The Diabetic Kidney… What to do?

Michael Cobble, MD, FNLA Director

Canyon Medical Center Sandy, Utah

Adjunct Faculty University of Utah

Salt Lake City, Utah

Statement of Sponsorship and Support This CME Symposium is sponsored by and supported by an educational grant from Janssen Biotech, Inc., administered by Janssen Scientific Affairs, LLC.

In collaboration with

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CME Information

This Live activity, Diabetic Kidney... What to Do, from 06/01/2019 - 05/31/2020, has been reviewed and is acceptable for up to 1.00 Prescribed credit(s) by the American Academy of Family Physicians. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Faculty Disclosure Statement Primary Care Education Consortium adheres to the conflict of interest policy of the ACCME and the AMA. It is the policy of PCEC to ensure balance, independence, objectivity, and scientific rigor in all of its educational activities. All individuals in a position to control the content in our programs are expected to disclose any relationships they may have with commercial companies whose products or services may be mentioned so that participants may evaluate the objectivity of the presentations. In addition, any discussion of off-label, experimental, or investigational use of drugs or devices will be disclosed by the faculty. Only those participants who have no conflict of interest or who agree to an identified resolution process prior to their participation were involved in the CME activity.

Disclosures Michael Cobble, MD, has disclosed that he is on the speakers bureau for Amarin, Amgen, AstraZeneca and Regeneron for the clinical conditions of Lipids, CAD and Diabetes. Stephen Brunton, MD, has disclosed that he is on the advisory board for Abbott Diabetes, AstraZeneca, Bayer, Janssen, Novo Nordisk, Sanofi and Xeris Pharmaceuticals; as well as on the speakers bureau for AstraZeneca, Bayer, Janssen, Lilly, and Novo Nordisk. Gregory Scott, PharmD, RPh, Editorial Support, disclosed no relevant financial relationship or interest with a proprietary entity producing, marketing, reselling or distributing health care goods or services.

Learning Objectives After participating in the activity, the clinician should be able to: • Appropriately screen for the presence of chronic kidney disease in

patients with T2DM. • Identify chronic kidney disease at an early stage in patients with

T2DM. • Individualize evidence-based therapy to slow the progression of

kidney disease in patients with T2DM and chronic kidney disease.

Chronic Kidney Disease Is Common • Prevalence: 30 million US adults (15%)1

• 1-in-3 US adults with diabetes • 1-in-5 US adults with hypertension

• 45% of new cases of ESRD are due to diabetes2 • 48% of those with severely reduced kidney function but not on

dialysis are not aware of having CKD1

1. US Centers for Disease Control and Prevention. https://www.cdc.gov/diabetes/pubs/pdf/kidney_factsheet.pdf. Accessed March 25, 2019. 2. United States Renal Data System. https://www.usrds.org/2017/download/2017_Volume_2_ESRD_in_the_US.pdf. Accessed March 25, 2019.

CKD, chronic kidney disease; ESRD, end-stage renal disease

End-Stage Renal Disease, United States

0

50

100

150

200

250

300

350

400

1980

1985

1990

1995

2000

2005

2010

2015

Inci

denc

e pe

r mill

ion/

year

, sta

ndar

dize

d

Year

Incidence Rate of ESRD

2017

United States Renal Data System. https://usrds.org/2019/download/USRDS_2019_ES_final.pdf. Accessed November 19, 2019.

341

End-Stage Renal Disease, United States, 2017 (cont)

124,500

108,131

12,572 3666

0

25,000

50,000

75,000

100,000

125,000

Total ESRD Hemodialysis Peritoneal Dialysis Transplant

Num

ber o

f new

cas

es

Incidence, 2017

United States Renal Data System. https://usrds.org/2019/download/USRDS_2019_ES_final.pdf. Accessed November 19, 2019.

Prevalence Is Increasing in Adults with Diabetes and Low eGFR in the Absence of Albuminuria

0

0.5

1

1.5

2

2.5

3

UACR <30 mg/g UACR 30-299 mg/g UACR ≥300 mg/g

Popu

latio

n es

timat

e (m

illio

ns)

Persons with Diabetes and eGFR <60 mL/min/1.73 m2

1988-1994 1999-2002 2003-2006 2007-2010

Kramer H, et al. Diabetes Care. 2018;41:775-781.

UACR, urine albumin-to-creatinine ratio

Mortality Is Increasing in Adults with Diabetes and Low eGFR in the Absence of Albuminuria

35

51

0

10

20

30

40

50

60

Mor

talit

y ra

te p

er 1

,000

per

son-

year

s

Mortality Rate in Persons with Diabetes with eGFR <60 mL/min/1.73 m2 and UACR <30 mg/g

1988-1994 2003-2006

Kramer H, et al. Diabetes Care. 2018;41:775-781.

From 1988-1994 to 2003-2006, the mortality rate in adults with diabetes and low eGFR in the absence of albuminuria has increased.

Slower Rate of Decline in eGFR with Nonalbuminuric CKD

1.00 1.00 1.00

1.72 1.82 1.88

4.52

2.38 2.37

0.76

1.42 1.44

0.00

1.00

2.00

3.00

4.00

5.00

End-Stage Kidney Disease All-Cause Mortality MACE

Haza

rd R

atio

*

Risk of ESKD, All-Cause Mortality, MACE by CKD Status

No CKD** Albuminuric non-CKD Albuminuric CKD Non-abuminuric CKD

M=10,185 patients with T2DM in the ACCORD study CKD=eGFR <60 mL/min/1.73 m2; albuminuria=UACR > 30 mg/g *Adjusted for age, sex, race/ethnicity, duration of diabetes, smoking, history of cardiovascular disease, serum lipid levels, systolic blood pressure, body mass index, glycated hemoglobin, use of RAAS inhibitor therapy **eGFR 90-120 mL/min/1.73 m2

Buyadaa O, et al. Diabetes Care. 2019;doi:10.2337/dc19-1438/-/DC1.

Risk Factors for CKD • Diabetes mellitus (uncontrolled)

• Hypertension (uncontrolled)

• Obesity • Heart failure • Age >60 years • Tobacco use • Family history • Ethnicity • Prior history of acute kidney injury

Gatwood J, et al. PLoS One. 2018;13(2):e0192712.

All-Cause Mortality Based on eGFR and UACR

0

1

2

3

4

5

6

7

8

9

15-30 30-45 45-60 60-75 75-90 90-105 >105

Rela

tive

risk

eGFR (mL/min/1.73 m2)

<10 10-29 30-299 300+

UACR (mg/g)

KDIGO. Kidney Int Suppl (2011). 2013;3(1):19-62.

UACR, urine albumin-to-creatinine ratio

Cardiovascular Mortality Based on eGFR and UACR

0

1

2

3

4

5

6

7

8

9

15-30 30-45 45-60 60-75 75-90 90-105 >105

Rela

tive

risk

eGFR (mL/min/1.73 m2)

<10 10-29 30-299 300+

UACR (mg/g)

KDIGO. Kidney Int Suppl (2011). 2013;3(1):19-62.

UACR, urine albumin-to-creatinine ratio

Cognitive Impairment in CKD Chronic Kidney

Disease

Reduced •●Processing •●Attention •●Response speed •●Short-term memory

Early stage

Deficits in ●Executive functioning ●Verbal fluency ●Logical memory ●Orientation ●Concentration

Moderate stage

Early stage + Moderate stage +

Deficits in ●Cognitive control ●Delayed/Immediate memory ●Visuospatial impairment ●Overall cognition

End stage

Brodski J, et al. J Int Neuropsychol Soc. 2019;25(1):101-114.

Case Scenario • Julio is a 63-yo male

diagnosed with T2DM x 7y • A1c had ranged from 6.8%

to 7.4% since diagnosis • Now 7.8%

• PMH: angina pectoris x 2y; stable

• Vital signs WNL • eGFR 64 mL/min/1.73 m2 • UACR 90 mg/g

• Current meds: • Metformin 1 g BID • Pioglitazone 45 mg

qAM • Atorvastatin 40 mg

qPM • Ramipril 10 mg qPM • Aspirin 81 mg qPM • NTG 0.3 mg SL prn

What change would you make to his antidiabetic therapy?

Intensive Therapy Results in Reduced Nephropathy

0

5

10

15

20

25

30

35

40

At 4 Years At 8 Years Post-Trial At 13 Years At 13 Years

Num

ber o

f Pat

ient

s

Intensive Therapy

Conventional Therapy

Diabetic Nephropathy ESRD

Requiring Dialysis

HR 0.44 95% CI: 0.25-0.77 P=0.004

P=0.04

• Patients with T2DM and persistent microalbuminuria

• 160 randomized • 130 continued

follow up

• Intensive* or conventional therapy for 7.8 y

• Follow-up for 5.5 y

Gaede P, et al. N Engl J Med. 2008;358:580-591.

*To achieve A1c <6.5%, total cholesterol <175 mg/dL, triglyceride <150 mg/dL, BP <130/80 mmHg; included renin-angiotensin-aldosterone inhibitor, low-dose aspirin

Effect of Intensive Glucose Lowering vs Standard Therapy on Renal Outcomes

Risk Ratio (intensive vs

standard therapy)

95% CI P

Microalbuminuria 0.86 0.76-0.96 0.009

Macroalbuminuria 0.74 0.65-0.85 0.001

Doubling of the SCr 1.06 0.92-1.22 0.44

ESRD 0.69 0.46-1.05 0.09

Death from renal disease 0.99 0.55-1.79 0.98

Systematic review of 7 trials involving 28,065 adults; 2-15 years of follow up Target A1C (or FPG) in the intensive group in each trial: A1c <7; 7.1; <6; ≤6.5; <6 and 1.5% less than standard; FPG <6 mg/dL; FPG <6 mg/dL Target A1C (or FPG) in the standard group in each trial: A1c 7-7.9; <9 and 1.5% higher than intensive; FPG 6.1-15 mg/dL; 6.1-15 mg/dL; not reported; local standards; avoidance of excessive hyperglycemia

Coca SG, et al. Arch Intern Med. 2012;172(10):761-769.

Screening for CKD in Diabetes Adults Children/Adolescents

Who? T1DM: Duration ≥5 years

T2DM: All

Comorbid hypertension: All with T1DM or T2DM

At puberty or age >10 years, whichever is earlier, once the child has had diabetes ≥5 years

How? Urinary albumin (eg, spot UACR)

and

eGFR

Urinary albumin (morning preferred) with spot UACR

When? At least once a year At least once a year

American Diabetes Association. Diabetes Care. 2019;42(Suppl 1):S124-S138. American Diabetes Association. Diabetes Care. 2019;42(Suppl 1):S148-S164.

This is correct regarding screening for kidney dysfunction in patients with type 2 diabetes: Measure estimated glomerular filtration rate and urine albumin-to-creatinine ratio annually.

Diabetic CKD vs non-Diabetic CKD Non-DKD DKD

Onset of proteinuria Rapid Gradual

Progression of CKD Rapid Gradual

Duration of diabetes <5 years >10 years

Urinalysis Active sediment (hematuria, pyuria, casts)

Bland sediment (crystals, protein, hyaline casts)

Retinopathy Absent Usually present

Republished with permission of American Society of Nephrology from Diagnosis and Management of Type 2 Diabetic Kidney Disease, Doshi SM, Friedman AN, volume 12, © 2017; permission conveyed through Copyright Clearance Center, Inc. Doshi SM, et al. Clin J Am Soc Nephrol. 2017;12:1366-1373.

Characteristics of CKD* in Adults with T2DM

45%

19%

28% 30%

0%

20%

40%

60%

80%

100%

Microalbuminuria Macroalbuminuria Retinopathy No retinopathy ormicro/macroalbuminuria

Perc

ent o

f Pat

ient

s with

CKD

*eGFR <60 mL/min/1.73 m2 13% (171/1197) of patients with T2DM had CKD

Kramer HJ, et al. JAMA. 2003;289:3273-3277.

n=171

Management Goals for DKD

• Identify patients at risk for CKD/DKD • Intervene early • Prevent further deterioration in kidney function

Treatment Principles for DKD • Control blood glucose, blood pressure, blood lipids • Tobacco cessation • Manage diet/lifestyle- reduce salt intake • Consider RAAS inhibitor (ACE-I or ARB) • Consider referral, especially for dialysis/transplantation • Monitor potentially nephrotoxic medications • Monitor medications cleared by the kidney • Implement shared decision-making • Provide patient education

American Diabetes Association. Diabetes Care. 2019;42(Suppl 1):S124-S138.

DKD Management Therapeutic Option Recommendation

Glycemic control A1c ≤7% reduces risk or slow the progression of CKD. Consider SGLT-2i or GLP-1RA shown to reduce CKD progression, CV events, or both

BP control 10-y ASCVD risk <15%: <140/90 mmHg 10-y ASCVD risk >15%: <130/80 mmHg

RAAS blockade ACE-I or ARB (nonpregnant with diabetes + HTN) -recommended if UACR 30-299 mg/24 h -strongly recommended if UACR ≥300 mg/24 h and/or

eGFR <60 mL/min/1.73 m2 -not recommended for 1° prevention if normal BP, UACR,

eGFR

Weight loss Demonstrated benefit

Close monitoring for disease progression and treatment-related complications is advised

American Diabetes Association. Diabetes Care. 2019;42(Suppl 1):S124-S138. Doshi SM, et al. Clin J Am Soc Nephrol. 2017;12:1366-1373.

Management Issues Clinicians Should Master

• Screen using eGFR and UACR • Utilize glucose-lowering medications shown to reduce

cardiovascular risk • Consider SGLT2i > GLP-1RA, DPP-4i depending on CV risk factor

• Achieve and maintain good control of blood glucose, blood pressure, blood lipids

• Consider renin-angiotensin-aldosterone inhibitor therapy • Facilitate/Support tobacco cessation

Considerations for Referral to Nephrology • Acute kidney injury or abrupt sustained fall in eGFR • eGFR <30 mL/min/1.73 m2 (G4-G5) • Consistent UACR ≥300 mg/g or AER ≥300 mg/24h • Progression of CKD • Urinary red cell casts, RBC >20 hpf sustained and not readily

explained • CKD and HTN refractory to ≥4 antihypertensive agents • Persistent abnormalities of serum K+ • Recurrent or extensive nephrolithiasis • Hereditary kidney disease • Progressive CKD with risk of kidney failure within 1 y ≥10% to 20%

KDIGO. Kidney Int Suppl (2011). 2013;3(1):19-62. AER, albumin excretion rate; hpf, high-power field; HTN, hypertension

*Referral threshold may vary †Anemia, metabolic bone disease, secondary hyperparathyroidism, resistant hypertension, electrolyte disturbances

American Diabetes Association. Diabetes Care. 2020;43(Suppl. 1):S135-S151.

Considerations for Nephrology Referral – ADA*

Uncertain etiology of kidney disease

Difficult management

issues†

eGFR <30 mL/min/1.73 m2

Rapidly progressing kidney disease

Results of CV Outcomes Trials

CV Safety

CV Benefit Renal Benefit

Dipeptidyl peptidase-4 inhibitors

Alogliptin

Linagliptin

Saxagliptin

Sitagliptin

Glucagon-like peptide-1 receptor agonists

Albiglutide*

Dulaglutide

Exenatide BID NR

Exenatide QW

Liraglutide

Lixisenatide

Semaglutide

Sodium glucose cotransporter-2 inhibitors

Canagliflozin Dapagliflozin Empagliflozin Ertugliflozin

CV safety • Non-inferiority • Not more than 30% increase in CV

risk compared to placebo as part of standard therapy

CV benefit • If non-inferiority is demonstrated,

can look for superiority • Superiority- CV risk significantly

reduced compared to placebo as part of standard therapy

*Will no longer be available as of December 2019.

Saxagliptin Improves UACR

*P value is based on a 2-tailed normal distribution approximation test for the proportion of patients who worsened. **P value is based on a χ2 test for independence. ***P value is based on a 2-tailed normal distribution approximation test for the proportion of patients who improved.

Mosenzon O, et al. Diabetes Care. 2017;40:69-76.

84% 82%

29% 23%

4% 3%

15% 17%

60%

60%

28% 23%

1% 1% 12%

17%

68% 74%

0%

20%

40%

60%

80%

100%

120%

Saxagliptin Placebo Saxagliptin Placebo Saxagliptin Placebo

<30 30-300 >300

Change in categorical UACR from baseline to end of treatment by baseline UACR category

P=0.021* P<0.001** P=0.049***

UACR <30 mg/g at baseline UACR 30-300 mg/g at baseline UACR >300 mg/g at baseline

Effect of GLP-1 Receptor Agonists on Renal Endpoints

GLP-1 Receptor Agonists- Liraglutide

Rate/100 patient-years

Hazard Ratio

(95% CI)

P

Active Placebo New onset of persistent macroalbuminuria or a doubling of SCr and eGFR ≤45 mL/min/1.73 m2, need for continuous renal-replacement therapy, or death from renal disease

1.5 1.9 0.78 (0.67-0.92)

0.003

New onset of persistent macroalbuminuria 0.9 1.21 0.74

(0.60-0.91) 0.004

Marso SP, et al. N Engl J Med. 2016;375(4):311-322. Mann JFE, et al. N Engl J Med. 2017;377(9):839-848.

Effect of GLP-1 Receptor Agonists on Renal Endpoints

GLP-1 Receptor Agonists- Semaglutide

Rate/100 patient-years

Hazard Ratio

(95% CI)

P

Active Placebo

Persistent macroalbuminuria or a doubling of SCr and eGFR ≤45 mL/min/1.73 m2, need for continuous renal-replacement therapy

1.86 3.06 0.64 (0.46-0.88)

0.005

Marso SP, et al. N Engl J Med. 2016;375(19):1834-1844.

Canagliflozin CREDENCE Trial • 4401 patients with T2DM

• Age ≥30 y • A1c 6.5% to 12.0% • eGFR 30 to <90 mL/min/1.73

m2 • UACR >300 to 5000 mg/g • Stabilized on ACE-I or ARB

therapy • 2-week, single-blind, placebo

run-in • Randomized (1:1) to

(stratified by eGFR): • Canagliflozin 100 mg or

placebo daily

Perkovic V, et al. N Engl J Med. 2019;380(24):2295-2306.

• Treatment continued until: • Trial completion • Initiation of dialysis • Kidney transplantation • Occurrence of diabetic

ketoacidosis • Pregnancy • Receipt of disallowed therapy

• Results suggested that there was no difference in amputation risk or fracture risk between canagliflozin and placebo

• Contrary to CANVAS

Effect of SGLT-2 Inhibitors on Renal Endpoints

SGLT-2 Inhibitors- Canagliflozin Rate/100 patient-years

Hazard Ratio

(95% CI)

P

Active Placebo

Dialysis, transplantation, sustained eGFR <15 mL/min/1.73 m2, doubling of SCr, or renal or CV death

4.32 6.12 0.70 (0.59-0.82)

0.00001

Doubling of SCr 2.07 3.38 0.60 (0.48-0.76)

<0.001

ESRD 2.04 2.94 0.68 (0.54-0.86)

0.002

ESRD, doubling of SCr, or renal death 2.70 4.04 0.66 (0.53-0.81)

<0.001

Dialysis, kidney transplantation, or renal death

1.36 1.86 0.72 (0.54-0.97)

–

Perkovic V, et al. N Engl J Med. 2019;380(24):2295-2306.

Canagliflozin in T2DM and Pre-existing Nephropathy: CREDENCE

N=4401 patients with T2DM, eGFR 30 to <90 mL/min/1.73 m2 and UACR >300 to 5000 mg/g Median follow-up 2.62 y NNT=22 for primary composite NNT=28 for renal-specific composite NNT=43 for ESKD

From The New England Journal of Medicine, Perkovic V, Jardine MJ, Neal B, Bompoint S, Heerspink HJL, Charytan DM, Edwards R, Agarwal R, Bakris G, Bull S, Cannon CP, Capuano G, Chu PL, de Zeeuw D, Greene T, Levin A, Pollock C, Wheeler DC, Yavin Y, Zhang H, Zinman B, Meininger G, Brenner BM, Mahaffey KW, Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy, volume 380, pages 2295-2306, Copyright © 2001 Massachusetts Medical Society. Reprinted with permission from Massachusetts Medical Society. Perkovic V, et al. N Engl J Med. 2019;380(24):2295-2306.

Effect of SGLT-2 Inhibitors on Renal Endpoints

SGLT-2 Inhibitors- Dapagliflozin

Kaplan-Meier event rate (4 y)

Hazard Ratio

(95% CI)

P

Active Placebo Sustained decrease in eGFR ≥40% to <60 mL/min/1.73 m2, ESRD, or CV or renal death

4.2% 5.3% 0.76 (0.67-0.87)

<0.0001

Sustained decrease in eGFR ≥40% to <60 mL/min/1.73 m2, ESRD, or renal death

1.5% 2.6% 0.53 (0.43-0.66)

<0.0001

Sustained decrease in eGFR ≥40% to <60 mL/min/1.73 m2 1.4% 2.5% 0.54

(0.43-0.67) <0.0001

ESRD 0.1% 0.2% 0.31 (0.13-0.79)

0.013

ESRD or renal death 0.1% 0.3% 0.41 (0.20-0.82)

0.012

Mosenzon O, et al. Lancet. Diabetes Endocrinol 2019;doi:10.1016/S2213-8587(19)30180-9

SGLT-2 Inhibitors- Empagliflozin Rate/100 patient-years

Hazard Ratio

(95% CI)

P

Active Placebo

Doubling of SCr, ESRD, or renal death 0.63 1.15 0.54 <0.001

Doubling of SCr and eGFR ≤45 mL/min/1.73 m2

1.0.55 0.97 0.56 (0.39-0.79)

<0.001

Doubling of SCr and eGFR ≤45 mL/min/1.73 m2, initiation of renal-replacement therapy, or renal death

0.63 1.15 0.54 (0.40-0.75)

<0.001

Initiation of renal-replacement therapy 0.10 0.21 0.45 (0.21-0.97)

0.04

Progression to macroalbuminuria 4.18 6.49 0.62 (0.54-0.72)

<0.001

Incident or worsening nephropathy 4.78 7.60 0.61 (0.53-0.70

<0.001

Wanner C, et al. N Engl J Med. 2016;375(4):323-334.

Effect of SGLT-2 Inhibitors on Renal Endpoints

As a class of medications, dipeptidyl peptidase-4 inhibitors are supported by little, if any, evidence demonstrating a cardiovascular benefit in a patient with T2DM and chronic kidney disease.

Updated Prescribing Information to Reflect CV Outcomes Trials MACE FDA Labeling Regarding CV Risk

GLP-1 Receptor Agonists

Albiglutide* –

Dulaglutide –

Exenatide once-weekly

Liraglutide …to reduce the risk of major adverse CV events (CV death, non-fatal myocardial infarction, or non-fatal

stroke) in adults with T2DM and established CV disease

Lixisenatide

Semaglutide –

SGLT-2 Inhibitors

Canagliflozin

…to reduce the risk of major adverse CV events in adults with T2DM and established CV disease …to reduce the risk of end-stage kidney disease (ESKD), doubling of serum creatinine, cardiovascular

(CV) death, and hospitalization for heart failure in adults with T2DM and diabetic nephropathy with albuminuria ˃ 300 mg/d

Dapagliflozin …to reduce the risk of hospitalization for heart failure in adults with T2DM and established CV disease or

multiple CV risk factors

Empagliflozin …to reduce the risk of CV death in adults with T2DM and established CV disease

Ertugliflozin

*No longer available as of December 2019

Tanzeum [package insert]. Research Triangle, NC: GlaxoSmithKline; December 2017. Trulicity [package insert]. Indianapolis, IN: Eli Lilly and Co.; September 2019. Bydureon [package insert]. Wilmington, DE: AstraZeneca Pharmaceuticals LP; February 2019. Victoza [package insert]. Plainsboro, NJ: Novo Nordisk Inc.; September 2019. Adlyxin [package insert]. Bridgewater, NJ: Sanofi-aventis U.S., LLC; January 2019. Ozempic [package insert]. Plainsboro, NJ: Novo Nordisk Inc.; November 2019. Rybelsus [package insert]. Plainsboro, NJ: Novo Nordisk Inc.; September 2019. Invokana [package insert]. Titusville, NJ: Janssen Pharmaceuticals, Inc.; December 2019. Farxiga [package insert]. Wilmington, DE: AstraZeneca Pharmaceuticals LP; October 2019. Jardiance [package insert]. Ridgefield, CT: Boehringer Ingelheim Pharmaceuticals, Inc.; January 2019. Steglatro [package insert]. Whitehouse Station, NJ: Merck Sharp

American Diabetes Association. Diabetes Care. 2020;43(Suppl 1):S98-S110. American Diabetes Association. Standards of medical care in diabetes-2020, American Diabetes Association, 2020. Copyright and all rights reserved. Material from this publication has been used with the permission of American Diabetes Association.

New Paradigm in T2DM Treatment

Patients with T2DM and Established ASCVD or CKD

American Diabetes Association. Diabetes Care. 2020;43(Suppl 1):S98-S110. American Diabetes Association. Standards of medical care in diabetes-2020, American Diabetes Association, 2020. Copyright and all rights reserved. Material from this publication has been used with the permission of American Diabetes Association.

Implications for Patient Care • CKD is common in patients with T2DM causing

significant increases in: • CV mortality • All-cause mortality

• Annual screening for CKD in patients with T2DM is critical

• Measure both eGFR and UACR

• Controlling blood glucose, blood pressure, and blood lipids is critical

• Recent clinical trial evidence demonstrates reduced renal events with several SGLT-2 inhibitors and GLP-1 receptor agonists

• Presents an additional opportunity to individualize therapy • Patient affordability may be a limiting factor

The Diabetic Kidney… What to do?

Thank you!