NEPHROLOGY NURSING JOURNAL September-October 2009 Vol. 36, No. 5 465

Understanding Diabetes Mellitus And Kidney Disease

Diabetes mellitus is a major pub-lic health problem that hasr e a ched epidemic proportions.The statistics on diabetes are

staggering, with nearly 24 millionpeople in the U.S., or 8% of the pop-ulation, having diabetes. This is anincrease of more than 3 million peo-ple in the last two years. The morestaggering statistic is that of the 24million people with diabetes, almost 8million have not yet been diagnosed(American Diabetes Association[ A DA], 20 09a). In addition, 57 mil-lion Americans are diagnosed withpre-diabetes, a condition that putsone at risk for developing diabetes.This number will no doubt increasein years to come. The purpose of thisarticle is to define diabetes mellitus,describe appropriate criteria for diag-nosis, and explain the term pre-dia-betes. In addition, discussion of theconnection between diabetes and kid-ney disease is presented.

Diabetes Mellitus Defined

Diabetes mellitus is a group ofmetabolic diseases affecting the abili-ty of the pancreas to produce or usethe hormone insulin, affecting insulinsecretion, insulin action, or both.Diabetes mellitus is characterized byvariable and chronic hyperglycemiaand other disturbances of carbohy-drate, lipid, and protein metabolism.It is also associated with a variety ofvascular and neurologic changes thatresults in considerable morbidity andm o r t a l i t y.

Originally in 1979, the Na t i o n a lDiabetes Data Group (NDDG) devel-oped criteria for the classification anddiagnosis of diabetes mellitus. In 1997and again in 20 03, the ExpertCommittee on the Diagnosis andClassification of Diabetes Me l l i t u srecommended changes to the originalNDDG classification (Expert Co m m i t t e eon the Diagnosis and Classification ofDiabetes Mellitus, 20 03). Such

changes were supported by the ADAand the National Institute of Kidney,Digestive, and Kidney Diseases( NIDDK ) .

Previously, diabetes mellitus wasreferred to as insulin-dependent dia-betes mellitus (IDDM) or non-insulin-dependent diabetes mellitus (NIDDM ) .This terminology often created confu-sion with insulin therapy becomingpopular with both types of diabetes.

James A. Fain

Diabetes mellitus is a chronic disease that can cause serious long-term complicationswhen blood sugars are not well controlled. Damage to small microscopic blood vessels inthe kidney that filter out waste products from the blood can eventually cause kidney dis -ease. Over time, the kidneys become overworked and start to leak. Because the kidneys aregood at compensating for failing blood vessels, kidney disease produces no symptoms untilfunction is almost completely gone. The purpose of this article is to define diabetes melli -tus, describe appropriate criteria for diagnosis, and explain the term pre-diabetes. Inaddition, discussion of the connection between diabetes and kidney disease is presented.

Copyright 2009 American Nephrology Nurses’ Association

Fain, J.A. (20 09). Understanding diabetes mellitus and kidney disease. N e p h rology NursingJournal, 36(5), 465 - 470 .

GoalTo provide an overview of diabetes mellitus and how it affects individuals with kid-ney disease.

Objectives1 . Define diabetes mellitus.2 . Explain the differences between type 1 diabetes mellitus and type 2 diabetes mel-

l i t u s .3 . Discuss the emergence of diabesity.4 . Explain the term “pre-diabetes.”5 . Discuss the relationship between diabetes and kidney disease.

James A. Fain, PhD, RN, BC-ADM, FAAN, isDean and Professor, University of MassachusettsDartmouth, College of Nursing, North Dartmouth,MA, and Editor-in-Chief, The DiabetesEducator.

Statement of Disclosure: The author reported noactual or potential conflict of interest in relation tothis continuing nursing education article.

This offering for 1.3 contact hours is being provided by the American Nephrology Nurses’Association (ANNA).

ANNA is accredited as a provider of continuing nursing education (CNE) by the AmericanNurses Credentialing Center’s Commission on Accreditation.

ANNA is a provider approved by the California Board of Registered Nursing, provider numberCEP 00910.

This CNE article meets the Nephrology Nursing Certification Commission’s (NNCC’s) continu-ing nursing education requirements for certification and recertification.

NEPHROLOGY NURSING JOURNAL September-October 2009 Vol. 36, No. 5466

Understanding Diabetes Mellitus and Kidney Disease

IDDM is now referred to as type 1diabetes mellitus (T1DM) andNIDDM is referred to as type 2 dia-betes mellitus (T2DM). The ADArecommends using Arabic numerals,type 1 and type 2, rather than Ro m a nnumerals, when referring to eithertype of diabetes.

Classification of Diabetes

There are four major classifica-tions or clinical states associated withdiabetes, including T1DM, T2DM ,gestational diabetes mellitus (GDM ) ,and other specific types of diabetes.An overview of each classification isprovided in Table 1.

T 1 DM is an auto-immune disorderwhereby the immune system mistak-enly identifies body tissue, in this casebeta cells of the pancreas, as foreign.As beta cells are attacked anddestroyed, individuals are eventuallyrendered insulin deficient. T2DM isthe result of a progressive insulin secre-tory defect along with insulin resist-ance. Exactly why cells become resist-ant to insulin is uncertain, although agenetic predisposition to obesity exists,with increasing demands on the pan-creas destroying beta cells that pro-duce insulin. GDM is the name fordiabetes that can possibly develop dur-ing pregnancy. GDM typically devel-ops in response to hormones secretedduring pregnancy, increasing thebody’s resistance to insulin. GDM usu-ally occurs during the second half ofthe pregnancy (third trimester) andaffects approximately 4% of pregnantwomen in the U.S. Women who havehad GDM have a 40% to 60% ch a n c eof developing diabetes in the next 5 to10 years. Finally, other specific typesof diabetes may occur as a result ofgenetic defects in beta cell functionand insulin action, diseases of theexocrine pancreas, or diseases in-duced by certain drugs/medications( A DA, 20 09 b ).

What Is Insulin?

The pancreas is a large fish-shaped vascular gland stretching outto about 6 inches in length. It is locat-ed in the back of the abdominal cavi-ty (behind the stomach) and is respon-sible for regulating blood glucose lev-els. The head of the pancreas is on theright side of the abdomen and con-nected to the duodenum. The narrowend, or tail of the pancreas, extends tothe left side of the body. The pancreasregulates blood glucose levels bymanufacturing, storing, and releasing

the hormone insulin. The pancreasalso manufactures and releases otherhormones and digestive enzymes thathelp breakdown food and convert itinto glucose.

Insulin is a hormone produced bythe beta cells of the pancreas.Insulin’s major function is to regulateblood glucose levels, facilitating thetransport of blood glucose into bil-lions of cells that make up the body.The presence of insulin stimulatesglucose transporters to move to thesurface of cells and help facilitate glu-cose entry into cells. Insulin also stim-ulates centers in the hypothalamus ofthe brain responsible for hunger andsatiety (Guthrie & Guthrie, 20 04 ) .

Insulin maintains the narrowrange of normal levels of glucose inthe blood by regulation of the liverand muscles, directing them to manu-facture and store glycogen; a starch ysubstance the body uses when bloodsugar falls too low. If blood sugar fallslow, alpha cells of the pancreasrelease glucagon, another hormoneinvolved in regulating blood glucoselevels. Glucagon signals the musclesand liver to convert their storedglycogen back into glucose (a processcalled glycogenolysis), which raisesblood sugar. When the body’s storesof glucose and glycogen have beenexhausted, the liver, and to a lesserextent kidneys and small intestines,transform some of the body’s proteinstores (for example, muscle mass intoglucose) (Guthrie & Guthrie, 20 04 ) .

Type 1 Diabetes Mellitus

T 1 DM is the most frequentlyoccurring chronic illness of ch i l d-hood. T1DM has its highest incidenceamong infants and toddlers, with alarge number of adolescents present-ing with diabetes in early puberty(Urban & Grey, 20 06). T1DM usual-ly strikes children and young adults,although the onset of T1DM canoccur at any age, making itself appar-ent quite suddenly, with symptomss u ch as weight loss and frequent thirstand urination. T1DM accounts for5% to 10% of all diagnosed cases ofdiabetes.

Table 1

Classification of Diabetes

Mellitus

1 . Type 1 diabetes mellitus (beta cell

d e s t ruction leading to absolute

insulin deficiency)

2 . Type 2 diabetes mellitus (insulin

resistance with relative insulin defi-

c i e n c y )

3 . Gestational diabetes

4 . Other specific types of diabetes

A . Genetic defe c t s

1 . M i t o c h o n d rial DNA defe c t

2 . Wo l f ra m ’s syndrome

B. Genetic defects in insulin action

1 . L e p r e c h a u n i s m

2 . L i p o d y s t r o p hy

C. Diseases of the ex o c rine

p a n c r e a s

1 . Pa n c r e a t i t i s

2 . Pa n c r e a t e c t o my

3 . N e o p l a s i a

4 . Cystic fibrosis

5 . H e m o c h r o m a t o s i s

D. E n d o c ri n o p a t h i e s

1 . Cushing syndrome

2 . A c r o m e g a l y

3 . A l d o s t e r o n o m a

4 . H y p e rt hy r o i d i s m

E . D rug or chemical induced

1 . G l u c o c o rt i c o i d s

2 . T hyroid horm o n e

3 . T h i a z i d e s

4 . P h e nytoin (Dilantin®)

5 . D i a zox i d e

F. Other genetic syndromes

1 . D ow n ’s syndrome

2 . Tu rner syndrome

3 . P rader-Willi syndrome

4 . H u n t i n g t o n ’s chorea

5 . M yotonic dystrophy

S o u rc e : H a rmel & Mathur, 2004.

NEPHROLOGY NURSING JOURNAL September-October 2009 Vol. 36, No. 5 467

T 1 DM is an autoimmune diseaseresulting from a cell-mediated auto-immune destruction of pancreaticbeta cells. Markers of immunedestruction (such as auto-antibodiesto islet cells, glutamic acid decarboxy-lase [GAD], and tyrosine phosphalasein the islet cells) are present in 80% to85% of individuals with fasting hyper-glycemia (Harmel & Mathur, 20 04 ) .S u ch antibodies alone are not suffi-cient or necessary to make the diag-nosis of T1DM. In addition, environ-mental factors (such as viruses, food,toxins, and vaccinations) are suspect-ed to trigger an immune response thatlikewise destroys beta cells.

The rate of beta cell destruction isvariable but generally more rapid inchildren than adults. Once beta cellreserves are depleted, individuals areinsulin deficient and cannot survivewithout insulin being administered ona daily basis. Absent levels of insulinalso lead the liver, kidneys, and intes-tines to perform gluconeogenesis –turning the body’s protein stores(muscle) into even more glucose thatthe body cannot utilize. Me a n w h i l e ,the kidneys try to rid the body ofinappropriately high levels of sugar,causing frequent urination, insatiablethirst, and dehydration.

Type 2 Diabetes Mellitus

T 2 DM is the most common typeof diabetes, affecting 90% of all indi-viduals with diabetes. T2DM is usual-ly diagnosed after the age of 40 and ismore common in older adults andminority groups, including Me x i c a nAmericans, African Americans, Na t i v eAmericans, and Pacific Islanders.T 2 DM is frequently undiagnosed formany years because the elevatedblood glucose levels are not highenough to elicit the classic symptomsof uncontrolled diabetes (Skelly,20 06). It is estimated that the lengthof time between the onset of hyper-glycemia and the diagnosis of T2DMis 9 to 12 years (Harris, Klein,Welborn, & Kniuman, 1992).

T 2 DM is a chronic disease ch a r a c-terized by progressive beta cell dys-function and varying degrees of

insulin resistance. In addition to thebody being less sensitive or respon-sive to insulin, there is a reduced abil-ity of the pancreas to make andsecrete a sufficient amount of insulinto keep blood glucose levels normal.The body’s response to insulin resist-ance is to enhance secretion of insulinby the beta cells to maintain normalglucose homeostasis. The develop-ment of T2DM from the impairedglucose tolerance (IGT) state occursas the result of an organized sequenceof events. Initially, glycogenolysisincreases, resulting in enhanced basalglucose metabolism. This is commonin all individuals with T2DM. Insulinresistance tends to become greaterand peak when fasting hyperglycemiadevelops because of the degree ofglycemic load, aging, sedentarylifestyle, obesity, and other factorsaffecting insulin resistance and sensi-tivity (Harmel & Mathur, 20 04 ;Skelly, 20 06 ) .

Obesity is a major cause of insulinresistance. Approximately 80% to85% of individuals with T2DM areoverweight and affected by a particu-lar form of obesity referred to asabdominal, truncal, or visceral.Individuals with excess fat concen-trated in the abdominal area ratherthan generalized are more likely to beinsulin resistant. Abdominal fat alsomakes an individual more likely tohave abnormal blood fats (dyslipi-demia), an increase in harmful fats inthe blood (triglycerides), and adecrease in beneficial high- densitylipoprotein (HDL) ch o l e s t e r o l(Guthrie & Guthrie, 20 04; Skelly,20 06 ) .

The Emergence of Diabesity

The incidence of T2DM will con-tinue to be on the rise, with over 10 %of the U.S. population having dia-betes. At the same time, the increasein diabetes mellitus mirrors theincreased incidence of obesity, whichhas likewise reached epidemic pro-portions in the U.S. and around theworld. There are currently 45 millionobese adults in the U.S. (Kaufman,20 05). This is almost 30% of the adult

population, all of whom are at risk fordiabetes. As experts became alarmedby the closely linked epidemics ofobesity and T2DM, some beganreferring to the two as a single prob-lem, referring to this dual epidemic asD i a b e s i t y® (Kaufman, 20 05). ShapeUp America, an organization found-ed in 1994 by the former U.S.Surgeon General C. Everett Ko o p ,l a u n ched a diabesity initiative to raiseawareness of the growing prevalenceof obesity and diabetes in the US .The term “diabesity” was trade-marked as part of their efforts to rais-ing awareness of obesity as a publichealth issue while providing informa-tion on healthy weight management( Forman, 20 01 ) .

Diagnosing Diabetes

To diagnose diabetes, a blood testmust be drawn on two separate occa-sions. A fasting blood glucose is thebest indicator of overall glucosehomeostasis and is the preferredmethod of diagnosing diabetes. If anindividual’s fasting blood glucose isgreater than 126 mg/dL after an 8-hour fast, a diagnosis of diabetes isconfirmed. Fasting blood glucose lev-els between 100 and 125 mg/dL isreferred to as impaired fasting glucose(Expert Committee on the Diagnosisand Classification of DiabetesMellitus, 20 03; Harmel & Mathur,20 04). Impaired fasting glucose is nota clinical entity; rather, it is a risk fac-tor for the future development of dia-betes and macrovascular disease.

Symptoms associated with dia-betes mellitus include frequent urina-tion (polyuria), increased thirst orfluid intake (polydipsia), weight lossdespite hunger, and increased foodintake (polyphagia). A casual (ran-dom) blood glucose level greater than200 mg/dL is also indicative of a pos-itive diagnosis for diabetes (ExpertCommittee on the Diagnosis andClassification of Diabetes Me l l i t u s ,20 03; Harmel & Mathur, 20 04 ) .Casual blood glucose samples can bedrawn any time of the day withoutregard to fasting.

A postprandial blood glucose

NEPHROLOGY NURSING JOURNAL September-October 2009 Vol. 36, No. 5468

Understanding Diabetes Mellitus and Kidney Disease

level can also be used to diagnose dia-betes. Postprandial blood glucosesamples are drawn 2 hours after ameal and reflect the efficiency ofinsulin-mediated glucose uptake byperipheral tissue. The oral glucose tol-erance test (OGTT) is used to assesspostprandial glucose levels. Afterdrinking about 8 ounces of a sweetliquid (75 grams of glucose), bloodglucose levels are measured after onehour and again after two hours. If theblood glucose level is 200 mg/dL orabove after two hours, a diagnosis ofdiabetes is confirmed. A blood glu-cose level between 140 and 199mg/dL after two hours is referred toas impaired glucose tolerance (ExpertCommittee on the Diagnosis andClassification of Diabetes Me l l i t u s ,20 03; Harmel & Mathur, 20 04 ) .Impaired glucose tolerance is not aclinical entity; rather, it is a risk factorfor the future development of dia-betes and macrovascular disease.

P r e - D i a b e t e s

Individuals who have a plasma glu-

cose level higher than normal but notdiagnostic for diabetes are referred toas having pre-diabetes. This categoryincludes impaired fasting glucose val-ues between 100 and 125 mg/dL (6.1to 6.9 mmol/L) and impaired glucosetolerance with values between 140 and199 mg/dL (7.8 to 11 mmol/L) in a 2-hour sample after a 75 gram OGT T(Expert Committee on the Diagnosisand Classification of Diabetes Me l l i t u s ,2003; Harmel & Mathur, 2004).Impaired fasting glucose and impairedglucose tolerance are part of the con-tinuum that can lead to T2DM.Having pre-diabetes does not meanthat progressing to T2DM isinevitable. Individuals with pre-dia-betes can take measures to help delayor prevent T2DM by changing behav-iors associated with meal planning andphysical activity.

Pre-diabetes is becoming morecommon in the U.S. From 20 03 to20 06, almost 30% of adults in the U.S.age 20 or older had impaired fastingglucose (ADA, 20 09a). Applying thispercentage to the entire U.S. popula-tion in 20 07 resulted in an estimated 57

million American adults with pre-dia-betes. Healthcare providers havereferred to impaired fasting glucoseand impaired glucose tolerance as bor-derline diabetes for many years. Onlyrecently has the term pre-diabetesbeen used by the ADA. Pre-diabetes isa clearer way of explaining what itmeans to have higher than normalblood glucose levels. By any name, thediagnosis should serve as a loud warn-ing signal. Research results haveshown that every year about 10% ofindividuals with pre-diabetes willdevelop diabetes ( A DA, 20 09 a ) .

Individuals with pre-diabetes areable to bring down their blood glucoselevels sufficiently to enable their bod-ies to use insulin effectively. Lifestylechanges can prevent T2DM becauseof the Diabetes Prevention Pr o g r a m( DPP) Study. The DPP is a major clin-ical trial aimed at discovering whethermodest weight loss through healthyeating and increased physical activityor treatment with an oral diabetesmedication (metformin) could preventor delay the onset of T2DM in individ-uals with impaired glucose tolerance.Results of the DPP indicated that par-ticipants in the lifestyle interventiongroup (those receiving individualcounseling and motivational supporton healthy eating, increased exercise,and behavior modification) reducedtheir risk of developing diabetes by58%. This finding was true across allethnic groups for both men andwomen. Lifestyle changes worked par-ticularly well for participants aged 60and over, reducing their risk by 71 %(Diabetes Prevention Program Re s e a r chGroup, 20 02, 20 05 ) .

The ADA recommends screeningto detect pre-diabetes and T2DM inadults who are overweight (for exam-ple, BMI greater than 25 kg/m2) andone or more additional risk factors.Risk factors associated with pre-dia-betes and T2DM are described inTable 2.

Diabetes and Kidney Disease

Diabetes mellitus is the singlemost important cause of kidney dis-ease in the United States (U.S. Re n a l

Table 2

Risk Factors Associated with Pre-Diabetes and T2DM

• H aving a family member (parent, brother, sister) with diabetes

• H aving an ethnic/racial back ground that is African American, Mexican Ameri c a n ,N a t i ve American, Asian American, Pacific Islander

• H aving high blood pressure (for ex a m p l e, 130/85 or above) or being treated fo rhigh blood pressure

• H aving a body mass index (BMI) greater than 25 kg/m2 (20% above ideal we i g h t )with abdominal obesity; waist size of greater than 35 inches for women andgreater than 40 inches for men

• H aving high levels of tri g l y c e rides (for ex a m p l e, greater than 150 mg/dL) and lowl evels of high-density lipoprotein (HDL) cholesterol (less than 40 mg/dL in menand less than 50 mg/dL in wo m e n )

• H aving polycystic ova ry syndrome

• H aving impaired fasting glucose or impaired glucose tolera n c e

• H aving a history of art e riosclerotic vascular disease

• H aving a history of gestational diabetes or delive ry of a high-birt h weight infa n t( greater than 9 lbs)

• Being physically inactive

S o u rc e : A m e rican Diabetes Association, 2009a.

NEPHROLOGY NURSING JOURNAL September-October 2009 Vol. 36, No. 5 469

Data System [USRDS], 20 08 ) .Diabetic kidney disease (DKD) is amicrovascular complication (involv-ing small blood vessels that feed oxy-gen and nutrients to the kidneys) andis referred to as diabetic nephropathy.The kidneys are vital organs responsi-ble for filtering wastes, glucose, drugs,and other potentially toxic materialfrom the blood. Years of ch r o n i c a l l yelevated blood glucose damages thefiltering structures of the kidneys. Inaddition to elevated blood glucoselevels, uncontrolled high blood pres-sure can also accelerate the decline ofkidney function.

DKD has a similar natural historyas T2DM in that it takes years todevelop and deteriorate to end stagerenal disease (ESRD). A major con-cern is that in the early stages whenaggressive therapy can prevent theprogression of DKD, there are no rec-ognizable symptoms. By the timesymptoms of late stage kidney diseasepresent themselves, the opportunityto prevent progression has past.

Not all individuals with diabetesdevelop DKD, which occurs in 30 %to 40% of individuals with diabetes,with only one-third developing kid-ney failure. Most individuals with dia-betes who are going to have kidneyproblems show signs during the first10 years of diagnosis. If properlyscreened, early kidney changes canbe found within two or three years ofthe onset of high blood glucose levels( Yee, 20 08 ) .

The first detectable abnormality inthe course of DKD is the presence ofalbumin in the urine, referred to asmicroalbuminuria. Albumin is a pro-tein not normally found at all or onlyin very small amounts in urine.Individuals with microalbuminuriahave a high likelihood of experienc-ing decreased kidney function if leftuntreated. Individuals with T1DMare to be screened for microalbumin-uria once a year beginning 5 yearsfrom the time of diagnosis.

Individuals with T2DM are to bescreened once a year from the time ofdiagnosis (ADA, 20 09b). Sc r e e n i n gtests for microalbuminuria involve atimed urine collection for albumin (12or 24 hours). In addition, measuringthe ratio of albumin in the urine tocreatinine (another substance thatbecomes elevated with kidney dys-function) in the blood is a popular testbecause 12 or 24-hour urine collec-tion does not need to be performed.Urinary albumin collections aremeasured in micrograms of albuminper milligram of creatinine. No r m a lalbuminuria is less than 30 mcg/mg,with microalbuminuria defined as 30to 299 mcg/mg and macroalbumin-uria defined as greater than 30 0mcg/mg (ADA, 20 09 b ) .

S u m m a ry and “Take Home” Points

Diabetes mellitus is a major publichealth problem that is increasing bothin the U.S. and worldwide. In addi-tion, obesity has become widespreadin the U.S., with the term d i a b e s i t ybeing coined for the dual epidemic ofdiabetes and obesity. Identified riskfactors, such as glucose tolerance,hypertension, hyperlipidemia, andbeing physically inactive, often pre-cede and accompany the diagnosis ofT 2 DM. Guidelines for screening anddiagnosing diabetes have been rec-ommended, providing a basis forearly detection, treatment, and inter-vention. Results of the DiabetesPrevention Program indicated thatindividuals at risk for developing dia-betes can prevent or delay the onsetof diabetes by changing behaviorsassociated with meal planning andphysical activity.

R e f e re n c e sAmerican Diabetes Association (ADA ) .

( 20 09a). Diabetes statistics. Re t r i e v e dfrom http://w w w. d i a b e t e s . o r g / d i a-b e t e s - s t a t i s t i c s . j s p

American Diabetes Association (ADA ) .( 20 09b). Standards of medical care indiabetes – 20 09. Diabetes Care ,3 2(Suppl. 1), S13 - S 61.

Diabetes Prevention Program Re s e a r chGroup. (20 02). The DiabetesPrevention Program (DPP): De s c r i p t i o nof lifestyle intervention. Diabetes Care ,25, 2165 - 2171.

Diabetes Prevention Program Re s e a r chGroup. (20 05). Impact of intensivelifestyle and metformin therapy oncardiovascular disease risk factors inthe diabetes prevention program.Diabetes Care, 28, 888 - 894 .

Expert Committee on the Diagnosis andClassification of Diabetes Me l l i t u s .( 20 03). Follow-up report on diagnosisand classification of diabetes melli-tus. Diabetes Care, 26, 3160 - 3167.

Forman, A. (20 01). Shape Up Americahosts Diabetsity® conference. N u t r i t i o nToday, 36, 266 - 271.

Guthrie, R., & Guthrie, D. (20 04 ) .Pathophysiology of diabetes mellitus.Critical Care Nursing Quarterly, 27 ,113 -125 .

Harmel, A.P., & Mathur, R. (20 04 ) .Classification of diabetes mellitus. InA . P. Harmel & R. Mathur (Ed s . ) ,Davidson’s diabetes mellitus (pp. 1-22 ) .Philadelphia: Elsevier.

Harris, M.I., Klein, R., Welborn, T.A., &Kniuman, M.W. (1992). Onset ofNIDDM occurs at least 4-7 yearsbefore clinical diagnosis. D i a b e t e sC a re, 15, 815 .

Kaufman, F.R. (20 05). D i a b e s i t y. Ne wYork: Bantam Dell Books.

Skelly, A.H. (20 06). Type 2 diabetes mel-litus. Nursing Clinics of North Am e r i c a ,41, 531 - 547.

Urban, A.D., & Grey, M. (20 06 ) . Type 1diabetes. Nursing Clinics of NorthAm e r i c a. 41, 513 - 530 .

U.S. Renal Data System (USRDS ) .( 20 08). Annual data report: Atlas ofch ronic kidney disease and end- stagerenal disease in the United States.Bethesda, MD: National Institutes ofHealth (NIH), National Institute ofDiabetes and Digestive and KidneyDiseases (NIDDK ) .

Yee, J. (20 08). Diabetes kidney disease:Chronic kidney disease and diabetes.Diabetes Spectrum, 21, 8-10 .

NEPHROLOGY NURSING JOURNAL September-October 2009 Vol. 36, No. 5470

Understanding Diabetes Mellitus and Kidney Disease ANNJ0911

Complete the Follow i n g :

N a m e : _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _

A d d r e s s : _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _

_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _

Te l e p h o n e : ______________________ Email: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __

C N N : ___ Yes ___ No C D N : ___ Yes ___ No C C H T: ___ Yes ___ No

Pay m e n t :

ANNA Member: ____ Yes ____ No Member #___________________________

C h e ck Enclosed A m e rican Express Visa M a s t e r C a r d

Total Amount Submitted: _________________

Credit Card Number: _______________________________ Exp. Date: _______

Name as it Appears on the Card: ______________________________________

Online submissions through a partnership with HDCN.com are accepted on this posttest at $20 for ANNA members and $30 regular price. CNE certificates will be available immediately

upon successful completion of the posttest.

Posttest Instructions• Select the best answer and circle the

a p p r o p riate letter on the answer gri db e l ow.

• Complete the eva l u a t i o n .• Send only the answer fo rm to the

ANNA National Office; East HollyAve nue Box 56; Pitman, NJ 08071-0 0 5 6 ; or fax this fo rm to (856) 589-7 4 6 3 .

• Enclose a check or money orderp aya ble to ANNA. Fees listed in pay-ment section.

• If you receive a passing score of 70%or better, a certificate for the contacthours will be awarded by ANNA.

• Please allow 2-3 weeks for processing.You may submit multiple answer fo rm sin one mailing, howeve r, because ofva rious processing procedures fo reach answer fo rm, you may not receiveall of your certificates returned in onem a i l i n g .

Note: If you wish to keep the journal intact, you may photocopy the answer sheet or access this posttest atwww.annanurse.org/journal

A NSW ER/EVA L UAT ION FORMUnderstanding Diabetes Mellitus and Kidney Disease

James A. Fain, PhD, RN, BC- A DM, FA A N

Special Note

Your posttest can be processed in 1 week for an additional rush charge of $5.00.� Ye s, I would like this posttest rush processed. I have included an additional fe e

of $5.00 for rush processing.

1.3 Contact HoursExpires: October 31, 2011ANNA Member Price: $15

Regular Price: $ 2 5

1 . What would be different in your practice if you applied what you have learn e d

from this activity?

____________________________________________________________

____________________________________________________________

____________________________________________________________

____________________________________________________________

____________________________________________________________

Strongly Strongly

Evaluation disagree agree

2. By completing this offering, I was able to meet the stated objectivesa . Define diabetes mellitus. 1 2 3 4 5b. Explain the differences between type 1 diabetes mellitus and type 2 diabetes mellitus. 1 2 3 4 5c. Discuss the emergence of diabesity. 1 2 3 4 5d . Explain the term “ p r e - d i a b e t e s.” 1 2 3 4 5e. Discuss the relationship between diabetes and kidney disease. 1 2 3 4 5

3 . The content was current and releva n t . 1 2 3 4 54. This was an effective method to learn this content. 1 2 3 4 55. Time required to complete reading assignment: _________ minutes.

I verify that I have completed this activity ________________________________________________________________________________

(Signature)

To provide an overview of diabetes mellitusand how it affects individuals with kidneydisease.

Please note that this continuing nursing education activity does not

contain multiple-choice questions. This posttest substitutes the mul-

tiple-choice questions with an open-ended question. Simply answer

the open-ended question(s) directly above the evaluation portion of

the Answer/Evaluation Form and return the form, with payment, to

the National Office as usual.

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.