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Module 1:

Kidney Disease Basics


Andrew Narva, MD, FASN &
Amy Barton Pai, PharmD, MHI, FASN, FCCP, FNKF
Faculty Disclosure Information

Andrew Narva, MD, FASN


No financial disclosures/conflicts of interest

Amy Barton Pai, PharmD, MHI, FASN, FCCP, FNKF


Disclosure: Consultant for Keryx

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About NKDEP
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 health system change to facilitate effective CKD detection and management.

To learn more about NKDEP, please visit: http://www.nkdep.nih.gov. For additional materials from NIDDK,
please visit: http://www.niddk.nih.gov.

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Meet our Presenters
Amy Barton Pai, PharmD, MHI, FASN, FCCP, FNKF

Dr. Barton Pai is Chair of the National Kidney Disease Education Program’s Pharmacy
Working Group
Dr. Amy Barton Pai, Pharm.D., MHI, FASN, FCCP, FNKF is Associate Professor of
Clinical Pharmacy at the University of Michigan College of Pharmacy. She obtained her
Bachelor of Science in Pharmacy from Albany College of Pharmacy in 1996 and then
completed a Pharmacy Practice Residency at St. Peter’s Hospital in Albany, New York.
She received her Doctor of Pharmacy from Albany College of Pharmacy in 1999. From
1999-2001 she was a Nephrology Research Fellow at the University of Illinois at
Chicago. Dr. Pai was on faculty at the University of New Mexico College of Pharmacy
and School of Medicine from 2001 to 2008 and at Albany College of Pharmacy and
Health Sciences from 2008 to 2016. She earned a Master's degree in Healthcare
Innovation in 2018.

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Meet our Presenters
Andrew S. Narva, M.D., F.A.C.P.

Dr. Narva is the Director of the National Kidney Disease Education Program
(NKDEP) at the National Institutes of Health. Prior to joining the NKDEP in 2006, he
served as Director of the Kidney Disease Program for the Indian Health Service
(IHS). Dr. Narva continues to serve as the Chief Clinical Consultant for Nephrology
for IHS and to provide care for patients at Zuni Pueblo through a telemedicine clinic.
Dr. Narva is a member of the American Board of Internal Medicine Nephrology
Subspecialty Board. He has served as a member of the Eighth Joint National
Committee (JNC 8) Expert Panel, the National Quality Forum Renal Steering
Committee, the Kidney Disease Outcomes Quality Initiative Work Group on Diabetes
in Chronic Kidney Disease, and the Medical Review Board of End Stage Renal
Disease Network 15.

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After completing this module, you will be able to:

• Describe kidney anatomy and physiologic functions


• Define and discuss the pathophysiology of chronic kidney disease
(CKD)
• Calculate estimated glomerular filtration rate (eGFR) and urine
albumin-to-creatinine ratio (UACR) to assess kidney function and
kidney damage and to determine diagnosis
• Describe the burden of chronic kidney disease in the US and how
pharmacists can improve outcomes for patients

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Kidneys and collecting system

• Kidneys
Kidneys
• Ureters
• Bladder
• Urethra
Ureters

Bladder
Urethra Image source: National Kidney Disease Education Program

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The nephron
Bowman’s
Capsule
Afferent
arteriole

Efferent
arteriole Glomerulus

Renal vein
• Glomerulus
Collecting duct
• Proximal tubule
• Loop of Henle Loop of Henle
with capillary
• Distal tubule network

• Collecting duct

Tubule Image source: National Kidney Disease Education Program

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The nephron functions to maintain balance
Bowman’s
Capsule
Afferent
arteriole
The functions include:
•Filtration Efferent
arteriole Glomerulus
 Glomeruli generate
ultrafiltrate of the plasma. Renal vein
•Reabsorption Collecting duct
 Tubules selectively reabsorb
substances from the Loop of Henle
with capillary
ultrafiltrate. network
•Secretion
 Tubules secrete substances
into the urine.

Tubule Image source: National Kidney Disease Education Program

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Glomeruli generate ultrafiltrate via
specialized capillary
• The specialized capillary tufts are located between the
afferent and efferent arterioles.
• Pressure differences result in a gradient
and movement of solutes across the semipermeable
glomerular basement membrane.

Image source: National Kidney Disease Education Program

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Filtration is based on size and charge

• Small solutes cross readily


• Larger substances are
generally restricted
• Negatively charged molecules
are restricted

Image source: National Kidney Disease Education Program

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Ultrafiltration of plasma is the main function of the
glomeruli

• Volume of ultrafiltrate = 135–180 liters(L)/day


• 99% water reabsorbed -> 1–1.5 L urine excreted

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The ultrafiltrate is modified by the tubules
• Reabsorption and secretion of substances occurs within the
tubules. Examples:

• Potassium (K) is reabsorbed from and secreted into the urine

• Sodium (Na) is generally reabsorbed

• Organic acids are secreted into the urine.

• Many drugs are actively secreted (e.g. cephalexin, renal clearance


rate 252 mL/min) or reabsorbed (e.g. levofloxacin, renal clearance
rate 96 mL/min)

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What happens in the tubules?
• Reabsorption and secretion of substances occurs within the
tubules.
Proximal Loop of Henle Distal Tubule Collecting
Tubule Duct

Sodium 67% 25% 5% reabsorbed 3% reabsorbed


reabsorbed reabsorbed

Potassium 80-90% - Actively Reabsorption


reabsorbed secreted when mediated by
high K+ intake aldosterone
occurs

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The kidneys have many functions
• Regulatory function
 Control composition and volume of blood
 Maintain stable concentrations of inorganic anions such as sodium (Na), potassium (K), and
calcium (Ca)
 Maintain acid-base balance

• Excretory function
 Produce urine
 Remove metabolic wastes
 Including nitrogenous waste

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The kidneys have many functions

• Endocrine function
 Produce renin for blood pressure control
 Produce erythropoietin which stimulates bone marrow
production of red blood cells
 Activate 25(OH)D to 1,25 (OH)2D (active vitamin D)

• Metabolic function
 Gluconeogenesis
 Metabolize drugs and endogenous substances (e.g., insulin)

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The kidneys are involved with drug excretion and
metabolism

Some drug transporters are located in the kidney (e.g., ATP-Binding cassette
transporters, P-glycoprotein, organic anion transporters, solute
carrier transporters)
Schwenk MH, Pai AB. Adv Chronic Kidney Dis 2016;23:76-81
Image source: National Kidney Disease Education Program

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The kidneys are involved with drug excretion and
metabolism
Metabolize:
•Drugs (e.g., Glucuronidation, Sulfonation)
•Endogenous substances (e.g., insulin)

Schwenk MH, Pai AB. Adv Chronic Kidney Dis 2016;23:76-81


Image source: National Kidney Disease Education Program

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CKD usually means fewer functioning nephrons.

Image source: National Kidney Disease Education Program

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Fewer nephrons disrupt the balance
• Urine volume may not change
 Composition of the urine changes
• Reduced waste excretion
 May not be apparent until CKD is advanced
• Altered hormone production
 Anemia (erythropoietin) and mineral & bone disorders
(vitamin D)
• Reduced catabolism
 Examples: Insulin, glucagon, drugs

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Fewer nephrons disrupt the balance

• Reduced renal clearance and accumulation of


 Advanced glycation end products
 Pro-inflammatory cytokines
 Reactive oxygen species (oxidation)
 Metabolic acids
• Insulin resistance (even in non-diabetics)
 Reduces insulin-mediated glucose uptake in skeletal muscles
 May be associated with inflammation as well

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Glomerular injury
• Glomerular disease is the most common type of
kidney disease.
• With disease progression, the vascular tuft is
replaced by scar tissue and function is lost.
• Damage to the filter allows larger molecular weight
substances such as albumin into the ultrafiltrate.
• Increased urine protein may be a cause as well as a
sign of kidney injury.

Image source: National Kidney Disease Education Program

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Risk factors for CKD

• Diabetes

• Hypertension

• Family history of kidney disease

• Cardiovascular disease

• Obesity

• Acute kidney injury

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Terms Used to Described States of Reduced GFR
1998 and 1999 ASN Abstracts
1. Chronic renal failure 13. Renal failure
2. Chronic renal insufficiency 14. Renal disease
3. Mild renal insufficiency 15. Renal insufficiency
4. Moderate chronic renal insufficiency 16. Predialysis
5. Moderate or advanced renal insufficiency 17. Mildly elevated serum creatinine
6. Severe renal insufficiency 18. Chronic renal failure patients not on
7. Renal dysfunction dialysis
8. Severe renal dysfunction 19. Pre–end-stage chronic renal failure
9. Decreased renal function 20. Pre–end-stage renal disease chronic renal
10. Pre–end-stage renal disease failure
11. Low clearance (predialysis) patients 21. Mild renal failure
12. Pre-uremic 22. Chronic renal disease
23. Chronic renal failure requiring dialysis
AJKD 2000; 36:415-418

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CKD, regardless of etiology, is reduced kidney
function and/or kidney damage
• Chronic Kidney Disease
 Kidney function
 Glomerular filtration rate (GFR) < 60 mL/min/1.73 m 2 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, i.e., proteinuria (albuminuria)
 Urine albumin-to-creatinine ratio (UACR) > 30 mg/g

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Each kidney has about 1 million nephrons; slow loss
may not be noticeable

• Large physiologic reserve.

• Slow, progressive loss of functioning nephrons may


not be noticeable.

• Often, there are no symptoms until more than three-


quarters of kidney function is lost.

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Importance of inflammation
• Inflammation may contribute to:
 Decline in kidney function with aging
 Albuminuria
 Cardiovascular disease
 Malnutrition
 Anemia
 Metabolic acidosis
• Causes reduced clearance and/or increased production of
pro-inflammatory cytokines
• Obesity may be an inflammatory state

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People with CKD still make urine

• The composition of the urine changes.


• Most people do not notice any difference in
urine volume.
• Slow, progressive loss of function may not
be noticeable.

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FUNCTIONAL ASSESSMENT

Identify and Monitor CKD.

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CKD is reduced kidney function and/or kidney damage
• Chronic Kidney Disease
 Kidney function
 Glomerular Filtration Rate (GFR) < 60 mL/min/1.73 m 2 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
Reference: National Kidney Foundation, 2002

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What is the GFR?

• GFR is equal to the sum of the filtration rates in all of the


functioning nephrons.
• GFR is not routinely measured in clinical settings.
• Estimation of the GFR (eGFR) gives a rough measure of the
number of functioning nephrons.

• Cardiac output (CO) = 6 L/min


 x 20% of CO goes to kidneys = 1.2 L/min
 x Plasma is 50% blood volume = 600 mL/min
 x Filtration Fraction of 20% = 120 mL/min

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Approaches to Estimate Kidney Function

• Cockcroft-Gault estimates creatinine clearance


• Modification of Diet in Renal Disease (MDRD)
• Chronic Kidney Disease Epidemiology
Collaboration (CKD-EPI)

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“Normal” serum creatinine may not be normal
• Serum creatinine levels reflect muscle mass, age, gender and race
• A typical “normal” reference range of
0.6–1.2 mg/dL listed on many lab reports does not account for
muscle mass, age, gender,
and race.
• A 28-year-old African American man with serum creatinine of
1.2 has an eGFR > 60.
• A 78-year-old white woman with serum creatinine of 1.2 has an
eGFR of 43.

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Cockcroft-Gault Background
• Developed to predict creatinine clearance (CrCl) using 24-hour creatinine
excretion per weight (kg)

• Used actual body weight

• Based on 249 men (aged 18-92)

• CrCl ranged between 30-130 mL/m2 (not adjusted for body surface area)

• The equation “assumes” females would be 15% lower creatinine clearance


at the same level of serum creatinine (sCr)
Cockcroft DW, Gault MH. Nephron 1976;16:31-41
Demirovic JA, Pai AB, Pai MP. Am J Health Syst Pharm. 2009;66(7):642-8.

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Estimating Equations for eGFR
• The Modification of Diet in Renal Disease (MDRD) and CKD-
EPI study equations are most widely used for estimating GFR.

• The variables are serum creatinine, age, race, and gender.

• MDRD eGFR = 175 x (Standardized Scr)-1.154 x (age)-0.203 x


(0.742 if female) x (1.212 if African American)

• CKD-EPI eGFR = 141 × min (Scr /κ, 1)α × max(Scr /κ, 1)-1.209
× 0.993 Age × 1.018 [if female] × 1.159 [if African American]

• The estimate is normalized to body surface area.


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eGFR estimates the measured GFR

• eGFR is not the measured GFR.


• Estimating equations are derived from population-based studies.
• The performance measurement of the estimating equation is the
P30
• P30 refers to the percent of GFR estimates that are within 30%
of mGFR

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What does this mean?
MDRD: There is an 77.2% chance that the estimated GFR (for patients with eGFR
<60) is +/- 30% of the measured GFR

 e.g a patient with an eGFR of 59 has an 77.2% chance of having a measured


GFR between 42 and 78
vs

CKD-Epi: There is an 79.9% chance that the estimated GFR (for patients with
eGFR <60) is +/- 30% of the measured GFR

 e.g a patient with an eGFR of 59 has an 79.9% chance of having a measured


GFR between 42 and 78
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Decreased Kidney Function vs Kidney Disease

• Estimating equations are less reliable at higher GFR


• Kidney function declines with age
• While there is an association between decreased eGFR and
morbidity, even in elderly, this association does not mean
causality
• Use diagnostic terms denoting disease with caution, especially
in older people without evidence of kidney damage (e.g. elderly
with eGFR 55)

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Creatinine-based estimates of kidney
function have limitations

• Do not use with:


 Rapidly changing creatinine levels
 Example: acute kidney injury
 Extremes in muscle mass, body size, or altered diet patterns
 Medications that interfere with the measurement of serum
creatinine

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How to explain eGFR results to patients

• Normal: > 60 mL/min/1.73 m2


• Kidney disease: 15–59 mL/min/1.73 m2
• Kidney failure: < 15 mL/min/m2

Image Source: National Kidney Disease Education Program

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KIDNEY DAMAGE

Use urine albumin-to-creatinine ratio (UACR) to assess


and monitor.

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CKD is reduced kidney function and/or
KIDNEY DAMAGE
• Chronic kidney disease
 Kidney function
 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

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Urine albumin results are used for screening,
diagnosing, and treating CKD

• An abnormal urine albumin level is often the earliest


marker for kidney disease complicating diabetes
• Important prognostic marker, especially in diabetes
• Used to monitor and guide therapy
• Tool for patient education and self-management (such as
A1C or eGFR)

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Proteins are filtered based on size and electrical charge

• Low-molecular-weight proteins cross the glomerulus.


• High-molecular-weight proteins do not cross the glomerulus
normally.
• Negatively charged molecules usually are restricted from
crossing the glomerulus.
• Drugs bound to albumin are not filtered into urine
• Reduced albumin from albuminuria reduces drug binding sites
and can increase free drug concentrations

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Damaged kidneys allow albumin to cross the filtration
barrier into the urine
• Increased glomerular permeability allows albumin (and other
proteins) to cross the glomerulus into the urine.
• Higher levels of protein within the tubule may exacerbate
kidney damage.
 Proteins may exceed tubules’ ability to reabsorb.

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Very little albumin or protein is normally
excreted into urine

• Currently accepted “normal” level ≤ 30 mg/g


 Albumin is a medium-size molecular-weight protein
with a negative charge.
 Most is reabsorbed by the tubules.
• Normal urine protein is < 150 mg/day
 Includes albumin and other proteins.

Reference: Danziger J. Mayo Clinical Proceedings, 2008

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Use urine albumin-to-creatinine ratio (UACR) for
urine albumin assessment
• UACR uses a spot urine sample.
• In adults, ratio of urine albumin to creatinine correlates closely
to total albumin excretion.
• Ratio is between two measured substances (not dipstick).

Urine albumin (mg/dL) = UACR (mg/g)  Albumin excretion in mg/day


Urine creatinine (g/dL)

• UACR of 30 mg/g is generally the most widely used cutoff for


“normal.”

Reference: http://nkdep.nih.gov/resources/uacr_gfr_quickreference.htm

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UACR quantifies all levels of urine albumin

• UACR is a continuous variable.


• The term albuminuria describes all levels of urine
albumin.
• The term microalbuminuria describes abnormal
urine albumin levels not detected by dipstick test.
 30 mg/g – 300 mg/g
• The term macroalbuminuria describes urine albumin
> 300 mg/g.

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Explaining urine albumin

Image Source: National Kidney Disease Education Program

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DESCRIBING THE BURDEN
OF CKD

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Thirty million U.S. adults may have
chronic kidney disease

Reference: CDC National Chronic Kidney Disease Fact Sheet , 2017

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Stages of Chronic Kidney Disease
NKF K/DOQI Clinical Practical Guidelines for Chronic Kidney Disease 2002

GFR
Stage Description
(mL/min/1.73 m2)

Albuminuria,
1  90
normal or  GFR

2 Albuminuria, mild  GFR 60-89

3 Moderate  GFR 30-59

4 Severe  GFR 15-29

5 Kidney Failure < 15 or ESRD

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KDIGO 2012 Practice
Guideline on Evaluation and
Management of CKD

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Uses of CKD Staging System

• Determining incidence and prevalence of CKD


• Association with cardiovascular risk
• Risk prediction for end stage kidney disease
• US and global burden of kidney disease
• Public health messaging
• Population health management

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Diabetes is the leading cause of ESRD,
followed by hypertension

Reference: USRDS Annual Data Report (NIDDK, 2016)

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Prevalence of Diabetes; United States, 2005-2008

2005-2008 National Health and Nutrition Examination Survey


2011 National Diabetes Fact Sheet

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Prevalence of Diabetic Kidney Disease (DKD)
Among Adults with Diabetes; United States, 2005-2008
Albuminuria = ACR ≥30 mg/g
Impaired GFR = eGFR <60 ml/min/1.73m²

JAMA 305:2532-2539, 2011

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10-Year Mortality in Type 2 Diabetes in the
United States
Mortality in persons without
diabetes or kidney disease

*Standardized to age, sex, and race


of study population

J Am Soc Nephrol 24:302-308, 2013

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Natural history of diabetic nephropathy: hyperglycemia
causes hyperfiltration, may be followed by albuminuria
180 >4

160 4.0
140 3.5

Urinary albumin, g/d


Clinical
120 nephropathy 3.0

GFR (mL/min)
100 2.5

80 2.0
60 1.5
Clinical
40 nephropathy 1.0

20 0.5

0 0
0 3 6 9 12 15 18 21 24 27

Hyperglycemia (year)

Reference: Adapted from Friedman, 1999

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…however

• Microalbuminuria can regress


 de Boer IH et al, Arch Int Med 2011

• Impaired GFR can develop without albuminuria


 Molitch M et al, Diabetes Care 2010

• Disease heterogeneity often not reflected by GFR


 Bohle et al. American Journal of Nephrology, 1987

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Trends in ESRD prevalence by modality, 1980-2015

Reference: USRDS Annual Data Report (NIDDK, 2017)

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Delaying the need for Renal Replacement Therapy
(RRT) may be cost-effective.

• Hemodialysis $26.7 billion ($88,195 per patient)


• Peritoneal Dialysis $ 2.1 billon ($75,140 per patient)
• Transplantation $ 3.3 billion ($34,800 per patient)

• ESRD data do not include Medicare Part D cost Reference: USRDS Annual Data Report (NIDDK, 2017)

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IMPORTANCE OF THE
PHARMACIST’S ROLE IN
CHRONIC KIDNEY DISEASE

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Key Issues in Managing CKD

• Ensure the diagnosis is correct


• Monitor progression
• Implement appropriate therapy to slow progression
• Screen for CKD complications
• Treat CVD risk
• Avoid acute kidney injury (e.g. NSAIDs)
• Refer to a dietitian
• Educate the patient about CKD
• Begin the conversation about renal replacement therapy

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Challenges to Improving CKD Care

• CKD remains under diagnosed


• Implementation of recommended care is poor
• Many clinicians feel inadequately educated
 Uncertain about how to interpret diagnostic tests
 Unclear about clinical recommendations
 Low confidence in their ability to successfully manage
CKD
 Indications for, and process of, referral poorly defined

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Awareness & Knowledge about CKD
in Patients Seen by Nephrologists
Low Self-Rating Perceived Knowledge N=676
No Knowledge of Hemodialysis / Peritoneal Dialysis 43% / 57%
Little or No Knowledge Re: Diagnosis 35%
Finkelstein, et al. Kidney International, 2008

Limited Awareness & Objective Knowledge N=401


Unaware of CKD diagnosis 31%
Do not understand CKD implications, e.g. heart disease 34%
Do not understand kidney functions, e.g. urine production 34%
Do not understand terminology, GFR 32%
Wright, et al. AJKD 2011

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Pharmacists are Pivotal Members
of the Multi-disciplinary Team!

“The clinician will need to adopt an appropriate system for


monitoring individual patients… Pharmacists are a valuable
resource for identifying potential drug interactions,
interpreting the clinical relevance of known interactions and
developing monitoring plans based on pharmacodynamic and
pharmacokinetic characteristics of individual agents”

http://www2.kidney.org/professionals/KDOQI/guidelines_bp/guide_7.htm

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Why is it important to have pharmacists on board?

• The prevalence of medication-related problems (MRPs) increases as


CKD progresses because the medication usage increases.
• Patients with stage 3 and 4 CKD are prescribed approximately 6 to 8
medications.
• Stage 5 patients are prescribed an average of 12 medications to treat
on an average 5 to 6 chronic medical conditions
• These patients are at a high risk for MRPs and it is associated with
significant costs to the healthcare system.

Cardone KE et al. Adv Chronic Kidney Dis. 2010 Sep;17(5):404-12.

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Medication-related Problems
Problem Description Example(s)
Indication without Patient is not receiving medication A patient with an elevated LDL level not
drug therapy (IWD) therapy for a diagnosed medical taking a lipid lowering medication
condition
Drug use without Use of a medication without a Failure to discontinue diuretic therapy in an
indication (DWI) medically valid indication anuric patient
Improper drug Medication of choice is not being Initiating a calcium-based phosphate binder in
selection (IDS) used a hypercalcemic hemodialysis patient
Subtherapeutic Patient has a medical problem that is A hemodialysis patient continues to receive
dosage (UD) being treated with too little of a the same dose of sevelamer carbonate despite
correct medication serum phosphorus levels of 6.3
Overdose (OD) Patient has a medical problem that is Not adjusting the dose of renally cleared
being treated with too much of the medications in patients with CKD
correct medication
Adverse drug reaction Drug effects that are unwanted, • Nonproductive cough associated with ACE
(ADR) unpleasant, or harmful inhibitor therapy
• Rhabdomyolysis resulting from statin use
Cardone KE et al. Adv Chronic Kidney Dis. 2010 Sep;17(5):404-12.

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Medication-related Problems
Problem Description Example(s)
Drug interaction (DI) Negative effects of drug-drug, drug- • Calcium acetate chelating a fluoroquinolone antibiotic
disease, or drug-food interaction like ciprofloxacin resulting in decreased
bioavailability
• NSAID use in CKD
• Excessive consumption of foods high in vitamin K
decreasing the efficacy of warfarin
Failure to receive drug Patient is not receiving prescribed • Nonadherence to medication regimen
(FRD) medication(s) • Medication is not accessible (e.g., nonformulary
medication)
• Inability to pay for medication (e.g., patient does not
have prescription insurance, patient cannot afford
medication)
Inappropriate laboratory Patient is not receiving appropriate • Failure to continually monitor INR at regular intervals
monitoring (LAB) laboratory tests to adequately during warfarin therapy
monitor medication therapy or to • High cardiovascular risk patient without a recent
determine if comorbid conditions fasting lipid profile
are being treated properly
Cardone KE et al. Adv Chronic Kidney Dis. 2010 Sep;17(5):404-12.

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Trials on Medication-related Problems in CKD/ESRD
Author(s) Year Result
Pai and 2009 HD patient group who had the drug regimen reviewed by a clinical pharmacist was associated
colleagues with fewer drug use, fewer all-cause hospitalizations and shorter cumulative time of
hospitalization compared with patient group who had the drug regimen reviewed by a nurse.

Hug and 2009 Of ADE that occurred in 900 patients with acute or chronic kidney damage, 91% were
colleagues preventable and 51% were significant. All preventable events could have been detected by renal
dosing checking.

Pai and 2009 Quality of Life at 1-year was significantly worse in several domains in the patient group who had
colleagues the drug regimen reviewed by a nurse compared with patient group who had the drug regimen
reviewed by a clinical pharmacist.

Cabello-Muriel 2014 Study showed significant improvement in CrCl among patients with advanced CKD and taking
and colleagues nephrotoxic medications in the pharmacist intervention group (Renal dose adjustments in
nephrotoxic med).
ADE: adverse drug events; CrCl: Creatinine Clearance; HD: hemodialysis; MRP: Medication-related problems; Pai AB et al, Pharmacotherapy 2009;29:1433-40.
RQLP: Renal Quality of Life Profile Hug BL et al. Kidney Int 2009;76:1192-98.
Pai AB, et al. Hemodial Int 2009; 13:72-9.
Cabello-Muriel A, et al. Int J Clin Pharm. 2014;36(5):896-903.

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Population Health and CKD

• CKD is best addressed through population management


• Improvement in care results from changes implemented
by in the community and in the clinic by all health
professionals
• Implemented through diabetes care delivery system; not
specialty clinic based

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Integrated Approaches Reduce Burden of CKD

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Pharmacists in Team-based care
• In a report to the Surgeon General from the Office of the Chief
Pharmacist four key focal points were outlined to expand the scope of
pharmacy practice:
 Pharmacists integrated as healthcare professionals in federal programs (e.g. Indian
Health Service and Veterans Affairs) improve quality and access to care.
 Pharmacists need to be recognized as providers
 Compensation mechanisms need to be expanded to support growth of pharmacist
in team-based care.
 The evidence is supporting pharmacists in team based care
models improving preventative medicine and reducing total cost of care is strong
Giberson S, Yoder S, Lee MP. Improving Patient and Health System Outcomes
through Advanced Pharmacy Practice. A Report to the U.S. Surgeon General.
Rockville, MD: Office of the Chief Pharmacist, US Public Health Service; 2011.

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