Educ Behav 2006; 38(6 suppl): S93S107.

Most protein-rich foods are a source of phosphorus Food Amount P (mg) Meat 1 ounce 62 Poultry

1 ounce 56 Fish 1 ounce 59 Beans & peas c. cooked

60 Egg 1 large 86 Egg white* 1 large 5 Nuts/seeds

ounce 70 Milk 1 cup 247 Soymilk (fortified)* 1 cup

250 More typical intake 6 ounces steak 372 mg phosphorus 1 cup beans 240 mg phosphorus Phytates reduce absorption Still high potassium 2 egg whites 10 mg phosphorus *

oodcomp/cgi-bin/list_nut_edit. pl Reference: Marcoe et al. J Nutr Educ Behav 2006; 38(6 suppl): S93S107. Use ingredient list to find phosphorus additives, look for PHOS Phosphorus is not required on Nutrition Facts labels. Nutrition Facts labels may list phosphorus, and the % Daily Value used is 1,000 mg. Read ingredients for PHOS additives. Choose a different food if PHOS is listed. References:; Nutrition/FoodLabelingGuide/ucm064928.htm

Anemia may develop as eGFR declines Reference: Adapted from USRDS Annual Data Report (NIDDK, 2009) Laboratory assessment for anemia in CKD Complete blood count (CBC) Hemoglobin (Hgb) Women: less than 12 g/dL; Men: less than 13 g/dL Iron indices Transferrin saturation Iron available for erythropoiesis < 16% may indicate iron-deficiency anemia in the general

population (Institute of Medicine) Ferritin Storage iron < 12 nanograms per milliliter may indicate iron depletion in the general population (Institute of Medicine) Reference: aspx . Possible interventions to treat anemia in CKD Iron supplementation Oral

325 milligrams (mg) dose of: Ferrous fumarate has 108 mg elemental iron Ferrous sulfate has 65 mg elemental iron Ferrous gluconate has 35 mg elemental iron Intravenous (parenteral) Possible oxidant Erythropoiesis-stimulating agents (ESAs) Injectable Potential risks include stroke and hypertension References:; A Physicians Guide to Oral Iron Supplementation, Nov 2008.; Zager, 2004; Zager, 2006; Horl, 2007

Additional factors for inadequate iron in CKD Both a spontaneous decrease in intake and aversion to foods with protein may occur as eGFR declines. Hepcidin may accumulate in CKD. Hepcidin is the hormone that controls iron levels. This hormone regulates iron absorption in the gut and mobilization of stored iron. Inflammation may reduce absorption of iron. Calcium supplements used to bind phosphorus may interfere with absorption of supplemental iron. References: Kopple et al. Kidney Int 2000; 57(4):16881703; Young et al. Clin J Am Soc Nephrol 2009;4(8):13841387.

Iron supplement improved anemia Serum potassium increases as eGFR decreases Reference: Adapted from USRDS 2009 Annual Data Report U.S. adults do not meet the AI for potassium intake Reference: (2009), FDA (2009), IOM (2006) Numerous sources contribute to potassium levels in CKD

Potassium-rich foods Medications: Salt substitutes K supplements Low-sodium products may have added KCl. Herbs and dietary supplement (examples) Noni juice (56 mmol/L) Alfalfa

Dandelion Horsetail Nettle KCl, K citrate Impair excretion ACEi ARBs K+-sparing diuretics Nonsteroidal antiinflammatory drugs Potassium food additives References: Palmer, N Eng J Med 2004;351(6):58592;

Hollander-Rodriguez & Calvert, Am Fam Physician. 2006;73(2):28390. Treating hyperglycemia and acidemia may lower serum potassium Control hyperglycemia with adequate insulin. Potassium follows glucose into the cells. Treating acidosis may lower serum potassium. Treatment may allow continued use of blood pressure medications that help lower urine albumin. Dietary protein may play a role here. Reference: Palmer, N Engl J Med 2004; 351(6):585592 What you have learned

SUMMARY Identify CKD Use estimated glomerular filtration rate (eGFR) and urine albumin-tocreatinine ratio (UACR). eGFR estimates kidney function. Persistent levels < 60 are considered CKD. UACR > 30 mg/g is considered as kidney damage. Patients with high levels of urine albumin are at greatest risk of rapid progression to kidney failure.

Slow progression Control blood pressure. Limit sodium to 2,400 mg sodium. Do not replace salt with salt substitutes (KCl). Medications that affect the renin-angiotensin-aldosterone system (RAAS) increase risk of hyperkalemia. Limit dietary potassium when serum level is elevated. Control diabetes. A1C is individualized. Spontaneous improvement in control may mean CKD progression. Treat hypoglycemia appropriately. Use juice low in potassium.

Avoid dark colas due to phosphorus content. Slow progression (continued) Urine albumin is an indicator of kidney damage. Medications that affect the RAAS may lower urine albumin. Lower sodium, planned weight loss, lower protein intake, tobacco cessation may help lower albuminuria. Cardiovascular disease is the leading cause of mortality for people with CKD. Nontraditional risk factors are important. Anemia Urine albumin Abnormal mineral metabolism (calcium and phosphorus)

Complications Anemia Inadequate erythropoietin and iron Hemoglobin and iron indices Hyperkalemia Limit dietary potassium when serum level is elevated. Hypoalbuminemia Poor oral intake (spontaneous reduction in protein) Inflammation Complications (continued) Metabolic acidosis Maintaining serum CO2 > 22 mEq/L may be beneficial.

Animal protein is a source of metabolic acids. Acidosis may be treated with supplemental bicarbonate. Bone disease in CKD Calcium, phosphorus, vitamin D, parathyroid hormone Use corrected calcium with hypoalbuminemia Vitamin D supplementation may increase risk of hypercalcemia and hyperphosphatemia. Diet changes as CKD progresses Limit sodium.

2,400 mg is the target. Eat adequate, not excessive, protein. Restrict phosphorus if serum level is elevated. Restrict potassium if serum level is elevated. Tools you have used Reference:

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