Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.
Module 2: Slow Progression of
Chronic Kidney Disease (CKD)
Hypertension, Diabetes, Urine Albumin,
and Cardiovascular Disea...
1. Use and interpret biochemical and patient data for
assessment of hypertension and CKD
2. Identify commonly prescribed c...
 Diabetes and hypertension are leading causes of
CKD in the United States.
 Urine albumin is a marker for kidney damage ...
 Chronic kidney disease
− Kidney function
 Glomerular filtration rate (GFR) < 60 mL/min/1.73 m2
for
> 3 months with or w...
Prevalence of co-morbidities by eGFR
Reference: Adapted from USRDS 2010 Annual Data Report
Prevalence of comorbidities by
urine albumin
Reference: Adapted from USRDS 2010 Annual Data Report
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 ...
Blood pressure is poorly controlled
in people with CKD
Reference: Adapted from USRDS 2009 Annual Data Report
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 pr...
A multinational epidemiological study found a
significant positive relationship between 24-hour
urinary sodium (Na) excret...
 About 90% of total sodium intake is from salt.
 Most (∼ 98%) is absorbed in small intestine.
 Sodium is freely filtere...
 ~ 60% in proximal tubule
 ~ 25% in loop of Henle
 5–7% in distal convoluted
tubule
 3–5% in collecting duct
Sodium is...
 Acid-base exchange
 Chloride dependent co-transporters
− Sodium, chloride, and/or potassium
 Aldosterone-sensitive cha...
 Renin is an enzyme produced by the juxtaglomerular
epitheloid cells in response to low renal perfusion.
 The renin-angi...
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 20...
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/...
 Original DASH
• “A diet rich in fruits, vegetables, and low-fat dairy
foods and with reduced saturated and total fat can...
DASH diet pattern for 2,000 calories
Reference: Your Guide to Lowering Your Blood Pressure with DASH, NIH Publication No.0...
The DASH combination diet pattern is higher
in protein and potassium
Reference: Adapted from Appel et al. N Engl J Med 199...
Urinary K increased with
increased K intake
Urea nitrogen reflected
protein intake
Urinary phosphorus (P)
may reflect prot...
 Compared to the control diet, the DASH combination
diet reduced systolic blood pressure (BP) by 5.5 mm
Hg and diastolic ...
 Typical and DASH pattern at different sodium levels
 3,450 mg; 2,300 mg; or 1,150 mg sodium
 Similar urinary excretion...
 The DASH pattern lowered blood pressure at all
levels of sodium intake.
 In the control diet, blood pressure was lowere...
Food Group Nutrients of Concern for CKD
Grains Whole grains: phosphorus,
potassium
Vegetables Potassium
Fruits Potassium
F...
 DASH and DASH-Sodium patterns lower blood
pressure.
 The lowest sodium level is the most effective, even
with the usual...
 Usually > 3 medications, including a diuretic
 1,500 mg sodium restriction
− Sodium restriction is key to blood pressur...
 These medications block aldosterone production,
and this may result in a reduction in potassium
excretion.
 The risk fo...
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
C...
 Specific level of eGFR does not determine need for
dietary potassium restriction.
 Restriction is to help achieve and m...
Serum potassium increases as
eGFR decreases
Reference: Adapted from USRDS 2009 Annual Data Report
 Their effects are beyond blood pressure control.
 They also reduce protein in the urine
(antiproteinuric).
 Sometimes ...
 Loop of Henle diuretics bind to co-transporter in loop
of Henle.
− Less sodium is reabsorbed, and blood pressure is
lowe...
 Assessment
− Potential food and anti-hypertensive medication
interactions (potassium)
 Intervention
− Control sodium in...
Case study: Food-medication interaction,
hyperkalemia, salt substitute
Reduced kidney function with high
level of urine al...
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 13...
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,...
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 4,4...
Breakfast Lunch Supper
2 fried eggs
•salt substitute
3–4 slices of bacon
3 slices of wheat
toast with soft
margarine
Coffe...
Food/beverage
intake
Recently stopped salt, now using salt substitute. Using orange juice
to treat low sugars. Includes ot...
 Food–medication interaction related to renal
dysfunction and blood pressure medication, as
evidenced by serum potassium ...
As eGFR declined, medication and
nutrient interaction increased serum K
 Initial nutrition education
 Priority modification: Reduce potassium intake by
eliminating salt substitute; use juice l...
Summary: CKD and hypertension
 BP ≤ 130/80 may be
beneficial for many
 Multiple medications
Assessment:
 Food–medicatio...
CONTROL DIABETES
Spontaneous 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 ...
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...
 Hyperfiltration
− The initial response to hyperglycemia is an increase in
GFR, followed by slow decline.
 Hypertrophy o...
Natural history of diabetic nephropathy:
hyperglycemia causes hyperfiltration,
may be followed by albuminuria
Reference: A...
 Advanced glycation end products (AGE) form by
nonenzymatic, sequential glycation and oxidation
reaction of sugars with f...
 Virtually any protein can be glycosylated.
 Slow turnover proteins are particularly prone to
modification.
− Glomerular...
 Receptors for AGEs upregulate as AGEs accumulate.
 Activation (binding) may induce release of pro-
inflammatory and pro...
 Glycohemoglobin (gHb) or glycosylated hemoglobin
 Sugars cross-link to hemoglobin
 Rate of formation is proportional t...
 A1C estimates average
glucose (eAG) level for past
2–3 months.
 eAG is similar to eGFR.
− Both “estimate” levels.
 Nor...
 < 1% of filtered insulin is excreted into urine.
 Insulin, pro-insulin, C-peptide are catabolized.
− About 1/3 total en...
Diabetes medications may be
discontinued or adjusted in CKD
Reference: Reilly & Berns Seminars in Dialysis 2010; 23(2):163...
Balancing Act
 Goal for the general population
− A1C < 7%
 Less stringent goal may be appropriate for:
− Frequent severe hypoglycemia
...
 There is evidence that control of newly diagnosed
diabetes may help prevent CKD.
− Type 1 diabetes (DM 1)
 Diabetes Con...
 Newly diagnosed, first 10 years
− Median age: 54 years (48–60 years)
 Intensive control defined as A1C < 7.0% (compared...
 The evidence is not strong.
 Control still matters for other organs.
 AGEs may have altered or destroyed slow turnover...
 45–60 grams per meal for most women
 60–75 grams per meal for most men
 15 grams per snack
 Adjust carbohydrates base...
Carbohydrate choice Nutrients of concern for CKD
Milk Protein, sodium, phosphorus,
potassium
Processed grains Sodium
Whole...
 Dietary protein may increase GFR and renal blood flow
rates. Animal protein may have greater effect than plant
protein.
...
 RDA = 0.8 g protein/kg body weight (wt)
 American Diabetes Association (2008) recommendations:
− Normal kidney function...
 Data are inconclusive for replacing animal protein
with vegetable protein to help lower urine albumin.
 Long-term consu...
 National Cholesterol Education Program (2002)
recommendations:
− 25–35% total calories from fat
 Saturated fat < 7% tot...
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 cata...
 The risk for hyperkalemia is increased in diabetic kidney
disease.
 Review medication list for ACEi or ARB.
− If prescr...
Any “juice” can treat hypoglycemia, even
those low in potassium
mg
Date 1/19 1/29 4/2 5/7 7/1
BP (mmHg) 168/98 138/82 136/78 142/60 146/70
Weight (lbs.) 200.5 196 191 189.4 189.4
eGFR (> 60...
Food/beverage
intake
Recently stopped salt, using salt substitute. Using orange juice to treat
low sugars. Includes other ...
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 skip...
Initial nutrition education
Priority modifications:
− Eat a small snack between brunch and supper on
weekends to prevent ...
 Renal threshold for glucose is 180–200 mg/dL.
 Sugars cross-linking to proteins changes their shapes
and functions (AGE...
 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 d...
 “Normal” UACR < 30 mg/g
− Current cut-off used to define normal levels
 Persistent UACR > 30 mg/g means kidney damage
...
 Increased glomerular permeability allows albumin
(and other proteins) to pass into the urine.
 Higher levels of protein...
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, Februa...
 Their effects are beyond blood pressure control.
 They also reduce protein in the urine.
 Sometimes these medications ...
 Dose-dependent increase in urine albumin in the
general population
 Independent predictor of elevated urine albumin in
...
 Literature review showed weight loss was associated
with decreased proteinuria.
− Dietary restrictions
− Exercise
− Anti...
 In the Netherlands, higher sodium intake was
associated with increased urine albumin excretion.
 In a 2006 literature r...
 The type of protein may make a difference.
 Animal protein may be associated with higher urine
albumin excretion.
 The...
 Two or more servings of red meat per week may increase
risk of microalbuminuria.
− Nurses Health Study (Lin J et al., 20...
 Baseline AER < 7 mg/24 hr.
− No difference found in AER between diet patterns at 8
weeks.
 Baseline AER ≥ 7 mg/24 hr.
−...
DASH: Baseline urine albumin may affect
AER response to change in dietary protein
Reference: Adapted from Jacobs et al., 2...
 A 1996 meta-analysis found low-protein diet may
slow increase in urinary albumin level in insulin-
dependent diabetes.
...
 Control blood pressure
 Reduce sodium intake
 Achieve good control of diabetes early; may help
prevent albuminuria
 R...
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
 Nut...
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
 Dyslipidemi...
 Increased triglycerides
− May be very elevated with massive proteinuria
(nephrotic syndrome)
 Decreased high-density li...
 Target lipid levels in CKD are unknown and may be
similar to those for the general population.
 Persons with CKD should...
 Statins reduce hepatic cholesterol synthesis.
 Statins significantly reduce all-cause and CVD
mortality in persons with...
 Inflammation may modify risk relationship between
cholesterol and CVD in this population.
 In patients with normal C-re...
 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 f...
 Spreads may reduce LDL cholesterol by 15%.
 Effectiveness in CKD patients is unknown.
 Spreads vary in sodium and calo...
 25–30 grams total fiber suggested per day.
 7–13 grams soluble fiber/day may reduce LDL.
 Effectiveness in CKD is unkn...
Legumes are rich in potassium and
phosphorus; counsel appropriately
References: http://www.nhlbi.nih.gov/health/public/hea...
Some fruits with soluble fiber are rich in
potassium; counsel appropriately
References: http://www.nal.usda.gov/fnic/foodc...
 More than 90% of phosphorus is absorbed from food
additives containing phosphorus.
− Read ingredient list for phosphorus...
 Nontraditional risk factors include:
− Albuminuria
− Anemia
− Abnormal calcium and phosphorus metabolism
 Statins are u...
Summary: CKD and hypertension
Assessment:
 Food–medication
interaction
− Hyperkalemia
 ACEi (____pril)
 ARBs (___sartan...
 Urine albumin excretion is associated with diabetic
kidney disease, but not all people will have high
urine albumin leve...
 Renal threshold for glucose is 180–200 mg/dL.
 Sugars cross-linking to proteins change their shapes and
functions (AGEs...
 Urine albumin is a marker of kidney damage.
 Control blood pressure.
− Particularly with high urine albumin, control is...
 Nontraditional risk factors include:
− Abnormal urine albumin
− Anemia
− Abnormal calcium and phosphorus metabolism
 St...
An educational handout you can use
to get started
Reference: http://www.nkdep.nih.gov/resources/nkdep-factsheet-overallpat...
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 initiat...
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 N...
Andrew S. Narva, M.D., F.A.C.P.
Dr. Narva is the director of the National Kidney Disease
Education Program (NKDEP) at the ...
American Dietetic Association. International Dietetics and Nutrition
Terminology (IDNT) Reference Manual: Standardized Lan...
Ellison DH. Chapter 2. Disorders of sodium balance. In: Berl T,
Bonventre JV, eds. Atlas of Disease of the Kidney. Vol. 1....
Institute of Medicine. Dietary Reference Intakes for Water,
Potassium, Sodium, Chloride, and Sulfate. Washington, D.C.:
Na...
Kunz R, Friedrich C, Wolbers M, Mann JFE . Meta-analysis: effect of
monotherapy and combination therapy with inhibitors of...
National Kidney Foundation Kidney Disease Outcome Quality
Initiative (KDOQI). Clinical practice guidelines for chronic kid...
Ravera M, Re M, Deferrari L, Vettoretti S, Deferrari G . Importance of
blood pressure control in chronic kidney disease. J...
Schiffrin EL, Lipman ML, Mann JFE. Chronic kidney disease effects on
the cardiovascular system. Circulation. 2007;116(1):8...
U.S. Department of Agriculture and U.S. Department of Health and
Human Services. Dietary Guidelines for Americans, 2010. 7...
Adler AI, Stevens RJ, Manley SE, et al. Development and progression
of nephropathy in type 2 diabetes: the United Kingdom
...
American Dietetic Association. International Dietetics & Nutrition
Terminology (IDNT) Reference Manual: Standardized Langu...
Cavanaugh KL. Diabetes management issues for patients with
chronic kidney disease. Clinical Diabetes. 2007;25(3):90–97.
Fr...
Gross JL, de Azevedo MJ, Silveiro SP, Canani LH, Caramori ML,
Zelmanovitz T. Diabetic nephropathy: diagnosis, prevention, ...
Molitch ME, Steffes M, Sun W, et al. Development and progression of
renal insufficiency with and without albuminuria in ad...
Reilly JB, Berns JS. Selection and dosing of medications for
management of diabetes in patients with advanced kidney
disea...
UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-
glucose control with sulphonylureas or insulin compared with...
U.S Renal Data System. USRDS 2010 Annual Data Report: Atlas of
Chronic Kidney Disease and End-Stage Renal Disease in the
U...
Afshinnia F, Wilt TJ, Duval S, Esmaeili A, Ibrahim HN. Weight loss
and proteinuria: systematic review of clinical trials a...
De Zeeuw D, Remuzzi G, Parving H, et al. Proteinuria, a target for
renoprotection in patients with type 2 diabetic nephrop...
Kunz R, Friedrich C, Wolbers M, Mann JFE. Meta-analysis: effect of
monotherapy and combination therapy with inhibitors of ...
Quick reference on UACR and GFR in evaluating patients with
diabetes and kidney disease. National Kidney Disease Education...
Peterson JC, Adler S, Burkart JM, et al. Blood pressure control,
proteinuria, and the progression of renal disease: the
Mo...
Verhave JC, Hillege HL, Burgerhof JGM, et al. Sodium intake affects
urinary albumin excretion especially in overweight sub...
Astor BC, Hallan SI, Miller ER III, Yeung E, Coresh J. Glomerular
filtration rate, albuminuria, and risk of cardiovascular...
Kendrick J, Chonchol MB. Nontraditional risk factors of
cardiovascular disease in patients with chronic kidney disease.
Na...
National Cholesterol Education Program. Third report of the National
Cholesterol Education Program (NCEP) Expert Panel on ...
National Kidney Disease Education Program. Your kidney test results.
Revised September 2011 . NIH publication 11–7407. Nat...
Ruan XZ, Varghese Z, Moorhead JF. An update on the lipid
nephrotoxicity hypothesis. Nature Reviews Nephrology.
2009;5(12):...
U.S. Department of Agriculture and U.S. Department of Health and
Human Services. Dietary Guidelines for Americans, 2010. 7...
Upcoming SlideShare
Loading in …5
×

CKD MNT Module 2: Slow Progression of Chronic Kidney Disease

14,398 views

Published on

This module reviews how intake of certain nutrients is reflected in urinary excretion; which antihypertensive medications increase the risk for hyperkalemia in CKD; and how diabetes control impacts CKD and how CKD progression may impact diabetes control. Interventions to lower albuminuria and control lipids in CKD are discussed. Using a case study format, follow Frank's journey as he rapidly approaches kidney failure to see how the diet and medications may interact in hypertension and diabetes in CKD.
At the end, you will be introduced to two other educational resources from NKDEP, Eating Right for Kidney Health and Your Kidney Test Results, and see how to use them when counseling patients.

Published in: Health & Medicine
  • I was needing Statement under 37 cfr 373b form yesterday and was informed of an online service that hosts a lot of sample forms . If people are searching for Statement under 37 cfr 373b form too , here's a https://goo.gl/Yior5j.
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here

CKD MNT Module 2: Slow Progression of Chronic Kidney Disease

  1. 1. Module 2: Slow Progression of Chronic Kidney Disease (CKD) Hypertension, Diabetes, Urine Albumin, and Cardiovascular Disease
  2. 2. 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:
  3. 3.  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
  4. 4.  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
  5. 5. Prevalence of co-morbidities by eGFR Reference: Adapted from USRDS 2010 Annual Data Report
  6. 6. Prevalence of comorbidities by urine albumin Reference: Adapted from USRDS 2010 Annual Data Report
  7. 7. CONTROL BLOOD PRESSURE Hypertension is the second leading cause of CKD in the United States
  8. 8.  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
  9. 9. Blood pressure is poorly controlled in people with CKD Reference: Adapted from USRDS 2009 Annual Data Report
  10. 10. Hypertension may cause CKD, and CKD may cause worsening hypertension
  11. 11.  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.
  12. 12. 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
  13. 13.  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.
  14. 14.  ~ 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
  15. 15.  Acid-base exchange  Chloride dependent co-transporters − Sodium, chloride, and/or potassium  Aldosterone-sensitive channel Sodium is reabsorbed by numerous mechanisms along the tubules
  16. 16.  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.
  17. 17. RAAS helps control sodium and potassium excretion
  18. 18. 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
  19. 19. Lifestyle modifications for blood pressure (BP) have not been studied extensively in the CKD population
  20. 20. The DASH diet lowers blood pressure in the general population Reference: http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/new_dash.pdf
  21. 21.  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.
  22. 22. 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/day Grains (mostly whole) 6–8 Vegetables 4–5 Fruits 4–5 Fat-free, low-fat milk, and milk products 2–3 Meats, poultry, and fish ≤6 ounces (oz.) Nuts, seeds, and legumes 4–5 per week Fats and oils 2–3 Sweets and added sugars ≤ 5 tablespoons (Tbsp.) per week
  23. 23. 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
  24. 24. 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 Combinati on Diet Potassium Run-in Intervention Change 1,385 1,531 146 1,459 2,757 1,298 1,416 2,916 1,500 Urea Nitrogen Run-in Intervention Change 8,592 9,026 434 8,775 9,456 681 8,729 11,583 2,834 Phosphorus Run-in Intervention Change 699 742 713
  25. 25.  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
  26. 26.  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
  27. 27.  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.
  28. 28. Food Group Nutrients of Concern for CKD Grains Whole grains: phosphorus, potassium Vegetables 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
  29. 29.  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
  30. 30.  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
  31. 31.  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
  32. 32. ACEi medications block the RAAS and increase the risk for hyperkalemia
  33. 33. ARBs block the RAAS and increase the risk of hyperkalemia
  34. 34. 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
  35. 35.  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
  36. 36. Serum potassium increases as eGFR decreases Reference: Adapted from USRDS 2009 Annual Data Report
  37. 37.  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.
  38. 38.  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)
  39. 39.  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
  40. 40. 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
  41. 41. 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 mg Diet changes Told to use less salt “stopping salt, trying salt substitute” Missed 2/19 RD appt
  42. 42. 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
  43. 43. 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
  44. 44. Breakfast Lunch Supper 2 fried eggs •salt substitute 3–4 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 food Double 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 substitute 2–3 slices bread 1 c. canned corn or peas Hot tea with artificial sweetener Uses orange juice to treat low sugars (↑ frequency) Frank’s “usual” diet intake
  45. 45. 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)
  46. 46.  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
  47. 47. As eGFR declined, medication and nutrient interaction increased serum K
  48. 48.  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
  49. 49. 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
  50. 50. CONTROL DIABETES Spontaneous improvement in diabetes control may indicate progression of kidney disease
  51. 51.  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
  52. 52. Diabetes is the leading cause of ESRD in the United States Reference: USRDS 2010 Annual Data Report
  53. 53.  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.
  54. 54.  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.
  55. 55. Natural history of diabetic nephropathy: hyperglycemia causes hyperfiltration, may be followed by albuminuria Reference: Adapted from Friedman, 1999
  56. 56.  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.
  57. 57.  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.
  58. 58.  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.
  59. 59.  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
  60. 60.  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
  61. 61.  < 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
  62. 62. Diabetes medications may be discontinued or adjusted in CKD Reference: Reilly & Berns Seminars in Dialysis 2010; 23(2):163–168.
  63. 63. Balancing Act
  64. 64.  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
  65. 65.  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
  66. 66.  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
  67. 67.  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
  68. 68.  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)
  69. 69. Carbohydrate choice Nutrients of concern for CKD Milk Protein, sodium, phosphorus, potassium Processed grains Sodium Whole grains Phosphorus, potassium Legumes Protein, phosphorus, potassium Starchy vegetables Potassium Fruit Potassium Sweets and added sugars May have added phosphorus Type of carbohydrate may matter in DKD
  70. 70.  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.
  71. 71.  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
  72. 72.  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;
  73. 73.  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
  74. 74. Guidelines provide guidance, but we still need to individualize
  75. 75. Spontaneous improvement and/or increased frequency of hypoglycemia may indicate CKD is progressing
  76. 76.  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.”
  77. 77.  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
  78. 78. Any “juice” can treat hypoglycemia, even those low in potassium mg
  79. 79. Date 1/19 1/29 4/2 5/7 7/1 BP (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
  80. 80. 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)
  81. 81. As eGFR declined, Frank’s DM medication was reduced, then changed
  82. 82.  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 Reference: American Dietetic Association, 2010
  83. 83. 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 Reference: American Dietetic Association, 2010
  84. 84.  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
  85. 85.  Baseline urine albumin level may predict risk of CKD progression Urine albumin
  86. 86.  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
  87. 87.  “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
  88. 88.  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
  89. 89. Risk factors for albuminuria Reference: de Jong & Brenner. Kidney Int 2004; 66(6):2109–2118.
  90. 90. 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.
  91. 91.  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.
  92. 92.  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.
  93. 93.  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.
  94. 94.  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.
  95. 95.  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
  96. 96.  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
  97. 97.  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.
  98. 98. DASH: Baseline urine albumin may affect AER response to change in dietary protein Reference: Adapted from Jacobs et al., 2009
  99. 99.  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.
  100. 100.  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
  101. 101. For Frank, an elevated urine albumin is a marker of kidney damage and prognosticator for rapid progression of CKD
  102. 102. CARDIOVASCULAR DISEASE CVD is the leading cause of morbidity and mortality in people with CKD
  103. 103.  CVD risks and CKD − Traditional − Nontraditional  Pattern of dyslipidemia in CKD  Statins  Nontraditional risks  Nutrition interventions Topics
  104. 104. Lipid abnormalities may increase as eGFR declines Reference: Astor et al. Am J Epidemiol 2008; 167(10):1226–1234.
  105. 105. 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
  106. 106.  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.
  107. 107.  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
  108. 108.  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.
  109. 109.  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.
  110. 110.  Albuminuria  Anemia  Abnormal metabolism of calcium and phosphorus Nontraditional risk factors for CVD
  111. 111.  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
  112. 112.  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.
  113. 113.  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.
  114. 114. 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
  115. 115. 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
  116. 116.  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.
  117. 117.  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
  118. 118. 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.
  119. 119.  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. Summary: CKD and diabetes
  120. 120.  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. Summary: CKD and diabetes
  121. 121.  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
  122. 122.  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
  123. 123. An educational handout you can use to get started Reference: http://www.nkdep.nih.gov/resources/nkdep-factsheet-overallpatient-508.pdf
  124. 124. Reference: http://www.nkdep.nih.gov/resources/nkdep-factsheet-overallpatient-508.pdf
  125. 125. Another educational tool you can start using: Reference: http://www.nkdep.nih.gov/resources/nkdep-ckd-amt-guide-508.pdf
  126. 126. 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.
  127. 127. 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
  128. 128. 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
  129. 129. American Dietetic Association. International Dietetics and Nutrition Terminology (IDNT) Reference Manual: Standardized Language for the Nutrition Care Process. 3rd ed. Chicago, IL: American Dietetic Association; 2011. American Dietetic Association evidence analysis library. Recommendations Summary Hypertension (HTN): Food/Nutrient- Medication Interactions. American Dietetic Association website. http://www.adaevidencelibrary.com/template.cfm? key=1965&cms_preview=1. April 2008. Accessed June 13, 2011. Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure. New England Journal of Medicine. 1997;336(16):1117–1124. 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. References: Hypertension
  130. 130. Ellison DH. Chapter 2. Disorders of sodium balance. In: Berl T, Bonventre JV, eds. Atlas of Disease of the Kidney. Vol. 1. http://www.kidneyatlas.org/book1/ADK1_02.pdf . 1999. Accessed June 19, 2011. Geleijnse JM, Kok FJ, Grobbee DE. Blood pressure response to changes in sodium and potassium intake: a metaregression analysis of randomised trials. Journal of Human Hypertension. 2003;17(7):471–480. 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. References: Hypertension
  131. 131. Institute of Medicine. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, D.C.: National Academy Press; 2004. Institute of Medicine website. http://iom.edu/Reports/2004/Dietary-Reference-Intakes-Water- Potassium-Sodium-Chloride-and-Sulfate.aspx. Accessed June 13, 2011. Intersalt Cooperative Research Group. Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion. British Medical Journal. 1988;297(6644):319–328. Jafar TH, Stark PC, Schmid CH, et al. Progression of chronic kidney disease: the role of blood pressure control, proteinuria, and angiotensin-converting enzyme inhibition: a patient level meta- analysis. Annals of Internal Medicine. 2003;139(4):244–252. References: Hypertension
  132. 132. 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. National Heart Lung Blood Institute. Your guide to lowering your blood pressure with DASH. Revised April 2006. NIH publication 06–4082. National Heart, Lung, and Blood Institute website. http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/new_dash .pdf Accessed June 13, 2011. References: Hypertension
  133. 133. National Kidney Foundation Kidney Disease Outcome Quality Initiative (KDOQI). Clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. American Journal of Kidney Diseases. 2002;39(2 suppl 1):S18–S266. National Kidney Foundation website. http://www.kidney.org/professionals/KDOQI/guidelines_ckd/toc.h tm. Accessed August 31, 2011. Neter JE, Stam BE, Kok FJ, Grobbee DE, Geleijnse JM. Influence of weight reduction on blood pressure: a meta-analysis of randomized control trials. Hypertension. 2003;42(5):878–884. Palmer BF. Managing hyperkalemia caused by inhibitors of the renin- angiotensin- aldosterone system. New England Journal of Medicine. 2004;351(6):585–592. References: Hypertension
  134. 134. 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. References: Hypertension
  135. 135. 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. References: Hypertension
  136. 136. 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/DietaryGuidelin es2010.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. References: Hypertension
  137. 137. 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
  138. 138. 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. References: Diabetes
  139. 139. 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. References: Diabetes
  140. 140. 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. References: Diabetes
  141. 141. 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. References: Diabetes
  142. 142. 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. Schmidt AM, Yan SD, Yan SF, Stern DM. The multiligand receptor RAGE as a progression factor amplifying immune and inflammatory responses. Journal of Clinical Investigation. 2001;108(7):949–955. The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. New England Journal of Medicine. 1993;329(14):977–986. References: Diabetes
  143. 143. 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. U.S. Department of Agriculture. Agricultural Research Service. 2010. USDA National Nutrient Database for Standard Reference, Release 23. Search the USDA national nutrient database for standard reference. U.S. Department of Agriculture website. http://www.nal.usda.gov/fnic/foodcomp/search/ Accessed August 30, 2011. References: Diabetes
  144. 144. 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. Wrone EM, Carnethon MR, Palaniappan L, Fortmann SP. Associations of dietary protein intake and microalbuminuria in healthy adults: Third National Health and Nutrition Examination Survey. American Journal of Kidney Diseases. 2003;41(3):580–587. References: Diabetes
  145. 145. 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
  146. 146. 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. References: Albuminuria
  147. 147. 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.pd f. Accessed June 13, 2011. References: Albuminuria
  148. 148. 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. References: Albuminuria
  149. 149. 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. References: Albuminuria
  150. 150. 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. Wrone EM, Carnethon MR, Palaniappan L, Fortmann SP. Association of dietary protein intake and microalbuminuria in healthy adults: Third National Health and Nutrition Examination Survey. American Journal of Kidney Diseases. 2003;41(3):580–587. References: Albuminuria
  151. 151. Astor BC, Hallan SI, Miller ER III, Yeung E, Coresh J. Glomerular filtration rate, albuminuria, and risk of cardiovascular and all- cause mortality in the US population. American Journal of Epidemiology. 2008;167(10):1226–1234. Beto JA, Bansal VK. Nutrition interventions to address cardiovascular outcomes in chronic kidney disease. Advances in Chronic Kidney Disease. 2004;11(4):391–397. Contreras G, Hu B, Astor BC, et al. Malnutrition-inflammation modifies the relationship of cholesterol with cardiovascular disease. Journal of the American Society of Nephrology. 2010;21(12):2131–2142. Kalantar-Zadeh K, Gutekunst L, Mehrotra R, et al. Understanding sources of dietary phosphorus in the treatment of patients with chronic kidney disease. Clinical Journal of the American Society of Nephrology. 2010;5(3):519–530. References: Cardiovascular Disease (CVD)
  152. 152. Kendrick J, Chonchol MB. Nontraditional risk factors of cardiovascular disease in patients with chronic kidney disease. Nature Clinical Practice Nephrology. 2008;4(12):672–681. Kwan BCH, Kronenberg F, Beddhu S, Cheung AK. Lipoprotein metabolism and lipid management in chronic kidney disease. Journal of the American Society of Nephrology. 2007;18(4):1246–1261. Molitch ME. Management of dyslipidemias in patients with diabetes and chronic kidney disease. Clinical Journal of the American Society of Nephrology. 2006;1(5):1090–1099. References: Cardiovascular Disease (CVD)
  153. 153. 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. National Cholesterol Education Program. Your guide to lowering your cholesterol with TLC. December 2005. NIH publication 06–5235. National Heart, Lung, and Blood Institute website. http://www.nhlbi.nih.gov/health/public/heart/chol/chol_tlc.pdf . Accessed June 19, 2011. National Kidney Disease Education Program. Eating right for kidney health tips for people with chronic kidney disease (CKD). Revised March 2011. NIH publication 11–7405. National Kidney Disease Education Program website. http://www.nkdep.nih.gov/resources/nkdep-factsheet- overallpatient-508.pdf. Accessed June 13, 2011 . References: Cardiovascular Disease (CVD)
  154. 154. National Kidney Disease Education Program. Your kidney test results. Revised September 2011 . NIH publication 11–7407. National Kidney Disease Education Program website. http://nkdep.nih.gov/resources/nkdep-kidney-test-results- 508.pdf. Accessed September 8,, 2011 . Navaneethan SD, Pansini F, Perkovic V, et al. HMG CoA reductase inhibitors (statins) for people with chronic kidney disease not requiring dialysis. Cochrane Database of Systematic Reviews. 2009. http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD007784/ abstract. Accessed August 26, 2011. Ninomiya T, Perkovic V, de Galan BE, et al. Albuminuria and kidney function independently predict cardiovascular and renal outcomes in diabetes. Journal of the American Society of Nephrology. 2009;20(8):1813–1821. References: Cardiovascular Disease (CVD)
  155. 155. Ruan XZ, Varghese Z, Moorhead JF. An update on the lipid nephrotoxicity hypothesis. Nature Reviews Nephrology. 2009;5(12):713–721. Rucker D, Tonelli M. Cardiovascular risk and management in chronic kidney disease. Nature Reviews Nephrology. 2009;5(5):287–296. Schiffrin EL, Lipman ML, Mann JFE. Chronic kidney disease: effects on the cardiovascular system. Circulation. 2007;116(1):85–97. Smogorzewski M. The myopathy of statins. Journal of Renal Nutrition. 2005;15(1):87–93. U.S Department of Agriculture. Agricultural Research Service. 2010. USDA National Nutrient Database for Standard Reference, Release 23. Search the USDA national nutrient database for standard reference. U.S. Department of Agriculture website. http://www.nal.usda.gov/fnic/foodcomp/search/ Accessed August 30, 2011. References: Cardiovascular Disease (CVD)
  156. 156. 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.cnpp.usda.gov/Publications/DietaryGuidelines/2010/P olicyDoc/Chapter3.pdf . 2010. Accessed June 14, 2011. Van Horn L, McCoin M, Kris-Etherton PM, et al. The evidence for dietary prevention and treatment of cardiovascular disease. Journal of the American Dietetic Association. 2008;108(2):287– 331. References: Cardiovascular Disease (CVD)

×