Chronic Kidney Disease (CKD) and Diet:

Assessment, Management, and Treatment

Treating CKD Patients Who Are Not on Dialysis

An Overview Guide for Dietitians

Revised April 2015
Table of Contents

I. About CKD .............................................................................................................................1

II. Assess Kidney Function and Damage ......................................................................2

III. Slow Progression................................................................................................................3

IV. Prevent, Monitor, and Treat Complications ............................................................5

V. Patient Education Materials .......................................................................................... 11

VI. References ..........................................................................................................................12
CKD and Diet | Assessment, Management, and Treatment 1

This document, developed by the National Kidney Disease Education Program (NKDEP), is intended to help registered dietitians (RDs) provide effective medical nutrition therapy (MNT) to CKD patients who are not on dialysis. 

I. About CKD

The kidneys regulate the composition and volume of blood, 

remove metabolic wastes in the urine, and help control the acid/

base balance in the body. They activate vitamin D needed for 

calcium absorption and produce erythropoietin needed for 

red-blood-cell synthesis.

CKD is typically a progressive disease. It is defined as:

n Reduction of kidney function—defined as an estimated 

glomerular filtration rate (eGFR) < 60 mL/min/1.73 m2 and/

 or

n Evidence of kidney damage, including persistent 

albuminuria—defined as > 30 mg of urine albumin 

per gram of urine creatinine 

Kidney failure is typically defined as an eGFR < 15 mL/min/1.73 m2.

CKD is detected and monitored by two tests:

n Estimated glomerular filtration rate (eGFR) and 

n Urine albumin-to-creatinine ratio (UACR) 

The purpose of diet therapy for CKD is to maintain good nutritional 

status, slow progression, and to treat complications. 

The key diet components to slowing progression of CKD are:

n Controlling blood pressure by reducing sodium intake 

n Reducing protein intake, if excessive

n Managing diabetes

As eGFR declines, complications occur more commonly and 

are more severe. These may include: 

n Malnutrition 

n Metabolic acidosis due to reduced acid (hydrogen ion) 

excretion

n Hyperkalemia

n Mineral imbalance and bone disorder (calcium, phosphorus, 

and vitamin D)

n Anemia due to impaired erythropoiesis and low iron stores

n Cardiovascular disease (CVD) (dyslipidemia)

CKD RISK FACTORS

Diabetes

Hypertension

Family history of kidney failure

Cardiovascular disease

Recurrent urinary tract infections

HIV infection

Immunological diseases
2

II. Assess Kidney Function and Damage

Test and Its Relevance Results Dietary Intervention

Estimated 

Glomerular 

Filtration Rate (eGFR) 

eGFR estimates kidney function. 

As eGFR declines, complications 

are more likely and more severe.

eGFR (mL/min/1.73m2)

Not diagnostic of CKD ≥ 60 

CKD 15–59 

Kidney failure < 15

● Evaluate eGFR to assess kidney function; track over time to monitor effectiveness of 

 diet therapy. 

● Stable eGFR may indicate therapy is working.

● Decline of eGFR reflects progression of CKD. 

Additional Information 

Each filtering unit of the kidney, or nephron, filters a tiny amount of plasma each minute. 

eGFR reflects the total filtration of all two million nephrons. As nephrons are damaged or 

destroyed, eGFR declines. The quantity or volume of urine may not change significantly 

as eGFR declines. However, what is excreted into the urine does change. Rapidly 

declining eGFR may warrant appropriate discussion of renal replacement therapies. 

In adults, recommended equations for estimating eGFR from serum creatinine include the 

Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) and Modification of Diet in 

Renal Disease (MDRD) Study equations (Levey et al, 1999; Levey et al, 2006; Levey et al, 

2009). NKDEP offers online calculators for estimating GFR from both CKD-EPI and MDRD 

Study equations. Serum creatinine level, age, gender, and race are needed for both 

calculators. Many laboratories routinely report eGFR with all serum creatinine 

determinations.

Urine Albumin-toCreatinine Ratio 

(UACR) 

UACR is the preferred measure 

for screening, assessing, and 

monitoring kidney damage. 

UACR estimates 24-hour urine 

albumin excretion. Unlike a dipstick test for urine albumin, UACR 

is unaffected by variation in urine 

concentration.

UACR (mg/g)

Normal 0–30 

Albuminuria > 30

● Evaluate UACR over time to assess response to therapy and monitor progression of CKD. 

● Elevated albuminuria may reflect higher risk for progression.

● A decrease in urine albumin may reflect response to therapy and may be associated with 

improved renal and cardiovascular outcomes.

Additional Information 

Each filtering unit of the kidney, or nephron, filters a tiny amount of plasma each minute. 

eGFR reflects the total filtration of all two million nephrons. As nephrons are damaged or 

destroyed, eGFR declines. The quantity or volume of urine may not change significantly as 

eGFR declines. However, what is excreted into the urine does change. Rapidly declining 

eGFR may warrant appropriate discussion of renal replacement therapies. 
3

III. Slow Progression 

Therapeutic Goal and 

Its Relevance Ranges/Goals Dietary Intervention

Control Blood 

Pressure 

Blood pressure control slows 

progression of CKD and lowers 

CVD risk.

Sodium plays a large role in 

Less than 140/90 mmHg ● Limit sodium intake to 2,300 mg a day or less (IOM, 2013). 

● Weight reduction may be beneficial.

● Monitor serum potassium in patients on renin angiotensin aldosterone system (RAAS) 

antagonists; limit dietary potassium intake when serum potassium > 5 mEq/L. 

Additional Information 

blood pressure control in CKD as 

a result of alterations in sodium 

excretion by the kidneys.

For patients with hypertension, reduction of dietary sodium has been associated with 

improved blood pressure control in clinical trials and epidemiological studies.

Multiple medications may be required to control blood pressure. RAAS antagonists, such 

as angiotensin-converting enzyme inhibitors (ACEi) or angiotensin receptor blockers 

(ARBs), are often used to control blood pressure, delay progression, reduce albuminuria, 

and protect against heart disease. These medications increase the risk of hyperkalemia.

Diuretics are prescribed to treat fluid overload and high blood pressure, and may help 

control serum potassium levels.

Reduce Albuminuria 

Decreased albuminuria is 

associated with slower progression of CKD, particularly in diabetics. Limiting dietary protein 

may reduce albuminuria and 

improve blood glucose control, 

hyperlipidemia, blood 

pressure, renal bone disease, 

and metabolic acidosis. (de 

Zeeuw et al, 2004).

Reduce or stabilize the amount of 

albumin lost in the urine 

(see UACR on page 2).

Limit excessive dietary protein as follows: 

● Nondiabetic: 0.8 g protein/kg/day.

● Diabetic: 0.8-1.0 g protein/kg/day.

Evidence suggests that further lowering to 0.6 g protein/kg/day in nondiabetic patients 

may be beneficial, but adherence is difficult. Some patients may be able to achieve this 

level with intensive counseling.

Additional Information 

Limiting excessive protein may activate adaptive responses that decrease albuminuria 

and increase serum albumin, without increasing risk for protein malnutrition. 

Reducing excessive protein also decreases nitrogen, phosphorus, and potassium intake. 

CKD and Diet | Assessment, Management, and Treatment
4 CKD and Diet | Assessment, Management, and Treatment

III. Slow Progression (continued)

Therapeutic Goal and 

Its Relevance Ranges/Goals Dietary Intervention

Manage Diabetes 

Blood glucose control may 

help slow progression of CKD 

(DCCT,1993; UKPDS,1998)

Good control of newly diagnosed 

diabetes may slow progression 

of CKD. Tight control in diabetes 

of long duration may not be 

indicated. 

Individualize A1C/eAG goal 

eAG = estimated average glucose

● Consider less-stringent control for patients with histories of hypoglycemia, the elderly, 

and patients with multiple co-morbid conditions. 

● Instruct patients to treat hypoglycemia with cranberry juice cocktail, grape or apple juice, 

glucose tablets, or 10 jelly beans to prevent hyperkalemia.

Additional Information 

As eGFR declines, renal metabolism of insulin and certain oral diabetes medications is 

reduced, potentially causing hypoglycemia in diabetes (Snyder and Berns, 2004). 

Unexplained improvement in glucose control may reflect progression of CKD.

Low-protein diets have been associated with improved insulin sensitivity and fasting 

serum insulin levels, lower insulin requirements and blood glucose levels, and a decrease 

in endogenous glucose production in patients with diabetes.
CKD and Diet | Assessment, Management, and Treatment 5

IV. Prevent, Monitor, and Treat Complications

Data is limited for CKD. Many of the recommendations for CKD are extrapolated from renal replacement therapies literature.

Complication and Its 

Relevance Ranges/Goals Dietary Intervention

Malnutrition 

Malnutrition is common in CKD; 

as eGFR declines, so may appetite. Malnutrition in CKD patients 

is associated with increased 

morbidity and mortality.

Albumin > 4.0 g/dL

Normal range: 3.4–5.0 g/dL

Serum albumin < 4.0 g/dL, 

prior to initiation of dialysis, may 

predict morbidity and mortality 

(Kaysen et al, 2008). 

Blood urea nitrogen (BUN) 

< 20 mg/dL

● Manage with adequate calories and nutrients. 

● A low protein diet (0.6 g/kg) may require supplemental riboflavin and cyanocobalamin. 

Supplemental pyridoxine may be beneficial due to medication-vitamin interactions. 

 It may be prudent to provide adequate amounts of thiamin and folic acid. High doses 

of vitamin C are not recommended. Data do not support routine supplementation with 

niacin and vitamins A, E, and K. In advanced CKD, certain vitamins may accumulate due 

to reduced excretion (Steiber & Kopple, 2011). 

Additional Information 

Serum albumin is used to monitor nutritional status. Hypoalbuminemia may result from 

reduced protein and/or calorie intake, uremia, metabolic acidosis, albuminuria, inflammation, or infection.

Although not used to indicate nutritional status, elevated BUN may be associated with aversion to certain high-biological-value protein foods. Appetite may improve in renal failure 

with adequate renal replacement therapy (i.e., dialysis treatment or kidney transplantation).

Metabolic Acidosis 

Patients with CKD are at risk for 

metabolic acidosis as a result of 

reduced excretion of acid load.

Bicarbonate (CO2) > 22 mEq/L

Normal range: 21–28 mEq/L

● Dietary protein is a source of metabolic acid. Serum bicarbonate levels may increase with 

dietary protein restriction. (Gennari et al, 2006) 

● Sodium bicarbonate supplementation may be prescribed to improve nutritional parameters and slow rate of CKD progression (de Brito-Ashurst et al, 2009). Monitor blood 

pressure closely when this medication is used, as some patients may experience elevated 

blood pressure associated with increased sodium load.

Additional Information 

Metabolic acidosis is thought to result in loss of bone and muscle mass, negative nitrogen 

balance, increased protein catabolism, and decreased protein synthesis (ibid).
6

IV. Prevent, Monitor, and Treat Complications (continued)

Complication and Its 

Relevance Ranges/Goals Dietary Intervention

Hyperkalemia 

Patients with CKD are at risk 

for hyperkalemia as a result of 

reduced potassium excretion, 

intake of high-potassium foods, 

metabolic acidosis, and medications that inhibit potassium excretion, such as RAAS antagonists 

for blood pressure control.

Potassium: 3.5–5.0 mEq/L

Hyperkalemia is usually not seen 

until CKD is advanced, but may 

be seen at higher eGFRs in 

people with diabetes.

● Counsel patients to restrict dietary potassium when serum level is 5.0 mEq/L or higher. 

● Caution patients to avoid potassium-containing salt substitutes. 

● Instruct patients with diabetes to treat hypoglycemia with cranberry juice cocktail, grape 

or apple juice, glucose tablets, or 10 jelly beans to prevent hyperkalemia. 

● Counsel patients to adhere to sodium bicarbonate therapy, if prescribed. Correction of 

acidosis may lower potassiums. 

Additional Information 

The potassium content of most vegetables can be decreased through a process of leaching. 

Leaching entails slicing and soaking the vegetable overnight in water, then draining and 

boiling the vegetable in new water. A recent study, however, shows that white potatoes do 

not need to be soaked overnight (Bethke & Jansky, 2008). The potassium content of other 

tuberous root vegetables commonly eaten in the Caribbean and South America has been 

shown to be reduced somewhat by double-cooking, however, most still remained higher 

than 200 mg per serving (Burrowes & Ramer, 2006).
CKD and Diet | Assessment, Management, and Treatment 7

IV. Prevent, Monitor, and Treat Complications (continued)

Complication and Its 

Relevance Ranges /Goals Dietary Intervention

CKD Mineral and 

Bone Mineral 

Disorder (CKD-MBD)

CKD-MBD is renal bone disease 

that occurs when the kidneys fail 

to maintain serum calcium and 

phosphorus levels.

See sections on calcium, 

phosphorus, parathyroid 

hormone (PTH), and vitamin D.

Existing guidelines on management of CKD-MBD reflect consensus rather than high-grade 

evidence. Early intervention may help prevent vascular calcification and secondary hyperparathyroidism.

The kidneys maintain calcium and phosphorus levels and activate vitamin D. As kidney function declines, complex interactions occur that affect calcium, phosphorus, vitamin D, and the 

parathyroid gland. Abnormal levels of PTH (measured as intact or iPTH) may be seen. Mineral 

and bone disorders may result from these interactions. See the specific sections that follow.

Additional Information 

Depending on the type of renal bone disease, calcium, phosphorus, and iPTH may be normal, decreased, or elevated (Martin & Gonzales, 2007).

• Secondary hyperparathyroidism is associated with high bone turnover, and elevated 

levels of calcium, phosphorus, iPTH, and alkaline phosphatase. 

• Osteomalacia results in low bone turnover with elevated serum calcium levels and 

normal-to-decreased serum phosphorus, iPTH, and alkaline phosphatase.

• Adynamic bone disease results in low bone turnover and may be characterized by 

normal-to-low iPTH and alkaline phosphatase. Serum calcium and phosphorus may be 

normal to elevated. 

• Mixed bone disease, as the name implies, has features of both low and high 

bone turnover.

Calcium Calcium: 8.5–10.2 mg/dL ● Dietary calcium recommendations for CKD have yet to be established.

Control of calcium and phospho- Maintain within normal range. ● Calcium-based phosphate-binding medications can increase total daily intake and elevate 

rus levels helps control PTH. calcium.

● Supplementation with active vitamin D increases the risk for hypercalcemia.

● Use formula to correct calcium with hypoalbuminemia: 

Corrected calcium (mg/dL) = serum calcium (mg/dL) + 0.8 (4.0 - serum albumin g/dL)
8

IV. Prevent, Monitor, and Treat Complications (continued)

Complication and Its 

Relevance Ranges /Goals Dietary Intervention

Phosphorus

Control of phosphorus and 

calcium levels helps control PTH.

Phosphorus: 2.7–4.6 mg/dL

Maintain within normal range. 

Serum phosphorus levels may be 

“normal” until CKD is advanced

● If serum phosphorus is elevated, dietary phosphorus restriction may be indicated. 

The recommended level of restriction has yet to be determined in CKD.

● Dietary protein restriction decreases phosphorus intake. If further restriction is needed, 

counsel patients to reduce intake of foods with added phosphorus. (Uribarri, 2007).

● Counsel patients to read ingredient lists for “phos” to identify foods with phosphate additives, as these additives may be absorbed more efficiently than food sources.

● Limiting whole grains may help if further reduction is needed.

● Phosphorus binders may be prescribed to lower phosphorus levels. Counsel patients to 

take binders with meals to help limit absorption of phosphorus from food and beverages.

Additional Information 

Calcium acetate and calcium carbonate are common calcium-containing phosphate binders. Calcium citrate is not recommended as a phosphate binder for CKD patients because it 

may increase aluminum absorption. Other binders, used more often in renal replacement 

therapy, are typically composed of resins (sevelamer carbonate) and earth metals (lanthanum carbonate).

Parathyroid Hormone 

(PTH) 

Secondary hyperparathyroidism 

(elevated PTH) is associated with 

the most common cause of bone 

disease in CKD.

Normal PTH < 65 pg/mL

Measured as iPTH

PTH varies by level of kidney 

function and type of bone 

disease

Dietary phosphorus restriction and use of active vitamin D or its analogs may help control 

PTH levels in CKD. Calcium supplementation may help as well.

Additional Information 

PTH is the hormone that regulates serum calcium levels. Low levels of 1,25(OH)2D, hypocalcemia, and hyperphosphatemia stimulate PTH secretion. Its metabolic actions include 

mobilizing calcium and phosphorus from bone, increasing intestinal absorption and renal 

tubular reabsorption of calcium, and decreasing renal tubular reabsorption of phosphorus. 

PTH enhances conversion of 25(OH)D to 1,25(OH)2D.
CKD and Diet | Assessment, Management, and Treatment 9

IV. Prevent, Monitor, and Treat Complications (continued)

Complication and Its 

Relevance Ranges /Goals Dietary Intervention

Vitamin D Vitamin D ≥ 20 ng/mL ● Supplementation may be indicated. Specific requirements in CKD have yet to be 

The kidneys activate 25(OH) Measured as 25(OH)D determined.

D (calcidiol) to 1,25(OH)2D 

(calcitriol or active vitamin D). 

Reduction of kidney function 

results in decreased production 

and conversion of calcidiol to 

Maintain within normal range 

(IOM, 2011).

● Ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3) may be used in early CKD to 

replete vitamin D.

● Active vitamin D (calcitriol) or its analogs (doxercalciferol, paricalcitol, or alfacalcidol) 

may be used as eGFR declines (ibid). 

calcitriol. There may be corre- Monitor for hypercalcemia and/or hyperphosphatemia when using supplements. 

sponding imbalances of calcium, Active vitamin D increases calcium and phosphorus absorption.

phosphorus, and PTH.

Anemia 

Anemia may develop early during the course of CKD due to 

inadequate synthesis of erythropoietin by the kidneys.

Hemoglobin 11–12 g/dL

Without CKD: 

Women: 12–16 g/dL 

Men: 14-17 g/dL

Transferrin Saturation (TSAT) >20%

Ferritin > 100 ng/mL

 Without CKD:

Women: 18–160 ng/mL 

Men: 18–270 ng/mL

Both iron supplementation and injectable erythropoiesis-stimulating agents (ESAs) have 

been used to correct anemia. The risks and benefits of these treatments in CKD are not 

yet defined. (Besarab & Coyne, 2010).

Additional Information 

Hemoglobin is used to assess anemia in CKD. Uncomplicated anemia of CKD is usually 

normocytic and normochromic.

TSAT is a measure of iron saturation. Transferrin transports iron absorbed by the intestines. 

Ferritin levels reflect iron stores. Existing guidelines regarding TSAT and ferritin levels in 

CKD reflect consensus rather than high grade evidence.
10

IV. Prevent, Monitor, and Treat Complications (continued)

Complication and Its 

Relevance Ranges/Goals Dietary Intervention

Cardiovascular 

Disease (CVD)

Patients with CKD are at high 

risk for developing CVD; the 

risk increases as eGFR declines.

CVD is the leading cause of 

mortality in CKD.

Total cholesterol < 200 mg/dL

LDL cholesterol < 100 mg/dL

HDL cholesterol > 40 mg/dL

Triglycerides < 150 mg/dL

Decreasing intake of saturated and trans fats (substituting for monounsaturated and 

polyunsaturated fats), along with physical activity, can help control hyperlipidemia and 

reduce inflammation.

Additional Information 

Controlling dyslipidemia may reduce the rate of decline in eGFR. 

To further decrease risk of developing CVD, pharmacological therapy may be necessary 

(Fried et al, 2001).

Nontraditional risk factors for CVD include anemia, albuminuria, and abnormal calcium 

and phosphorus metabolism (Kendrick & Choncol, 2008).
CKD and Diet | Assessment, Management, and Treatment 11

V. Patient Education Materials 

NKDEP offers a suite of materials to support RDs in providing MNT to patients with CKD. These free materials—designed to distill key 

information about CKD and diet for RDs and patients—are available to download in English and Spanish from the NKDEP website at 

nkdep.nih.gov/nutrition.

	 n Eating Right for Kidney Health: Tips for People with CKD—a handout on the basics of nutrition and CKD

	 n Nutrition Tips for People with CKD—individual nutrient handouts on: 

● Protein

● Phosphorus

● Potassium

● Sodium

● Food-label reading 

	 n Your Kidney Test Results—a tool for assessment and education of test results with patients 
12

VI. References 

Besarab A, Coyne DW. Iron Supplementation to Treat Anemia in 

Patients with Chronic Kidney Disease. Nature Reviews. Nephrology. 

2010;6(12): 699-710.

Bethke PC, Jansky SH. The Effects of Boiling and Leaching on the 

Content of Potassium and Other Minerals in Potatoes. Journal of 

Food Science. 2008;73(5):H80-85.

Burrowes JD, Ramer NK. Removal of Potassium from Tuberous Root 

Vegetables by Leaching. Journal of Renal Nutrition. 2006;16(4):

304-311.

de Brito-Ashurst I, Varagunam M, Raftery MJ, Yaqoob MM. 

Bicarbonate Supplementation Slows Progression of CKD and 

Improves Nutritional Status. Journal of the American Society of 

Nephrology. 2009;20(9):2075-2084.

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.

Diabetes Control and Complications Trial (DCCT) Research Group. 

The Effect of Intensive Treatment of Diabetes on the Development 

and Progression of Long-Term Complications in InsulinDependent Diabetes Mellitus. New England Journal of Medicine. 

1993;329(14):977-986.

Fried LF, Orchard TJ, Kasiske BL for the Lipids and Renal Disease 

Progression Meta-Analysis Study Group. Effect of Lipid Reduction 

on the Progression of Renal Disease: A Meta-Analysis. Kidney 

International. 2001;59(1):260-269.

Gennari FJ, Hood VL, Greene T, Wang X, Levey AS. Effect of Dietary 

Protein Intake on Serum Total CO2 Concentration in Chronic 

Kidney Disease: Modification of Diet in Renal Disease Study 

Findings. Clinical Journal of the American Society of Nephrology. 

2006;1(1):52-57.

Hemmelgarn BR, Manns BJ, Lloyd A et al. Relation Between Kidney 

Function, Proteinuria, and Adverse Outcomes. Journal of the 

American Medical Association. 2010;303(5):423-429.

IOM (Institute of Medicine). Dietary Reference Intakes for 

Calcium and Vitamin D. Washington, DC: The National Academies 

Press; 2011.

IOM (Institute of Medicine). Dietary Reference Intakes for Vitamin 

A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, 

Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. 

Washington, D.C.: National Academy Press; 2001. 

IOM (Institute of Medicine). Sodium Intake in Populations: 

Assessment of Evidence. Washington, D.C.: National Academy 

Press; 2013. 

James PA, Oparil S, Carter BL, Cushman WC, DennisonHimmelfarb C, Handler J, Lackland DT, LeFevre ML, MacKenzie 

TD, Ogedegbe O, Smith SC Jr, Svetkey LP, Taler SJ, Townsend RR, 

Wright JT Jr, Narva AS, Ortiz E. 2014 evidence-based guideline 

for the management of high blood pressure in adults: report 

from the panel members appointed to the Eighth Joint National 

Committee (JNC 8). JAMA. 2014; 311(5):507-20. 
CKD and Diet | Assessment, Management, and Treatment 13

VI. References

Kaysen GA, Johansen KL, Cheng S, Jin C, Chertow GM. Trends 

and Outcomes Associated with Serum Albumin Concentrations 

Among Incident Dialysis Patients in the United States. Journal of 

Renal Nutrition. 2008; 18(4):323-331. 

Kendrick J, Chonchol MB. Nontraditional Risk Factors for 

Cardiovascular Disease in Patients with Chronic Kidney Disease. 

Nature Clinical Practice Nephrology. 2008;4(12):672-681. 

Levey, AS, Bosch, JP, Breyer Lewis, J, Greene T, Rogers N, Roth D 

for the Modification of Diet in Renal Disease Study Group. A More 

Accurate Method to Estimate Glomerular Filtration Rate from 

Serum Creatinine: A New Prediction Equation. Annals of Internal 

Medicine. 1999;130(6):461-470. 

Levey AS, Coresh J, Greene T, Stevens LA, Zhang YL, Hendriksen 

S, Kusek JW, Van Lente F; Chronic Kidney Disease Epidemiology 

Collaboration. Using standardized serum creatinine values in 

the modification of diet in renal disease study equation for 

estimating glomerular filtration rate. Ann Intern Med. 2006 Aug 

15;145(4):247-54.

Levey AS, Stevens LA, Schmid CH, Zhang YL, Castro AF, 3rd, 

Feldman HI, et al. A new equation to estimate glomerular 

filtration rate. Ann Intern Med. 2009;150(9):604-12.

Martin KJ, Gonzalez EA. Metabolic Bone Disease in Chronic 

Kidney Disease. Journal of American Society of Nephrology. 

2007;18(3):875-885. 

Snyder RW, Berns JS. Use of Insulin and Oral Hypoglycemic 

Medications in Patients with Diabetes Mellitus and Advanced 

Kidney Disease. Seminars in Dialysis. 2004;17(5):365-370.

Steiber AL, Kopple JD. Vitamin Status and Needs for People with 

Stages 3-5 Chronic Kidney Disease. Journal of Renal Nutrition. 

2011;21(5):355-368. 

UK Prospective Diabetes Study Group: Intensive BloodGlucose Control with Sulphonylureas or Insulin Compared with 

Conventional Treatment and Risk of Complications in Patients with 

Type 2 Diabetes (UKPDS 33). The Lancet. 1998;352(9131):837-853.

Uribarri J. Phosphorus Homeostasis in Normal Health and in 

Chronic Kidney Disease Patients with Special Emphasis on Dietary 

Phosphorus Intake. Seminars in Dialysis. 2007;20(4):295-301.
The National Kidney Disease Education Program (NKDEP) works to improve the understanding, detection,

 and management of kidney disease. NKDEP is a program of the National Institutes of Health (NIH). 

www.nkdep.nih.gov 

Revised April 2015 • NIH Publication No. 15-7406 • NIH...Turning Discovery Into Health®

National Kidney Disease

Education Program