CKD MNT Module 2: Slow Progression of Chronic Kidney Disease

Module 2: Slow Progression of Chronic Kidney Disease (CKD)

Hypertension, Diabetes, Urine Albumin, and Cardiovascular Disease

1. Use and interpret biochemical and patient data for assessment of hypertension and CKD

2. Identify commonly prescribed classes of anti-hypertensive medications that may affect serum potassium levels in CKD

3. Associate spontaneous improvement in diabetes mellitus (DM) control with possible CKD progression

4. Modify recommendations for appropriate treatment of hypoglycemia in DM and CKD

5. Identify at least two nontraditional risk factors for cardiovascular disease in CKD

Participants will be able to:

Diabetes and hypertension are leading causes of CKD in the United States.

Urine albumin is a marker for kidney damage and cardiovascular disease (CVD); it also marks severity of kidney damage.

People with CKD are more likely to die due to CVD than progress to end-stage renal disease (ESRD).

Brief review

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

CKD is reduced kidney function and/or kidney damage

Reference: National Kidney Foundation, 2002

Prevalence of co-morbidities by eGFR

Reference: Adapted from USRDS 2010 Annual Data Report

Prevalence of comorbidities by urine albumin


CONTROL BLOOD PRESSURE

Hypertension is the second leading cause of CKD in the United States

Hypertension Sodium intake and excretion Dietary Approaches to Stop Hypertension (DASH)

diet pattern − Lowers blood pressure− May not be appropriate for CKD

Anti-hypertensive medications used in CKD and the risk for hyperkalemia

Topics

Blood pressure is poorly controlled in people with CKD


Hypertension may cause CKD, and CKD may cause worsening hypertension

Target of < 130/80 mmHg is often recommended but without strong evidence.

Uncontrolled hypertension (systolic blood pressure > 160) is a major challenge.

Individualized blood pressure goals in CKD

References: Chobanian et al. J Am Med Assoc 2003; 289(19):2560–2571; Jafar et al. Ann Intern Med 2003; 139(4):244–252.

A multinational epidemiological study found a significant positive relationship between 24-hour urinary sodium (Na) excretion and blood pressure.

Blood pressure may increase as sodium intake increases

Reference: Intersalt Cooperative Research Group. BMJ 1988; 297(6644):319–328

About 90% of total sodium intake is from salt.

Most ( 98%) is absorbed in small intestine.

Sodium is freely filtered by glomerulus.

About 99% is reabsorbed within the tubules.

Sodium intake excretion

Reference: Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate, 2004. Institute of Medicine of the National Academies. The National Academies Press Washington D.C.

~ 60% in proximal tubule

~ 25% in loop of Henle

5–7% in distal convoluted tubule

3–5% in collecting duct

Sodium is reabsorbed along the tubules

Reference: http://www.kidneyatlas.org/book1/adk1_02.pdf

Acid-base exchange

Chloride dependent co-transporters

− Sodium, chloride, and/or potassium

Aldosterone-sensitive channel

Sodium is reabsorbed by numerous mechanisms along the tubules

Renin is an enzyme produced by the juxtaglomerular epitheloid cells in response to low renal perfusion.

The renin-angiotensin-aldosterone system (RAAS) controls blood pressure.

Kidneys produce renin to increase sodium reabsorption

Reference: Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate, 2005. Institute of Medicine of the National Academies. The National Academies Press Washington D.C.

RAAS helps control sodium and potassium excretion

Lifestyle modifications help lower blood pressure in the general population

References: Chobanian et al. J Am Med Assoc 2003; 289(19):2560–2571; Neter et al. Hypertension 2003; 42(5):878–884; Dietary Guidelines, 2010

Modification Recommendation Lowers Systolic Blood Pressure by (Range)

Weight reduction •Maintain normal body weight•Body mass index (BMI) 18.5–24.9 kg/m2

5–20 mm Hg / 10 kg 4 mm Hg / 5 kg

DASH •Increase potassium (fruits and vegetables) and calcium (dairy)•DASH may be too high in protein, potassium and phosphorus for CKD

8–14 mm Hg

Physical activity •At least 30 minutes most days 4–9 mm Hg

Moderate alcohol consumption

•Women: ≤ 1 drink per day •Men: ≤ 2 drinks per day

2–4 mm Hg

Sodium restriction •2,300 mg per day•1,500 mg per day for hypertension, diabetes, and CKD

2–8 mm Hg

Modification Recommendation Lowers Systolic Blood Pressure by (Range)

Weight reduction •Maintain normal body weight•Body mass index (BMI) 18.5–24.9 kg/m2

5–20 mm Hg / 10 kg 4 mm Hg / 5 kg

DASH •Increase potassium (fruits and vegetables) and calcium (dairy)•DASH may be too high in protein, potassium and phosphorus for CKD

8–14 mm Hg

Physical activity •At least 30 minutes most days 4–9 mm Hg

Moderate alcohol consumption

•Women: ≤ 1 drink per day •Men: ≤ 2 drinks per day

2–4 mm Hg

Sodium restriction •2,300 mg per day•1,500 mg per day for hypertension, diabetes, and CKD

2–8 mm Hg

Lifestyle modifications for blood pressure (BP) have not been studied extensively in the CKD population

The DASH diet lowers blood pressure in the general population

Reference: http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/new_dash.pdf

Original DASH • “A diet rich in fruits, vegetables, and low-fat dairy

foods and with reduced saturated and total fat can substantially lower blood pressure.”

DASH-Sodium • “The reduction of sodium intake to levels below the

current recommendation of 100 mmol* per day and the DASH diet both lower blood pressure substantially, with greater effects in combination than singly.”

*100 mmol Na = 2,300 mg Na

Both DASH and DASH-Sodium lower blood pressure

References: Appel et al. N Engl J Med 1997; 336(16):1117–1124; Sacks et al. N Engl J Med 2001; 344(1):3–10.

DASH diet pattern for 2,000 calories

Reference: Your Guide to Lowering Your Blood Pressure with DASH, NIH Publication No.06-4082, April 2006 http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/new_dash.pdf

Food Group Servings/dayGrains (mostly whole) 6–8Vegetables 4–5Fruits 4–5Fat-free, low-fat milk, and milk products

2–3

Meats, poultry, and fish ≤6 ounces (oz.) Nuts, seeds, and legumes 4–5 per weekFats and oils 2–3 Sweets and added sugars ≤ 5 tablespoons

(Tbsp.) per week

The DASH combination diet pattern is higher in protein and potassium

Reference: Adapted from Appel et al. N Engl J Med 1997; 336(16):1117–1124

Control Diet Fruits & Vegetables Diet

Combination Diet

Nutrient Level per menu Level per menu Level per menu

Protein (% of total kcal)

13.8 15.1 17.9

Potassium (mg/day)

1,752 4,101 4,415

Sodium (mg/day)

3,028 2,816 2,859

Urinary K increased with increased K intake

Urea nitrogen reflected protein intake

Urinary phosphorus (P)may reflect protein intake

Urinary Na excretion intake

Urinary excretion depended on intake in DASH

Reference: Adapted from Appel et al. N Engl J Med 1997; 336(16):1117–1124

Substance excreted (mg per 24 hours)

Control Diet

Fruits & Veg Diet

Combination Diet

PotassiumRun-in

InterventionChange

1,385

1,531

146

1,459

2,757

1,298

1,416

2,916

1,500Urea Nitrogen

Run-inIntervention

Change

8,592

9,026

434

8,775

9,456

681

8,729

11,583

2,834

PhosphorusRun-in

InterventionChange

699

739

40

742

708

-35

713

851

137Sodium

Run-inIntervention

Change3,038

3,181

142

3,228

2,996

-232

3,144

3,071

-73

Compared to the control diet, the DASH combination diet reduced systolic blood pressure (BP) by 5.5 mm Hg and diastolic BP by 3.0 mm Hg.

Compared to control diet, the fruits and vegetables diet reduced systolic BP by 2.8 mm Hg and diastolic BP by 1.1 mm Hg.

The combination diet pattern was most effective in lowering blood pressure

Reference: Appel et al. N Engl J Med 1997; 336(16):1117–1124

Typical and DASH pattern at different sodium levels

3,450 mg; 2,300 mg; or 1,150 mg sodium

Similar urinary excretion patterns

DASH-Sodium showed lower blood pressures with lower sodium intake

Reference: Sacks et al. N Engl J Med 2001; 344(1):3–10

The DASH pattern lowered blood pressure at all levels of sodium intake.

In the control diet, blood pressure was lowered with the lowest sodium intake.

Combining the DASH pattern and low sodium intake provided the greatest reduction in blood pressure than either alone.

Sodium restriction lowered blood pressure in DASH-Sodium, even in the control diet

Reference: Sacks et al. N Engl J Med 2001; 344(1):3–10.

Food Group Nutrients of Concern for CKDGrains Whole grains: phosphorus,

potassiumVegetables Potassium

Fruits Potassium

Fat-free, low-fat milk , and milk products

Protein, sodium, phosphorus, potassium

Meats, poultry, and fish Protein, phosphorus, potassium, sodium (“enhanced” and processed)

Nuts, seeds, and legumes Protein, phosphorus, potassium, sodium (if salted)

Fats and oils May have sodium

Sweets and added sugars May have added phosphorus

DASH diet pattern and potential nutrients of concern in CKD

DASH and DASH-Sodium patterns lower blood pressure.

The lowest sodium level is the most effective, even with the usual (control) diet.

The DASH pattern may be too high in protein, potassium, and phosphorus for CKD.

Summary: The DASH diet may help prevent CKD, but it is not generally used with CKD

Usually > 3 medications, including a diuretic

1,500 mg sodium restriction

− Sodium restriction is key to blood pressure control.

May need multiple medications and Na restriction to control blood pressure in CKD

Reference: Chobanian et al. J Am Med Assoc 2003; 289(19):2560–2571

These medications block aldosterone production, and this may result in a reduction in potassium excretion.

The risk for hyperkalemia increases with their use.

These medications include:

− Angiotensin-Converting Enzyme Inhibitor (ACEi)

− Angiotensin Receptor Blocker (ARB)

Anti-hypertensive medications that block RAAS increase the risk for hyperkalemia

ACEi medications block the RAAS and increase the risk for hyperkalemia

ARBs block the RAAS and increase the risk of hyperkalemia

Medications that increase risk for hyperkalemia in CKD

Referece: Chobanian et al. J Am Med Assoc 2003; 289(19):2560–2571

Commonly prescribed

Angiotensin-Converting Enzyme Inhibitor (ACEi)– End with “____pril”

Angiotensin Receptor Blockers (ARB)– End with “___sartan

Used cautiously in CKD

Aldosterone antagonists

Renin inhibitors

Potassium-sparing diuretics

Specific level of eGFR does not determine need for dietary potassium restriction.

Restriction is to help achieve and maintain a safe serum potassium level ( < 5 mEq/L).

The level of potassium restriction should be individualized.

Potassium restriction is not indicated in the absence of hyperkalemia

Serum potassium increases as eGFR decreases


Their effects are beyond blood pressure control.

They also reduce protein in the urine (antiproteinuric).

Sometimes these medications are prescribed to lower urine albumin levels in normotensive people.

ACEi and ARBs may be renoprotective

References: Chobanian et al. J Am Med Assoc 2003; 289(19):2560–2571; Strippoli et al. Cochrane Database Syst Rev 2010.

Kunz et al. Ann Intern Med 2008; 148(1):30–48.

Loop of Henle diuretics bind to co-transporter in loop of Henle.− Less sodium is reabsorbed, and blood pressure is

lowered.− Less potassium is reabsorbed, and serum level may

decrease.

Many people with CKD on loop diuretics do not become hypokalemic due to ACEi or ARB use and fewer functioning nephrons.

Loop diuretics may cause hypokalemia (low potassium)

Assessment− Potential food and anti-hypertensive medication

interactions (potassium)

Intervention− Control sodium intake

< 1,500 mg daily

− Reduce potassium intake if hyperkalemic Avoid salt substitutes

− DASH may not be indicated for CKD.

Nutrition Care Process for CKD & HTN

Reference: ADA Evidence Library. Evidence-Based Practice Guideline for Hypertension

Case study: Food-medication interaction, hyperkalemia, salt substitute

Reduced kidney function with high level of urine albumin

Height 66.5”, weight 200.5 pounds (lb.)

Frank is a 55-year-old man Type 2 DM since 2002 Not taking any medications for past 5 years History: amputation of left fourth toe Comes to clinic 1/19 for right foot swelling BP 168/98 – started on ACEi eGFR 34 UACR 6,437

People with CKD and on ACEi need to use less salt and avoid salt substitutes

Date 1/19 1/29 4/2

BP (mmHg) 168/98 138/82 136/78

Weight (lb.) 200.5 196 191

eGFR (> 60) 34 34 29

UACR (mg/g) (< 30)

6,437

K mmol/L (3.5–5.0)

4.9 4.6 5.5 *High

Medications - - -• Lisinopril 40 mg• Furosemide 20 mg 40 mgDiet changes Told to

use less salt

“stopping salt, trying

salt substitute”

Missed 2/19 RD appt

Date 1/19 1/29 4/2 5/7

BP 168/98 138/82 136/78 142/60

Weight 200.5 196 191 189.4

eGFR (> 60) 34 34 29

UACR (< 30) 6,437 4,483

K (3.5-5.0) 4.9 4.6 5.5 H 5.5 H

Medications - - - -• Lisinopril (ACEi) 40 mg Stopped

• Furosemide 20 mg 40 mg 40 mg

• Losartan (ARB) 50 mg

Diet changes Told to use less salt

“Stopping salt, trying

salt substitute”

Missed 2/19 RD

appt

Missed 4/19 RD appt

ACEi lowered blood pressure and urine albumin (UACR) and increased K

Date 1/29 4/2 5/7 7/1

BP 138/82 136/78 142/60 146/70

Weight 196 191 189.4 189.4

eGFR (> 60) 34 29 22

UACR (< 30) 6,437 4,483

K (3.5–5.0) 4.6 5.5 H 5.5 H 5.5 H

Medications - - - -• Lisinopril Stopped • Furosemide 40 mg 40 mg 40 mg• Losartan 50 mg 50 mg

Diet changes “stopping salt, trying salt substitute”

Missed 2/19 RD

appt

Missed 4/19 RD

appt

Direct referral to

RD

Change to ARB did not reduce K

Breakfast Lunch Supper2 fried eggs •salt substitute3–4 slices of bacon 3 slices of wheat toast with soft margarine

Coffee: at least 3 cups with artificial sweetener

Wife makes fried potatoes on weekends

Fast foodDouble meat burger Medium fries (trying to limit carbs; doesn’t add more salt now)

Diet soda pop

May skip lunch on weekends (bigger breakfast)

6–8 oz. fried steak•salt substitute2–3 slices bread1 c. canned corn or peas

Hot tea with artificial sweetener

Uses orange juice to treat low sugars ( frequency)

Frank’s “usual” diet intake

Food/beverage intake

Recently stopped salt, now using salt substitute. Using orange juice to treat low sugars. Includes other potassium-rich foods, fast foods. Won’t use glucose tablets.

Diet order 2,200 calories; 1,500 mg sodium; potassium restriction

Diet experience Instructed on diabetic diet when diagnosed, tries to limit carbs.

Medications 50 mg Losartan (changed from 40 mg Lisinopril), 40 mg Furosemide

Anthropometrics Height 66.5”, weight 189.4# down 11# since Jan., BMI now 30.1.Left foot 4th toe amputation

Biochemical data

K 5.5 x 3 months; eGFR 22, was 34 (Jan.); UACR 4,483 mg/g (May), was 6,437 mg/g (Jan.)

Personal history 55-year-old male, English is his second language

Patient history DM 2 for 8 years, no meds x 5 years. BP 146/70. Originally came to clinic due to right foot swelling. Seeing a nephrologist.

Social history Sedentary job, sits for long periods of time. No sick leave, couldn’t make dietitian appointment. Lives in apartment with wife, 2 sons.

Assessment (7/1)

Food–medication interaction related to renal dysfunction and blood pressure medication, as evidenced by serum potassium level of 5.5.

Excessive potassium intake related to food-related knowledge deficit as evidenced by use of salt substitute and other foods rich in potassium.

Nutrition Care Process (NCP) Diagnoses

As eGFR declined, medication and nutrient interaction increased serum K

Initial nutrition education

Priority modification: Reduce potassium intake by eliminating salt substitute; use juice low in potassium (cranberry juice) to treat low sugars.

Collaborate with primary care provider in regard to patient’s hyperkalemia, CKD, and diabetes.

Intervention

Summary: CKD and hypertension

BP ≤ 130/80 may be beneficial for many

Multiple medications

Assessment:

Food–medication interaction− Hyperkalemia

ACEi (____pril) ARBs (___sartan)

Intervention:

Limit sodium− Keep to ≤ 1,500 mg/day− Avoid salt substitutes

Limit potassium when serum level is elevated− Individualized

CONTROL DIABETESSpontaneous improvement in diabetes control may indicate progression of kidney disease

Glucose and the nephrons

Insulin and other DM medications

Advanced glycation end products (AGEs)

Diabetes control in CKD

Treatment of hypoglycemia

Risk for hyperkalemia with ACEi and ARBs

Topics

Diabetes is the leading cause of ESRD in the United States

Reference: USRDS 2010 Annual Data Report

Glucose is filtered by glomeruli and almost completely reabsorbed by proximal tubules.

Glucosuria occurs when filtered load exceeds tubules ability to reabsorb the glucose.

Renal threshold is 180–200 mg/deciliter(dL).

Glucose is often co-absorbed with sodium.

The nephrons are involved in gluconeogenesis.− 20% of overall endogenous release

Glucose and the nephrons

References: Gerich et al. Diabetes Care 2001; 24(2):382–391;Meyer & Gerich. Curr Diab Rep 2002; 2(3):237–241.

Hyperfiltration− The initial response to hyperglycemia is an increase in

GFR, followed by slow decline.

Hypertrophy of glomerulus and tubule− Nephrons may be damaged or destroyed.

Diabetic kidney disease generally, but not always, associated with progressive albuminuria.− Monitor eGFR and UACR.

Hyperglycemia is associated with hyperfiltration

References: Molitch et al. Diabetes Care 2010; 33(7):1536–1543; Retnakaran et al. Diabetes 2006; 55(6):1832–1839.

Natural history of diabetic nephropathy:

hyperglycemia causes hyperfiltration, may be followed by albuminuria

Reference: Adapted from Friedman, 1999

Advanced glycation end products (AGE) form by nonenzymatic, sequential glycation and oxidation reaction of sugars with free amino groups on proteins, lipids, and nucleic acids.

The initial reaction is reversible, depending on concentration.

They may accumulate in plasma and tissues.− Increased levels are found in DM and CKD− May accumulate with aging

Advanced glycation end products form spontaneously

Reference: Bohlender et al. Am J Physiol Renal Physiol 2005; 289(4):F645–F659.

Virtually any protein can be glycosylated.

Slow turnover proteins are particularly prone to modification.− Glomerular basement membrane thickening

− Blood vessel stiffness Altered collagen and elastin

− Altered low-density lipoprotein (LDL) cholesterol May not be able to attach to receptor on endothelial cells for

clearance

AGEs alter protein structure and function

Reference: Goldin et al. Circulation 2006; 114(6):597–605; Peppa et al. Clinical Diabetes 2003; 21(4):186–187.

Receptors for AGEs upregulate as AGEs accumulate.

Activation (binding) may induce release of pro-inflammatory and pro-fibrogenic cytokines.

AGEs binding to receptors may promote inflammatory response

Reference: Schmidt et al. J Clin Invest. 2001; 108(7):949–955.

Glycohemoglobin (gHb) or glycosylated hemoglobin

Sugars cross-link to hemoglobin

Rate of formation is proportional to glucose level and duration

Hemoglobin lifespan is about 4 months

A1C is used to assess long-term DM control

A1C levels correlate with DM complications

Hemoglobin A1C is an AGE

A1C estimates average glucose (eAG) level for past 2–3 months.

eAG is similar to eGFR.− Both “estimate” levels.

Normal A1C is 4–5.6%

A1C > 6.5% is now used to diagnose DM.

Average glucose levels can be estimated from the A1C

Reference: http://professional.diabetes.org/GlucoseCalculator.aspx

A1C (%) eAG (mg/dL)14 355

12 298

10 240

9 212

8 183

7 154

6.5 140

6.0 126

< 1% of filtered insulin is excreted into urine.

Insulin, pro-insulin, C-peptide are catabolized.− About 1/3 total endogenous insulin catabolism− Primary site for exogenous insulin catabolism

− Major site for pro-insulin catabolism

Circulating insulin levels are higher as CKD advances.

The risk for hypoglycemia increases with CKD.

Insulin is catabolized by the kidneys

Reference: Himmelfarb J. In: Mitch WE, Ikizler TA, 2010

Diabetes medications may be discontinued or adjusted in CKD

Reference: Reilly & Berns Seminars in Dialysis 2010; 23(2):163–168.

Balancing Act

Goal for the general population − A1C < 7%

Less stringent goal may be appropriate for:− Frequent severe hypoglycemia− Limited life expectancy− Advanced microvascular (CKD) or macrovascular

complications

A1C goal is individualized in CKD

Reference: Diabetes Care, (suppl 1) 2011

There is evidence that control of newly diagnosed diabetes may help prevent CKD.

− Type 1 diabetes (DM 1) Diabetes Control and Complications Trial (DCCT)

− Type 2 diabetes (DM 2) United Kingdom Prospective Diabetes Study (UKPDS)

Good glycemic control early may reduce CKD later

Newly diagnosed, first 10 years− Median age: 54 years (48–60 years)

Intensive control defined as A1C < 7.0% (compared to 7.9%)

34% reduction in albuminuria

Long-term data not as clear

UKPDS: Control of newly diagnosed type 2 DM may lower risk of albuminuria

Reference: UKPDS 33, 1998; UKPDS 64, 2003

The evidence is not strong.

Control still matters for other organs.

AGEs may have altered or destroyed slow turnover proteins (glomerular barrier).

Good control of diabetes of long duration may not be as effective in slowing CKD

45–60 grams per meal for most women

60–75 grams per meal for most men

15 grams per snack

Adjust carbohydrates based on weight, glycemic targets, and individual preference

Carbohydrates still count in people with diabetic kidney disease (DKD)

Carbohydrate choice Nutrients of concern for CKD

Milk Protein, sodium, phosphorus, potassium

Processed grains SodiumWhole grains Phosphorus, potassiumLegumes Protein, phosphorus, potassiumStarchy vegetables PotassiumFruit PotassiumSweets and added sugars May have added phosphorus

Type of carbohydrate may matter in DKD

Dietary protein may increase GFR and renal blood flow rates. Animal protein may have greater effect than plant protein.

Dietary protein is a source of nitrogen, phosphorus, potassium, and metabolic acids that need to be filtered and excreted by the kidneys.

Animal protein intake may be a risk factor for increased urine albumin excretion in hypertension and diabetes.

High protein diets are not recommended for DKD

References: Friedman. Am J Kidney Dis 2004; 44(6):950–962; Bernstein et al. J Am Diet Assoc 2007; 107(4):644–650;

Wrone et al. Am J Kidney Dis 2003; 41(3):580–587.

RDA = 0.8 g protein/kg body weight (wt)

American Diabetes Association (2008) recommendations:− Normal kidney function: 15–20% protein calories (usual)− Early CKD: “reduction” to 0.8–1.0 g/kg body wt− Advanced CKD: 0.8 g/kg body wt

American Dietetic Association Evidence Library for Chronic Kidney Disease (accessed 2/4/2011)− 0.8–0.9 g/kg body wt − Protein-restriction may improve urine albumin (albuminuria)

Level of protein for DM and CKD may mean avoiding excessive intake

Reference: Diabetes Care, 2008

Data are inconclusive for replacing animal protein with vegetable protein to help lower urine albumin.

Long-term consumption of high-protein diets (animal or vegetable protein) may cause renal injury and/or accelerate CKD.− Definition of high-protein

> 0.8 g/kg/day (no CKD)

or > 0.6 g/kg/day (CKD)

Reducing total amount of protein may be more important than type of protein

References: Diabetes Care, 2008; Bernstein et al. J Am Diet Assoc 2007; 107(4):644–650;

National Cholesterol Education Program (2002) recommendations:− 25–35% total calories from fat

Saturated fat < 7% total calories Polyunsaturated fat < 10% Monounsaturated fat < 20%

− Cholesterol < 200 mg/day

− Plant stanols or sterols 2 grams per day

− Increase soluble fiber to 10–25 grams per day

Diet should be heart-healthy to reduce risk for CVD in DM (and CKD)

Reference: http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3full.pdf

Guidelines provide guidance, but we still need to individualize

Spontaneous improvement and/or increased frequency of hypoglycemia may indicate CKD is progressing

The risk for hypoglycemia may increase as CKD progresses.

Circulating levels of insulin are higher due to reduced catabolism.

Insulin prescription may be reduced.

Oral medications may change.

“I don’t have diabetes any more; my doctor stopped my diabetes pills.”

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.

Treat hypoglycemia without adding potassium or phosphorus

Any “juice” can treat hypoglycemia, even those low in potassium

mg

Date 1/19 1/29 4/2 5/7 7/1BP (mmHg) 168/98 138/82 136/78 142/60 146/70

Weight (lbs.) 200.5 196 191 189.4 189.4

eGFR (> 60) 34 34 29 27 22

UACR (mg/g) (< 30)

- 6,437 - 4,483 -

K (mmol/L )(3.5-5.0)

4.9 4.6 5.5 5.5 5.5

Glucose (70–99) 211 77 63 - 69

A1C (eAG) 9.4 (223) - 7.9 (180) - 6.1 (128)

Medications Glyburide 5 mg

- Glyburide 2.5 mg

Glipizide 5 mg

-

He reports - A few low sugars

More low sugars

Still has low sugars

-

For Frank: Hypoglycemia and improved glycemic control may indicate CKD progression

Food/beverage intake

Recently stopped salt, using salt substitute. Using orange juice to treat low sugars. Includes other potassium-rich foods, fast foods. Won’t use glucose tablets. Low sugars when he skips meals.

Diet order 2,200 calories; 1,500 mg sodium; potassium restriction

Diet experience Instructed on diabetic diet when diagnosed, tries to limit carbs.

Medications 50 mg Losartan (changed from 40 mg Lisinopril), 40 mg Furosemide;5 mg Glipizide (2.5 mg Glyburide discontinued due to low sugars)

Anthropometrics Height 66.5”, weight 189.4# down 11# since Jan., BMI now 30.1. Left foot, 4th toe amputation

Biochemical data K 5.5 x 3 months; eGFR 22, was 34 (Jan.); UACR 4,483 mg/g (May), 6,437 mg/g (Jan.); A1C 6.1, 7.9% (Apr); random blood sugar 69

Personal history 55-year-old male, English is his second language

Patient history DM type 2 for 8 years, no meds x 5 yrs. BP 146/70. Originally came to clinic due to right foot swelling. Seeing a nephrologist.

Social history Sedentary job, sits for long periods of time. No sick leave, couldn’t make dietitian appointment. Lives in apartment with wife, 2 sons.

Reference: American Dietetic Association, 2010

Assessment (7/1)

As eGFR declined, Frank’s DM medication was reduced, then changed

Inconsistent carbohydrate intake related to limited adherence to nutrition-related recommendations, as evidenced by skipped meals and low blood glucose levels

Excessive potassium intake related to nutrition-related knowledge deficit, as evidenced by use of orange juice to treat low blood glucose levels

NCP diagnoses


Initial nutrition education

Priority modifications: − Eat a small snack between brunch and supper on

weekends to prevent hypoglycemia.− Use glucose tablets or juice with less potassium to

treat hypoglycemia.

Intervention


Renal threshold for glucose is 180–200 mg/dL. Sugars cross-linking to proteins changes their shapes and

functions (AGEs). 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 occurs with ACEi and ARBs.− Use low-potassium juice to treat hypoglycemia.− Light-colored soda pop is lower in phosphorus than cola.

Summary: CKD and diabetes

Baseline urine albumin level may predict risk of CKD progression

Urine albumin

Urine albumin measures albuminuria.

Urine albumin may be earliest sign of CKD.

Urine albumin may exacerbate kidney damage.

The level reflects severity of kidney damage.

Reducing albuminuria may be associated with slower progression.

Urine albumin is a risk factor for cardiovascular disease (CVD).− Increased inflammation− Oxidative stress− Marker of endothelial dysfunction

Brief review: Urine albumin

“Normal” UACR < 30 mg/g − Current cut-off used to define normal levels

Persistent UACR > 30 mg/g means kidney damage

Spot urine sample

Monitor trends over time

Use UACR to assess and monitor kidney damage

Increased glomerular permeability allows albumin (and other proteins) to pass into the urine.

Higher levels of protein within the tubule may exacerbate kidney damage.− Protein may exceed tubule’s ability to reabsorb.

Damaged kidneys allow albumin to cross the filtration barrier into the

urine

Risk factors for albuminuria

Reference: de Jong & Brenner. Kidney Int 2004; 66(6):2109–2118.

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):2309–2320.

Their effects are beyond blood pressure control.

They also reduce protein in the urine.

Sometimes these medications are prescribed to lower urine albumin levels in normotensive people.

ACEi and ARBs may be renoprotective

References: Chobanian et al. J Am Med Assoc 2003; 289(19):2560–2571; Strippoli et al. Cochrane Database Syst Rev 2010.

Kunz et al. Ann Intern Med 2008; 148(1):30–48.

Dose-dependent increase in urine albumin in the general population

Independent predictor of elevated urine albumin in primary hypertension

Independent risk factor for onset and progression of albuminuria in DM 1 and DM 2

May increase risk for progression of renal failure in patients with primary renal disease

Smoking is associated with albuminuria

Reference: Orth. J Am Soc Nephrol 2002; 13(6):1663–1672.

Literature review showed weight loss was associated with decreased proteinuria.− Dietary restrictions− Exercise− Anti-obesity medications− Bariatric surgery

No data to evaluate effect on CKD progression.

Intentional weight loss is associated with decreased proteinuria

Reference: Afshinnia et al. Nephrol Dial Transplant 2010; 25(4):1173–1183.

In the Netherlands, higher sodium intake was associated with increased urine albumin excretion.

In a 2006 literature review, increasing salt consumption was associated with worsening urine albumin.

Reducing sodium intake may reduce urine albumin levels

References: Verhave et al. J Intern Med 2004; 256(4):324–330; Jones-Burton et al. Am J Nephrol 2006; 26(3):268–275.

The type of protein may make a difference.

Animal protein may be associated with higher urine albumin excretion.

The relationship may depend on baseline urine albumin level.

Relationship between urine albumin and dietary protein intake varies

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)

Animal protein intake may be associated with higher urine albumin

Baseline AER < 7 mg/24 hr. − No difference found in AER between diet patterns at 8

weeks.

Baseline AER ≥ 7 mg/24 hr. − 8-week AER was similar in control and DASH.

DASH was 3.8% higher in protein than control diet.

− 8-week AER was lower in fruits and vegetables diet. ~ 1% higher protein compared to control diet ~ 10 g/day reduction in animal protein

Although higher in protein, DASH pattern did not increase urine albumin excretion

Reference: Jacobs et al. Am J Kidney Dis 2009; 53(4):638–646.

DASH: Baseline urine albumin may affect AER response to change in dietary protein

Reference: Adapted from Jacobs et al., 2009

A 1996 meta-analysis found low-protein diet may slow increase in urinary albumin level in insulin-dependent diabetes.

The use of a supplemented very-low-protein diet is associated with decrease in proteinuria.

Lowering dietary protein may help reduce urine albumin or proteinuria

References: Pedrini et al. Ann Intern Med 1996; 124(7):627–632; Chauveau et al. J Renal Nutr 2007; 17(4):250–257.

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

Interventions for reducing urine albumin

For Frank, an elevated urine albumin is a marker of kidney damage and prognosticator for rapid

progression of CKD

CARDIOVASCULAR DISEASE

CVD is the leading cause of morbidity and mortality in people with CKD

CVD risks and CKD− Traditional− Nontraditional

Pattern of dyslipidemia in CKD

Statins

Nontraditional risks

Nutrition interventions

Topics

Lipid abnormalities may increase as eGFR declines

Reference: Astor et al. Am J Epidemiol 2008; 167(10):1226–1234.

CKD complications are nontraditional risk factors for CVD

Traditional risk factors Hypertension Diabetes Dyslipidemia Smoking Age Inflammation

Nontraditional risk factors Albuminuria Anemia Abnormal metabolism of

calcium and phosphorus

Increased triglycerides− May be very elevated with massive proteinuria

(nephrotic syndrome)

Decreased high-density lipoprotein levels

Low or normal low-density lipoprotein levels− Smaller, denser LDL particles

More prone to oxidation and accumulation in vessel walls

Pattern of dyslipidemia in CKD may increase risk of CVD

References: Molitch. Clin J Am Soc Nephrol 2006; 1(5):1090–1099; Ruan et al. Nat Rev Nephrol 2009; 5(12):713–721.

Target lipid levels in CKD are unknown and may be similar to those for the general population.

Persons with CKD should be considered at high risk for CVD.

Not many CVD studies include CKD patients.

Targets for lipid levels may be similar for 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.

Statins are used with caution in patients with CKD

Reference: Navaneethan et al. Cochrane Database Syst Rev 2009.

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)

Inflammation may play a role in CVD in CKD

Reference: Contreras et al. J Am Soc Nephrol 2010; 21(12):2131–2142.

Albuminuria

Anemia

Abnormal metabolism of calcium and phosphorus

Nontraditional risk factors for CVD

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

Nutrition recommendations addressing CVD in persons with CKD may be similar

to those for the general population

Reference: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2010/PolicyDoc/ExecSumm.pdf

Spreads may reduce LDL cholesterol by 15%.

Effectiveness in CKD patients is unknown.

Spreads vary in sodium and calories:− 80–110 mg sodium/Tbsp.

− 45–70 kcal/Tbsp.

Substitute isocalorically.

Some may contain potassium sorbate.

Plant stanol and sterol spreads may help lower LDL in general population

Reference: Van Horn et al. J Am Diet Assoc 2008; 108(2):287–331.

25–30 grams total fiber suggested per day.

7–13 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.

Soluble fiber may help reduce heart disease in the general population

References: Van Horn et al. J Am Diet Assoc 2008; 108(2):287–331; Beto & Bansal. Advances Chronic Kidney Dis 2004; 11(4):391–397.

Legumes are rich in potassium and phosphorus; counsel appropriately

References: http://www.nhlbi.nih.gov/health/public/heart/chol/chol_tlc.pdf; http://www.nal.usda.gov/fnic/foodcomp/search/

Serving of ½ 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

Some fruits with soluble fiber are rich in potassium; counsel appropriately

References: http://www.nal.usda.gov/fnic/foodcomp/search/; http://www.nhlbi.nih.gov/health/public/heart/chol/chol_tlc.pdf

Food Soluble fiber (grams)

K(mg)

P(mg)

Na(mg)

Apple (3” diameter–medium) 1 195 20 2

Apple, peeled 2.1 (total fiber) 145 18 0

Banana (7”–7 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

More than 90% of phosphorus is absorbed from food additives containing phosphorus.− Read ingredient list for phosphorus.

Phosphorus in animal foods is absorbed more readily than that in plant food.

Phytates in plant foods reduce absorption of phosphorus (e.g., foods rich in soluble fiber).

Source of phosphorus affects absorption: additives > animal > plant

Reference: Kalantar-Zadeh et al. Clin J Am Soc Nephrol 2010; 5(3):519–530.

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.

Summary: CKD and CVD

Summary: CKD and hypertension

Assessment: Food–medication

interaction− Hyperkalemia

ACEi (____pril) ARBs (___sartan)

Intervention: Limit sodium.

− 1,500 mg per day− Avoid salt substitutes

Limit potassium when serum level is elevated.

− Individualized

Blood pressure control is key to slowing progression.

Multiple medications are used.

Urine albumin excretion is associated with diabetic kidney disease, but not all people will have high urine albumin levels.

High levels of urine albumin may mean more rapid progression of CKD.

Good control of diabetes early may help reduce the risk of albuminuria later.

Tight versus good control may not slow progression.


Renal threshold for glucose is 180–200 mg/dL. Sugars cross-linking to proteins change their shapes and

functions (AGEs). A1C goal is individualized. Spontaneous improvement in glycemic control may indicate CKD

progression.− Medications may change.

Risk for hypoglycemia with CKD, hyperkalemia with ACEi and ARBs.− Use low-potassium juice to treat hypoglycemia.− Light-colored soda pop is lower in phosphorus than colas.


Urine albumin is a marker of kidney damage. Control blood pressure.

− Particularly with high urine albumin, control is important.− ACEi and ARBs may be antiproteinuric.

Reduce sodium intake to 1,500 mg. Good control of diabetes early may help prevent

albuminuria. Weight reduction (if obese) may reduce inflammation. Reduce protein intake, if excessive. Tobacco cessation is important.

Summary: CKD and urine albumin

Nontraditional risk factors include:− Abnormal urine albumin − Anemia− Abnormal calcium and phosphorus metabolism

Statins are used in CKD with some caution.

Some foods rich in soluble fiber may be higher in K and P than recommended for CKD.

Phosphorus in food additives is absorbed more readily.

Summary: CKD and CVD

An educational handout you can use to get started

Reference: http://www.nkdep.nih.gov/resources/nkdep-factsheet-overallpatient-508.pdf

Reference: http://www.nkdep.nih.gov/resources/nkdep-factsheet-overallpatient-508.pdf

Another educational tool you can start using:

Reference: http://www.nkdep.nih.gov/resources/nkdep-ckd-amt-guide-508.pdf

This professional development opportunity was created by the National Kidney Disease Education Program (NKDEP), an initiative of the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health. With the goal of reducing the burden of chronic kidney disease (CKD), especially among communities most impacted by the disease, NKDEP works in collaboration with a range of government, nonprofit, and health care organizations to:

• raise awareness among people at risk for CKD about the need for testing;• educate people with CKD about how to manage their disease;• provide information, training, and tools to help health care providers better

detect and treat CKD; and• support changes in the laboratory community that yield more accurate, reliable,

and accessible test results.To learn more about NKDEP, please visit: http://www.nkdep.nih.gov. For additional

materials from NIDDK, please visit: http://www.niddk.nih.gov.

Theresa A. Kuracina, M.S., R.D., C.D.E., L.N.

Ms. Kuracina is the lead author of the American Dietetic Association’s CKD Nutrition Management Training Certificate Program and NKDEP’s nutrition resources for managing patients with CKD.Ms. Kuracina has more than 20 years of experience in clinical dietetics with the Indian Health Service (IHS). She is a senior clinical consultant with the National Kidney Disease Education Program (NKDEP) at the National Institutes of Health. She also serves as a diabetes dietitian and coordinator for a diabetes self-management education program at the IHS Albuquerque Indian Health Center in New Mexico, a role in which she routinely counsels patients who have chronic kidney disease (CKD).

Meet our Presenters

Andrew S. Narva, M.D., F.A.C.P.

Dr. Narva is the director of the National Kidney Disease Education Program (NKDEP) at the National Institutes of Health (NIH). Prior to joining NIH in 2006, he served for 15 years as the Chief Clinical Consultant for Nephrology for the Indian Health Service (IHS). Via telemedicine from NIH, he continues to provide care for IHS patients who have chronic kidney disease. A highly recognized nephrologist and public servant, Dr. Narva has served as a member of the Medical Review Board of ESRD Network 15 and as chair of the Minority Outreach Committee of the National Kidney Foundation (NKF). He serves on the NKF Kidney Disease Outcomes Quality Initiative Work Group on Diabetes in Chronic Diabetes and is a member of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure 8 Expert Panel.

Meet our Presenters

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References: Hypertension

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Kunz R, Friedrich C, Wolbers M, Mann JFE . Meta-analysis: effect of monotherapy and combination therapy with inhibitors of the renin-angiotensin system on proteinuria in renal disease. Annals of Internal Medicine. 2008;148(1):30–48.

Lancaster KJ. Dietary treatment of blood pressure in kidney disease. Advances in Chronic Kidney Disease. 2004;11(2):217–221.

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Ravera M, Re M, Deferrari L, Vettoretti S, Deferrari G . Importance of blood pressure control in chronic kidney disease. Journal of the American Society of Nephrology. 2006;17(4 suppl 2):S98–S103.

Russell JM. Sodium-potassium-chloride cotransport. Physiological Reviews. 2000;80(1):211–276.

Sacks FM, Svetkey LP, Vollmer WM, et al . Effects on blood pressure on reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. New England Journal of Medicine. 2001;344(1):3–10.

Schaefer TJ, Wolford RW. Disorders of potassium. Emergency Medicine Clinics of North America. 2005;23(3):723–747.


Schiffrin EL, Lipman ML, Mann JFE. Chronic kidney disease effects on the cardiovascular system. Circulation. 2007;116(1):85–97.

Strippoli GFM, Bonifati C, Craig ME, Navaneethan SD, Craig JC. Angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists for preventing progression of diabetic kidney disease (review). Cochrane Database of Systematic Reviews. 2010. http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD006257/abstract. Accessed August 26, 2011.

U.S. Department of Agriculture. Agricultural Research Service. 2010. Nutrient intakes from food: mean amounts consumed per individual, by gender and age. What We Eat in America, NHANES 2007–2008. U.S. Department of Agriculture website. http://www.ars.usda.gov/SP2UserFiles/Place/12355000/pdf/0708/Table_1_NIN_GEN_07.pdf. Revised August 2010. Accessed June 14, 2011.


U.S. Department of Agriculture and U.S. Department of Health and Human Services. Dietary Guidelines for Americans, 2010. 7th ed. Washington, D.C.: U.S. Government Printing Office, December 2010. U.S. Department of Agriculture website. http://www.health.gov/dietaryguidelines/dga2010/DietaryGuidelines2010.pdf. Accessed June 14, 2011.

U.S. Renal Data System. USRDS 2010 Annual Data Report: Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2010. United States Renal Data System website. http://www.usrds.org/adr.htm. Accessed August 31, 2011.

U.S. Renal Data System. USRDS 2009 Annual Data Report: Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2009. United States Renal Data System website. http://www.usrds.org/adr.htm. Accessed August 31, 2011.


Adler AI, Stevens RJ, Manley SE, et al. Development and progression of nephropathy in type 2 diabetes: the United Kingdom Prospective Diabetes Study (UKPDS 64). Kidney International. 2003;63(1):225–232.

American Diabetes Association. Nutrition recommendations and interventions for diabetes: a position statement of the American Diabetes Association. Diabetes Care. 2008;31(suppl 1):S61–S78.

American Diabetes Association. DiabetesPro: professional resources online. Estimated average glucose: eAG. American Diabetes Association website. http://professional.diabetes.org/GlucoseCalculator.aspx. Accessed June 13, 2011.

American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care. 2011;34(suppl 1):S11–S61.

References: Diabetes

American Dietetic Association. International Dietetics & Nutrition Terminology (IDNT) Reference Manual: Standardized Language for the Nutrition Care Process. 3rd ed. Chicago, IL: American Dietetic Association; 2010.

American Dietetic Association evidence analysis library. Recommendations summary chronic kidney disease (CKD) protein intake. July 2010. American Dietetic Association website. http://www.adaevidencelibrary.com/tmp/pq95.pdf. Accessed August 26, 2011.

Bernstein AM, Treyzon L, Zhaoping L. Are high-protein, vegetable-based diets safe for kidney function? A review of the literature. Journal of the American Dietetic Association. 2007;107(4):644–650. [review]

Bohlender JM, Franke S, Stein S, Wolf G. Advanced glycation end products and the kidney. American Journal of Renal Physiology. 2005;289(4):F645–F659.


Cavanaugh KL. Diabetes management issues for patients with chronic kidney disease. Clinical Diabetes. 2007;25(3):90–97.

Friedman AN. High-protein diets: potential effects on the kidney in renal health and disease. American Journal of Kidney Diseases. 2004;44(6):950–962.

Friedman EA. Chapter 1. Diabetic nephropathy: impact of comorbidity. In: Klahr S, ed. Atlas of Disease of the Kidney. Vol. 4. http://www.kidneyatlas.org/book4/adk4-01.pdf. 1999. Accessed June 19, 2011.

Gerich JE, Meyer C, Woerle HJ, Stumvoll M. Renal gluconeogenesis its importance in human glucose homeostasis. Diabetes Care. 2001;24(2):382–391.

Goldin A, Beckman JA, Schmidt AM, Creager MA. Advanced glycation end products sparking development of diabetic vasculature injury. Circulation. 2006;114(6):597–605.


Gross JL, de Azevedo MJ, Silveiro SP, Canani LH, Caramori ML, Zelmanovitz T. Diabetic nephropathy: diagnosis, prevention, and treatment. Diabetes Care. 2005;28(1): 176-188.

Himmelfarb J, de Boer I, Kestenbaum B. Effects of chronic kidney disease on metabolism and hormonal function. In: Mitch WE, Ikizler TA, eds. Handbook of Nutrition and the Kidney. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2010; 34–49.

Krishnamurti U, Steffes MW. Glycohemoglobin: a primary predictor of the development or reversal of complications of diabetes mellitus. Clinical Chemistry. 2001;47(7):1157–1165.

Meyer C, Gerich JE. Role of the kidney in hyperglycemia in type 2 diabetes. Current Diabetes Reports. 2002;2(3):237–241.


Molitch ME, Steffes M, Sun W, et al. Development and progression of renal insufficiency with and without albuminuria in adults with type 1 diabetes in the Diabetes Control and Complications Trial and the Epidemiology of Diabetes Interventions and Complications Study. Diabetes Care. 2010;33(7):1536–1543.

National Cholesterol Education Program. Third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). September 2002. NIH publication 02–5215. National Heart, Lung, and Blood Institute website. http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3full.pdf . Accessed June 13, 2011.

Peppa M, Uribarri J, Vlassara H. Glucose, advanced glycation end products, and diabetes complications: what is new and what works. Clinical Diabetes. 2003;21(4):186–187.


Reilly JB, Berns JS. Selection and dosing of medications for management of diabetes in patients with advanced kidney disease. Seminars in Dialysis. 2010;23(2):163–168.

Retnakaran R, Cull CA, Thorne KI, Adler AI, Holman RR for the UKPDS Study Group. Risk factors for renal dysfunction in type 2 diabetes: U.K. Prospective Diabetes Study 74. Diabetes. 2006;55(6):1832–1839.

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UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet. 1998;352(9131):837–853.

Uribarri J, Tuttle KR. Advanced glycation end products and nephrotoxicity of high- protein diets. Clinical Journal of the American Society of Nephrology. 2006;1(6):1293–1299.

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Afshinnia F, Wilt TJ, Duval S, Esmaeili A, Ibrahim HN. Weight loss and proteinuria: systematic review of clinical trials and comparative cohorts. Nephrology Dialysis Transplantation. 2010;25(4):1173–1183.

Chauveau P, Combe C, Rigalleau V, Vendrely B, Aparicio M. Restricted protein diet is associated with decrease in proteinuria: consequences on the progression of renal failure. Journal of Renal Nutrition. 2007;17(4):250–257.

Chobanian, AV, Bakris GL, Black HR, et al. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. The JNC 7 report. Journal of the American Medical Association. 2003;289(19):2560–2571.

de Jong PE, Brenner BM. From secondary to primary prevention of progressive renal disease: the case for screening for albuminuria. Kidney International. 2004;66(6):2109–2118.

References: Albuminuria

De Zeeuw D, Remuzzi G, Parving H, et al. Proteinuria, a target for renoprotection in patients with type 2 diabetic nephropathy: lessons from RENAAL. Kidney International. 2004;65(6):2309–2320.

Jacobs DR, Gross MD, Steffen L, et al. The effects of dietary patterns on urinary albumin excretion: results of the Dietary Approaches to Stop Hypertension (DASH) Trial. American Journal of Kidney Diseases. 2009;53(4):638–646.

Jafar TH, Stark PC, Schmid CH, et al. Proteinuria as a modifiable risk factor for the progression of non-diabetic renal disease. Kidney International. 2001;60(3):1131–1140.

Jones-Burton C, Mishra SI, Fink JC, et al. An in-depth review of the evidence linking dietary salt intake and progression of chronic kidney disease. American Journal of Nephrology. 2006;26(3):268–275.


Kunz R, Friedrich C, Wolbers M, Mann JFE. Meta-analysis: effect of monotherapy and combination therapy with inhibitors of the renin-angiotensin system on proteinuria in renal disease. Annals of Internal Medicine. 2008;148(1):30–48.

Lin J, Hu FB, Curhan GC. Associations of diet with albuminuria and kidney function decline. Clinical Journal of the American Society of Nephrology. 2010;5(5):836–843.

National Kidney Disease Education Program. Explaining your kidney test results. Revised January 2010. NIH publication 10–6220. National Kidney Disease Education Program website. http://nkdep.nih.gov/resources/NKDEP_GFR_UA_Tearpad_508.pdf. Accessed June 13, 2011.


Quick reference on UACR and GFR in evaluating patients with diabetes and kidney disease. National Kidney Disease Education Program website. http://nkdep.nih.gov/resources/uacr_gfr_quickreference.htm. Reviewed June 30, 2010. Accessed June 13, 2011.

Nettleton JA, Steffen LM, Palmas W, Burke, GL, Jacobs DR Jr. Associations between microalbuminuria and animal foods, plant foods, and dietary patterns in the Multiethnic Study of Atherosclerosis. American Journal of Clinical Nutrition. 2008;87(6):1825–1836.

Orth SR. Smoking and the kidney. Journal of the American Society of Nephrology. 2002;13(6):1663–1672.

Pedrini MT, Levey AS, Lau J, Chalmers TC, Wang PH. The effect of dietary protein restriction on the progression of diabetic and nondiabetic renal diseases: A meta-analysis. Annals of Internal Medicine. 1996;124(7):627–632.


Peterson JC, Adler S, Burkart JM, et al. Blood pressure control, proteinuria, and the progression of renal disease: the Modification of Diet in Renal Disease study. Annals of Internal Medicine. 1995;123(10):754–762.

Ravera M, Re M, Deferrari L, Vettoretti S, Deferrari G. Importance of blood pressure control in chronic kidney disease. Journal of the American Society of Nephrology. 2006;17(4 suppl 2):S98–S103.

Strippoli GFM, Bonifati C, Craig ME, Navaneethan SD, Craig JC. Angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists for preventing progression of diabetic kidney disease (review). Cochrane Database of Systematic Reviews. 2010. http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD006257/abstract. Accessed August 26, 2011.


Verhave JC, Hillege HL, Burgerhof JGM, et al. Sodium intake affects urinary albumin excretion especially in overweight subjects. Journal of Internal Medicine. 2004;256(4):324–330.

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CKD MNT Module 2: Slow Progression of Chronic Kidney Disease

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