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Guided by Inflammation: Applying New Insights to CKD & ASCVD Care-FIN

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Guided by Inflammation: Applying New Insights to CKD and ASCVD Care

Supported by an educational grant from Novo Nordisk.

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Index

Pre-test

Learning Objectives

Faculty Disclosures

The interconnectedness of CKD, systemic inflammation, and ASCVD

Overlapping Risk Factors for CKD and ASCVD

Systemic Inflammation and High-Sensitivity C-Reactive Protein (hs-CRP)

Anti-inflammatory effects of current & emerging treatment options

Patient Case Vignettes

References

Claim CME/CE Credit

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Learning Objectives

Explain the impact of CKD and systemic inflammation as risk factors for atherosclerotic cardiovascular disease (ASCVD) Recognize the anti-inflammatory effects of current & emerging therapies for CKD

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Faculty Disclosures

Michael Blaha, MD, MPH

Advisory Board: Novartis, Novo Nordisk, Bayer, Eli Lilly, Astra Zeneca*, Boehringer Ingelheim*, Idorsia*, Agepha, Genentech*, New Amsterdam
Grant Funding: Novo Nordisk, Bayer
Speakers’ Bureau: Novo Nordisk
Steering Committee: Novartis

Sylvia Rosas, MD, MSCE

Advisory Board: Novo Nordisk
Research Funding (paid to institution): Bayer, ProKidney, NIDDK
Steering Committee: Bayer (finerenone)

Conan Tu, MD, MBA, DACD, BC-ADM

Consultant/Advisory Board: Novo Nordisk, Insulet, Sanofi, Eli Lilly*
Speakers’ Bureau: Abbott, Sanofi, Intuity Medical*, Astra Zeneca*
Research funding: Boehringer Ingelheim

*Relationship has ended.

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Pre-test

Before reviewing the material, please take a few moments to complete the Pre-test. When you're ready, click the "next" button below.

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Pre-test, Question 1

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Pre-test, Question 2

Pre-test, Question 3

Pre-test, Question 4

The Interconnectedness of CKD, Systemic Inflammation, and ASCVD

Figure 1. Association Between eGFR/uACR and Cardiovascular Mortality

Chronic kidney disease (CKD) is a major public health concern, affecting nearly 15% of adults in the United States.1 Most people living with CKD are more likely to have an atherosclerotic cardiovascular disease (ASCVD) event (i.e. myocardial infarction, stroke, peripheral artery disease) than to reach kidney failure. This increased risk has been demonstrated not only in people with an estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73m2, but also individuals with albuminuria (including urine albumin-creatinine ratio (uACR) concentrations >10 mg/g), independent of eGFR (Figure 1).2–7

Abbreviations: eGFR, estimated glomerular filtration rate; HR, hazard ratio; uACR, urine albumin-creatinine ratio Acknowledgement: Adapted from Van Der Velde M, Matsushita K, Coresh J, et al. Lower estimated glomerular filtration rate and higher albuminuria are associated with all-cause and cardiovascular mortality. A collaborative meta-analysis of high-risk population cohorts. Kidney Int. 2011;79(12):1341-1352.

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The Interconnectedness of CKD, Systemic Inflammation, and ASCVD

Figure 2. KDIGO CKD Heat Map

Persistent albuminuria categoriesDescription and Range

A1

A2

A3

Normal to mildly increased

Moderately increased

Severely increased

KDIGO: Prognosis of CKD by GFR and albuminuria categories

This phenomenon of dual risk markers is clearly visible in the KDIGO CKD heat map (Figure 2), with increasing risk levels observed along both axes (i.e. increased risk as uACR increases and eGFR declines).8 Furthermore, cardiovascular (CV) mortality accounts for approximately 40-50% of all deaths in patients with stage 4 or 5 CKD.2,9,10

<30 mg/g <3 mg/mmol

30-300 mg/g3-30 mg/mmol

>300 mg/g>30 mg/mmol

Normal or high

≥90

G1

G2

60-89

Mildly decreased

Mildly to moderately decreased

G3a

45-59

GFR categories (ml/min/1.73 m2Description and Range

Moderately to severely decreased

30-44

G3b

Severely decreased

G4

15-29

G5

<15

Kidney Failure

Acknowledgement: Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int. 2024;105(4S):S126.

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Overlapping Risk Factors for CKD and ASCVD

Table 1. Overlapping Risk Factors for CKD and ASCVD

Health Conditions

Lifestyle Factors

Miscellaneous Risk Factors

Smoking and/or use of tobacco products

Family history/genetic predisposition

Hypertension

Dyslipidemia

Diabetes

Metabolic syndrome

Albuminuria

Obesity

Hyperuricemia

Physical inactivity

Poor nutrition

Older age

Systemic inflammation

Social and area deprivation

Low socioeconomic status

Vascular calcification

Environmental toxins

An overview of the most common overlapping risk factors for CKD and ASCVD is provided in Table 1. Traditional CV risk factors are often present in patients with CKD, and their contribution to ASCVD in this patient population is noteworthy, especially in the earlier stages of CKD.2,11,12 In more advanced stages of CKD, the interplay between inflammation, albuminuria, elevated uric acid levels, oxidative stress, and circulatory dysfunction also contributes to a pro-atherogenic environment that accelerates the progression of atherosclerosis and increases the likelihood of ASCVD events.2,13,14

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Overlapping Risk Factors for CKD and ASCVD

Figure 3. The Impact of Social Determinants of Health on Systemic Inflammation and CVD

Furthermore, various social determinants of health (SDoH) are also associated with increased levels of chronic systemic inflammation, especially among people experiencing discrimination, segregation, and/or social and economic disadvantage, thereby contributing a further increased risk for developing CKD and ASCVD (Figure 3).15–17

Acknowledgement: Adapted from Powell-Wiley TM, Baumer Y, Baah FO, et al. Social Determinants of Cardiovascular Disease. Circ Res. 2022;130(5):782-799.

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Systemic Inflammation and High-Sensitivity C-Reactive Protein (hs-CRP)

Figure 4. Inflammatory pathways involved in atherosclerosis

Systemic inflammation is a significant driver of CKD progression and CV pathology. People living with CKD often have high levels of circulating pro-inflammatory markers (Figure 4), including C-reactive protein, interleukin-6 (IL-6), and tumor necrosis factor (TNF).18 Of these markers, high-sensitivity C-reactive protein (hs-CRP) is most likely to be readily available to clinicians outside of the setting of a clinical trial. While hs-CRP is a well-known marker of inflammation, it is important to acknowledge that it is non-specific, as it may be increased for any number of reasons (e.g. infection, trauma, smoking, autoimmune conditions, chronic inflammatory conditions).19

Abbreviations: CRP, C-reactive protein; MMPs, matrix metalloproteinases; IFN-γ, interferon-gamma; IL-1α, interleukin-1-alpha; IL-1β, interleukin-1-beta; IL-2, interleukin-2; IL-6, interleukin-6; IL-10, interleukin-10; IL-18, interleukin-18; Lp-PLA2, lipoprotein-associated phospholipase A2; TGF-β, transforming growth factor beta; Th-1, T-helper-1 lymphocyte; TNF-α, tumor necrosis factor alpha; T-reg, regulatory T lymphocyte. Acknowledgment: Nguyen MT, Fernando S, Schwarz N, Tan JTM, Bursill CA, Psaltis PJ. Inflammation as a therapeutic target in atherosclerosis. J Clin Med. 2019;8(8):1109.

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Systemic Inflammation and High-Sensitivity C-Reactive Protein (hs-CRP)

Table 2. Summary of guideline recommendations regarding hs-CRP and primary ASCVD risk prevention

Guideline

Recommendation

2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease25 2018 AHA/ACC/AACVPR/AAPA/ ABC/ACPM/ADA/AGS/APhA/ASPC/ NLA/PCNA Guideline on the Management of Blood Cholesterol26

Consider an elevated hs-CRP level (≥ 2.0 mg/L) as one of several ASCVD Risk Enhancers to inform further risk stratification for patients with a borderline or intermediate risk for developing ASCVD (i.e. 10-year ASCVD risk of 5-<20% using their ASCVD risk calculator).

NLA Recommendations for Patient-Centered Management of Dyslipidemia: Part 127

Consider other factors for risk refinement, particularly in patients with moderate risk (2 major ASCVD risk factors), The presence of an elevated hs-CRP level (≥ 2.0 mg/L) may warrant moving a patient into a higher risk category based on clinical judgment. Because of high intraindividual variability, multiple hs-CRP values should be obtained before concluding that the level is elevated. hs-CRP should not be tested in patients who are ill, have an infection, or are injured

American Society for Preventive Cardiology28

Consider the presence, quantity, and/or extent of any risk enhancing factors, including the severity of certain inflammatory factors such as hs-CRP to further inform treatment decisions (beyond the calculated 10-year ASCVD risk score)

Understanding the association between chronically elevated hs-CRP levels and a person’s ASCVD risk has been a highly researched area for decades.20,21 A summary of current guideline recommendations from various organizations regarding hs-CRP concentrations for primary ASCVD prevention can be found in Table 2. For patients with established ASCVD, the utility of hs-CRP as a tool for assessing “residual inflammatory risk” after LDL-C goals are achieved is an area of ongoing research, with early data suggesting prognostic value.22–24

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Systemic Inflammation and High-Sensitivity C-Reactive Protein (hs-CRP)

Figure 5. Relationship of increasing quartiles of baseline hsCRP to associated cardiovascular and mortality risks for individuals with eGFR < 60 mL/min/1.73m2 in CANTOS trial

Within the context of CKD, an elevated hs-CRP concentration has consistently been associated with an increased risk of ASCVD, although the strength of this correlation has varied from study to study.29–32 In a CANTOS sub-study, increasing quartiles of plasma hs-CRP were positively associated with increased risks of recurrent major adverse CV events (MACE), CV mortality, and all-cause mortality for statin-treated patients with CKD and a prior history of MI, independent of baseline LDL-C concentrations (Figure 5).33 Furthermore, increasing levels of hs-CRP were observed with worsening stages of CKD in a long-term follow-up analysis of data from the MESA study, and contributed to increasing risk of CV events and incidence of chronic inflammation-related disease (i.e. medical conditions with a chronic inflammatory or infectious milieu and deemed likely to lead to hospitalization or death).7

p<0.05 compared to reference group

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Anti-inflammatory Effects of Current & Emerging Treatment Options

While hs-CRP and other markers of systemic inflammation are not direct treatment targets per se, current evidence supports considering a patient’s systemic inflammation when considering a patient’s cardiovascular risk and leveraging treatment approaches that offer anti-inflammatory effects. As cornerstones of a holistic approach to CKD treatment and risk modification, it is important to emphasize that physical activity, healthy diet, and weight loss (when indicated) can contribute significant reductions in systemic inflammation and are essential for all patients with CKD.34–39 Additionally, many medications currently available to treat CKD, reduce ASCVD risk, and manage comorbid conditions within the broader Cardiovascular-Kidney-Metabolic (CKM) syndrome provide variable anti-inflammatory effects beyond their main pharmacologic mechanism of action, also known as “pleiotropic effects”. While some agents may not directly impact systemic inflammation and/or reduce systemic hs-CRP concentrations, there is value in more localized anti-inflammatory effects (e.g. at the vascular, glomerular, and/or tubular levels), with potential downstream effects on overall systemic inflammation. Click the buttons to the right to learn more about the pleiotropic anti-inflammatory effects for these medications.

Lipid-lowering Agents

CKD Agents

Anti-inflammatory Agents for Reducing CV Risk (Focus on CKD)

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Anti-inflammatory effects of current & emerging treatment options

Figure 6. Residual Risk Pathways in Secondary ASCVD Prevention

The recommended approach to CKD management prioritizes agents which can offer additional benefits to patients beyond slowing CKD progression (e.g. RAS inhibitors also lower blood pressure, SGLT2 inhibitors also help manage blood glucose, heart failure, and CV risk). As part of this treatment paradigm, it is important to consider the anti-inflammatory effects of available interventions, especially in patients with a high level of systemic inflammation at baseline.13 This is especially important given the high level of residual cardiovascular risk that many patients with CKD experience despite maximizing lifestyle interventions and guideline-directed medical therapy (Figure 6).61,62

Abbreviations: ApoB, apolipoprotein B; GLP-1, glucagon-like peptide-1; hs-CRP, high-sensitivity C-reactive protein; LP(a), lipoprotein(a); LDL-C, low density lipoprotein-cholesterol; TG, triglycerides; SGLT2, sodium-glucose cotransporter-2 *In addition to standard evidence-based therapies, more aggressive blood pressure targets may be considered. Acknowledgment: Lawler PR, Bhatt DL, Godoy LC, et al. Targeting cardiovascular inflammation: next steps in clinical translation. Eur Heart J. 2021;42(1):113-131.

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Patient Case Vignettes

Review each case and answer the questions that follow.

Review Patient Case 1

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Case 1, Question 1

Case Summary

Case 1, Question 1 Rationale

Victor’s uACR of 160 mg/g places him in stage A2 albuminuria, and stage G3bA2 CKD is considered very high-risk for CKD progression and ASCVD risk. Further intervention to reduce his uACR can help lower his ASCVD risk (in addition to slowing CKD progression). Victor’s blood pressure and diabetes appear to be reasonably well-managed according to current guidelines, especially considering his comorbidities. Although there may be room for modest improvements, these areas are not the most likely contributors to his ongoing ASCVD risk. Similarly, while COPD may be a factor in his limited physical activity, we lack enough information to determine its impact or whether it is the primary barrier. Overall, these issues are less likely to yield meaningful reductions in ASCVD risk compared to addressing other modifiable factors, such as his chronic kidney disease (albuminuria).

Case 1, Question 2

Case Summary

Case 1, Question 2 Rationale

Of the options available, finerenone is likely the best option to initiate for Victor (assuming his serum potassium concentration is within the normal range). It will help reduce his albuminuria while also providing additional anti-inflammatory and anti-fibrotic effects without significantly impacting blood pressure. Finerenone has also been shown to provide ASCVD and heart failure benefits in cardiovascular outcomes trials. Furthermore, the risk of hyperkalemia may be lowered as a result of his concurrent SGLT2 inhibitor use. While each of the remaining interventions—low-dose colchicine, icosapent ethyl, and spironolactone—has potential clinical value, they are not the most appropriate or impactful options for Victor at this time:

Low-dose colchicine has shown benefit in patients with ASCVD, but patients with stage G3b CKD (like Victor) were not included in the LoDoCo2 trial. It also does not address his albuminuria, which is a more pressing concern.
Icosapent ethyl: Victor’s mildly elevated triglycerides do not represent a major driver of his ASCVD risk compared to his persistent albuminuria.
Spironolactone: Although spironolactone can reduce albuminuria, it carries a higher risk of hyperkalemia in advanced CKD and could lower blood pressure excessively given Victor’s current well-managed levels.

Case 1, Question 3

Case Summary

Case 1, Question 3 Rationale

According to several major guidelines on lowering cardiovascular risk, a hs-CRP ≥2 mg/L can be considered an ASCVD risk enhancer as it conveys an increased risk of ASCVD relative to a hs-CRP concentration less than 2 mg/L. While it is true that a hs-CRP level ≥2 mg/L is associated with increased ASCVD risk, current guidelines do not recommend targeting a specific hs-CRP level as a treatment goal. Additionally, although type 2 diabetes is often associated with chronic inflammation, the presence of diabetes does not automatically negate its value. Furthermore, Victor’s A1C suggests his diabetes is reasonably well managed, making it unlikely to be the primary driver of his elevated hs-CRP. Lastly, ASCVD risk-enhancing factors like hs-CRP are relevant even in patients with established ASCVD, as they can guide treatment decisions in this patient population in whom traditional ASCVD risk calculators are not recommended.

Patient Case Vignettes

Review each case and answer the questions that follow.

Review Patient Case 2

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Case 2, Question 1

Click here to access PREVENT (Predicting Risk of cardiovascular disease EVENTs) risk calculator.

Case Summary

Case 2, Question 1 Rationale

Maria’s estimated 10-year risk of ASCVD using the full model (i.e. including uACR and A1C) is 6.4%, which is considered “intermediate/moderately elevated”. Of note, the PREVENT calculator does not include hs-CRP within the model – it is a risk enhancing factor that can be considered after calculating a patient’s 10-year ASCVD risk to help with clinical decision making,

Case 2, Question 2

Case Summary

Case 2, Question 2 Rationale

Of the available options, bempedoic acid will provide ASCVD risk reduction by reducing LDL-C in addition to reducing systemic inflammation, especially since Maria has a markedly elevated LDL-C level and is intolerant to statins. While each of the remaining interventions—rosuvastatin, aspirin, and low-dose colchicine—has potential clinical value, these options are less ideal for Maria at this time:

Rosuvastatin: While it is true that statins are the cornerstone of ASCVD risk reduction, Maria has documented statin intolerance despite multiple trials and rechallenges, making them no longer a viable option.
Aspirin: Although aspirin may modestly reduce ASCVD risk and inflammation, its role in primary prevention remains uncertain, and if considered, would typically be used at a lower dose of 81 mg daily.
Low-dose colchicine: Lastly, although low-dose colchicine might help lower inflammation given her elevated hs-CRP, it does not address her elevated LDL-C which is also a significant driver of ASCVD risk. In contrast, bempedoic acid effectively lowers LDL-C and is specifically indicated for patients who are statin intolerant, making it a more suitable and targeted option for Maria at this time (with the option to add low-dose colchicine later if hs-CRP remains elevated after initiating bempedoic acid).

Claim CME/CE Credit

Eligible learners can claim up to 0.5 hours of CME/CE credit for this program. Visit the NKF Professional Education Resource Center (PERC) to register for this program and complete the requirements. Credit available until August 15, 2026.

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References

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03

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18

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23

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24

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Lopaschuk GD, Verma S. Mechanisms of Cardiovascular Benefits of Sodium Glucose Co-Transporter 2 (SGLT2) Inhibitors: A State-of-the-Art Review. JACC Basic Transl Sci. 2020;5(6):632-644. doi:10.1016/j.jacbts.2020.02.004

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Buttice L, Ghani M, Suthakar J, et al. The effect of sodium-glucose cotransporter-2 inhibitors on inflammatory biomarkers: A meta-analysis of randomized controlled trials. Diabetes Obes Metab. 2024;26(7):2706-2721. doi:10.1111/dom.15586

Yoo TT, Baek IH, Stoletniy L, Hilliard A, Sakr A, Doycheva D. Impact of sodium-glucose transport protein-2 (SGLT2) inhibitors on the inflammasome pathway in acute myocardial infarction in type 2 diabetes mellitus: a comprehensive review. Cardiovasc Diabetol. 2025;24(1):227. doi:10.1186/s12933-025-02777-7

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Morales J, Handelsman Y. Cardiovascular Outcomes in Patients With Diabetes and Kidney Disease. J Am Coll Cardiol. 2023;82(2):161-170. doi:10.1016/j.jacc.2023.04.052

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Barrera-Chimal J, Lima-Posada I, Bakris GL, Jaisser F. Mineralocorticoid receptor antagonists in diabetic kidney disease — mechanistic and therapeutic effects. Nat Rev Nephrol. 2022;18(1):56-70. doi:10.1038/s41581-021-00490-8

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Wang QR, Yang Y. Mineralocorticoid receptor antagonists promote renal immunosenescence. Int Urol Nephrol. Published online April 30, 2025. doi:10.1007/s11255-025-04530-1

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Berger M, MacNamara A, Ferreira JP, et al. Finerenone effects on biomarkers: an analysis from the FIGARO-DKD trial. Eur Heart J. 2025;ehaf316. doi:10.1093/eurheartj/ehaf316

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Ren Y, Chen Y, Zheng W, et al. The effect of GLP‐1 receptor agonists on circulating inflammatory markers in type 2 diabetes patients: A systematic review and meta‐analysis. Diabetes Obes Metab. 2025;27(7):3607-3626. doi:10.1111/dom.16366

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Deftereos SG, Beerkens FJ, Shah B, et al. Colchicine in Cardiovascular Disease: In-Depth Review. Circulation. 2022;145(1):61-78. doi:10.1161/CIRCULATIONAHA.121.056171

Punnanithinont N, Kambalapalli S, Iskander B, et al. “Anti-inflammatory Therapies in Atherosclerosis – Where are we going?” Curr Atheroscler Rep. 2024;27(1):19. doi:10.1007/s11883-024-01267-7

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Table 2. Summary of guideline recommendations regarding hs-CRP and primary ASCVD risk prevention

Guideline

Recommendation

2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease25 2018 AHA/ACC/AACVPR/AAPA/ ABC/ACPM/ADA/AGS/APhA/ASPC/ NLA/PCNA Guideline on the Management of Blood Cholesterol26

NLA Recommendations for Patient-Centered Management of Dyslipidemia: Part 127

American Society for Preventive Cardiology28

Managing Intermediate ASCVD Risk

Maria is a 55-year-old female with a past medical history of hypertension, type 2 diabetes, hyperlipidemia, and stable CKD (Stage G2A1) secondary to IgA nephropathy. She has a strong family history of premature ASCVD and confirmed statin intolerance (significant muscle symptoms with 3 different statins, including rechallenges).

Medications: • Dapagliflozin 10 mg daily • Ezetimibe 10 mg daily • Lisinopril 40 mg daily • Metformin 1000 mg twice daily

Laboratory values: • TC 224 mg/dL, HDL-C 41 mg/dL, LDL-C 155 mg/dL, triglycerides 140 mg/dL • SCr 0.99 mg/dL, eGFR 67 mL/min/1.73m2, uACR 10 mg/g (was markedly elevated prior to initiating lisinopril and dapagliflozin) • A1C: 6.6% • hs-CRP: 4.8 mg/L

Vitals: • BP 126/72 mmHg; HR 72 beats/min • BMI: 32.1 kg/m2

Social history: • Has never used tobacco • ~3 hours of moderate-intensity exercise/week

CKD Agents

Proposed mechanism(s) for anti-inflammatory effects

Clinical Pearls for use in CKD

Medication/Class

Impact on hs-CRP

Reduce albuminuria-mediated inflammation
Block angiotensin II/aldosterone-mediated inflammation

Continue until dialysis (if tolerated)

RAAS inhibitors46

No effect

Reduce albuminuria-mediated inflammation
Reduce hyperglycemia-mediated inflammation
Reduce intraglomerular pressure
May inhibit NLRP3 inflammasome activation

Initiate as long as eGFR ≥20
Continue until dialysis (if tolerated)

Possible decrease (conflicting results)

SGLT2 inhibitors46–49

Steroidal:

Reduce albuminuria-mediated inflammation
Block aldosterone-mediated inflammation
Suppress pro-inflammatory cytokines (e.g. IL-6, TNF-α, IL-1β)
May inhibit NLRP3 inflammasome activation

Use with caution due to hyperkalemia risk, especially if eGFR <45

_____________________

Mineralocorticoid Receptor Antagonists50–53

No effect

Nonsteroidal:

Approved in CKD (eGFR ≥25) with T2D and albuminuria
Lower hyperkalemia risk vs. steroidal MRAs

No dose adjustments needed based on eGFR (except exenatide)

Fat mass reduction
Reduce albuminuria-mediated inflammation
Reduce hyperglycemia-mediated inflammation
Suppress pro-inflammatory cytokines (e.g. IL-6, TNF-α, IL-1β)

Decrease

GLP-1 RAs54

Lipid-lowering Agents

Proposed mechanism(s) for anti-inflammatory effects

Clinical Pearls for use in CKD

Medication/Class

Impact on hs-CRP

Inhibit mevalonate pathway
Reduce LDL-C mediated inflammation
Suppress pro-inflammatory cytokines (e.g. IL-6, TNF-α, IL-1β)
Improve endothelial function
Inhibit immune cell activation in vasculature

Do not exceed rosuvastatin 10 mg daily if eGFR <30
No atorvastatin dose adjustments needed based on eGFR
Dialysis: do not initiate statin, but continue if tolerated

Statins40,41

Decrease

Decrease (in combination with statin)

No dose adjustments needed based on eGFR

Reduces LDL-C mediated inflammation
Suppresses pro-inflammatory cytokines (e.g. IL-6, TNF-α, IL-1β)

Ezetimibe41

Reduces LDL-C mediated inflammation
Improves endothelial function

Bempedoic acid 42,43

No dose adjustments needed for eGFR ≥30
Limited data in eGFR <30

Decrease

No dose adjustments needed based on eGFR
Limited evidence in eGFR <30

Reduce LDL-C mediated inflammation
Suppress pro-inflammatory cytokines (e.g. IL-6, TNF-α, IL-1β)
Increase IL-10 (anti-inflammatory interleukin)

PCSK-9 inhibitors 41,44

No effect

No dose adjustments needed based on eGFR

Suppresses pro-inflammatory cytokines (e.g. IL-6, TNF-α, IL-1β)
Increases IL-10 (anti-inflammatory interleukin)

Icosapent Ethyl45

Decrease

Figure 5. Relationship of increasing quartiles of baseline hsCRP to associated cardiovascular and mortality risks for individuals with eGFR < 60 mL/min/1.73m2 in CANTOS trial

p<0.05 compared to reference group

Managing Residual Risk in CKD with Established CAD

Victor is a 69-year-old male with a past medical history of coronary artery disease (STEMI 18 months ago), type 2 diabetes, hypertension, COPD, and stable CKD (Stage G3bA2).

Laboratory values: • TC 154 mg/dL, HDL-C 34 mg/dL, LDL-C 84 mg/dL, triglycerides 180 mg/dL • SCr 1.83 mg/dL, eGFR 39 mL/min/1.73m2, uACR 160 mg/g • A1C: 7.1%

Medications:• Aspirin 81 mg daily • Atorvastatin 80 mg daily • Empagliflozin 25 mg daily • Ezetimibe 10 mg daily • Losartan/HCTZ 100/25 mg daily • Metoprolol succinate 50 mg daily • Semaglutide 2 mg weekly • Umeclidinium-vilanterol 62.5/25 mcg once daily

Vitals: • BP 128/76 mmHg; HR 64 beats/min • BMI: 26.4 kg/m2

Social history:

• Does not currently smoke (quit last year, 25 pack-year history) • ~75 minutes of moderate-intensity exercise/week • Retired, has commercial insurance

Case Study: 35-Year Old Woman with Type 1 Diabetes, Hypertension, and Dyslipidemia

A 35-year old woman presents with type 1 diabetes, hypertension, and dyslipidemia. She is on an ACE-inhibitor with good blood pressure control. Within the past 3 years, her eGFR has dropped from 46 mL/min/1.73m2 to 28 mL/min/1.73 m2. Her current albuminuria consistently remains ≥300 mg/g. Her lab results reveal that she has recently developed CKD-related mineral and bone disorder (CKD-MBD), with an iPTH of 220 pg/ml and serum phosphorus of 4.8 mg/dl. Based on the “CKD Risk Map,” you know that: 1) her CKD can be classified as A3/G4 2) her risk of progression is very high 3) referral to a nephrologist is recommended; and 4) she should be monitored 4 or more times per year.

Managing Residual Risk in CKD with Established CAD

Victor is a 69-year-old male with a past medical history of coronary artery disease (STEMI 18 months ago), type 2 diabetes, hypertension, COPD, and stable CKD (Stage G3bA2).

Laboratory values: • TC 154 mg/dL, HDL-C 34 mg/dL, LDL-C 84 mg/dL, triglycerides 180 mg/dL • SCr 1.83 mg/dL, eGFR 39 mL/min/1.73m2, uACR 160 mg/g • A1C: 7.1%

Vitals: • BP 128/76 mmHg; HR 64 beats/min • BMI: 26.4 kg/m2

Social history:

• Does not currently smoke (quit last year, 25 pack-year history) • ~75 minutes of moderate-intensity exercise/week • Retired, has commercial insurance

Managing Residual Risk in CKD with Established CAD

Victor is a 69-year-old male with a past medical history of coronary artery disease (STEMI 18 months ago), type 2 diabetes, hypertension, COPD, and stable CKD (Stage G3bA2).

Laboratory values: • TC 154 mg/dL, HDL-C 34 mg/dL, LDL-C 84 mg/dL, triglycerides 180 mg/dL • SCr 1.83 mg/dL, eGFR 39 mL/min/1.73m2, uACR 160 mg/g • A1C: 7.1%

Vitals: • BP 128/76 mmHg; HR 64 beats/min • BMI: 26.4 kg/m2

Social history:

• Does not currently smoke (quit last year, 25 pack-year history) • ~75 minutes of moderate-intensity exercise/week • Retired, has commercial insurance

Managing Intermediate ASCVD Risk

Maria is a 55-year-old female with a past medical history of hypertension, type 2 diabetes, hyperlipidemia, and stable CKD (Stage G2A1) secondary to IgA nephropathy. She has a strong family history of premature ASCVD and confirmed statin intolerance (significant muscle symptoms with 3 different statins, including rechallenges).

Medications: • Dapagliflozin 10 mg daily • Ezetimibe 10 mg daily • Lisinopril 40 mg daily • Metformin 1000 mg twice daily

Vitals: • BP 126/72 mmHg; HR 72 beats/min • BMI: 32.1 kg/m2

Social history: • Has never used tobacco • ~3 hours of moderate-intensity exercise/week

Anti-inflammatory Agents for Reducing CV Risk (focus on CKD)

Proposed mechanism(s) for anti-inflammatory effects

Clinical Pearls for use in CKD

Medication/Class

Impact on hs-CRP

Inhibits immune cell activation in vasculature
Inhibits NLRP3 inflammasome activation
Suppresses pro-inflammatory cytokines (e.g. IL-6, TNF-α, IL-1β)

Excreted by kidneys
Use with caution in eGFR <30

Low-dose colchicine55

Decrease

Neutralizes IL-6 signaling

Phase 3 ZEUS trial ongoing in adults with CKD (eGFR 15-59 mL/min/1.73m2 or uACR ≥200 mg/g), hsCRP ≥2 mg/L, and clinical ASCVD

Ziltivekimab56,57 (investigational)

Decrease

Clazakizumab58,59 (investigational)

Phase 2b/3 POSIBIL6ESKD trial ongoing in adults with ESKD undergoing dialysis, hs-CRP ≥2 mg/L, and diabetes or ASCVD

Neutralizes IL-6 signaling

Decrease

Neutralizes IL-6 signaling

Phase 2 TRANQUILITY trial ongoing in adults with CKD (eGFR 15-59 mL/min/1.73m2 or uPCR ≥200 mg/g), hs-CRP ≥2 mg/L and <15 mg/L

Pacibekitug60 (investigational)

Decrease

Table 1. Overlapping Risk Factors for CKD and ASCVD

Health Conditions

Lifestyle Factors

Miscellaneous Risk Factors

Smoking and/or use of tobacco products

Family history/genetic predisposition

Hypertension

Dyslipidemia

Diabetes

Metabolic syndrome

Albuminuria

Obesity

Hyperuricemia

Physical inactivity

Poor nutrition

Older age

Systemic inflammation

Social and area deprivation

Low socioeconomic status

Vascular calcification

Environmental toxins

Managing Residual Risk in CKD with Established CAD

Victor is a 69-year-old male with a past medical history of coronary artery disease (STEMI 18 months ago), type 2 diabetes, hypertension, COPD, and stable CKD (Stage G3bA2).

Laboratory values: • TC 154 mg/dL, HDL-C 34 mg/dL, LDL-C 84 mg/dL, triglycerides 180 mg/dL • SCr 1.83 mg/dL, eGFR 39 mL/min/1.73m2, uACR 160 mg/g • A1C: 7.1%

Vitals: • BP 128/76 mmHg; HR 64 beats/min • BMI: 26.4 kg/m2

Social history:

• Does not currently smoke (quit last year, 25 pack-year history) • ~75 minutes of moderate-intensity exercise/week • Retired, has commercial insurance

Managing Intermediate ASCVD Risk

Maria is a 55-year-old female with a past medical history of hypertension, type 2 diabetes, hyperlipidemia, and stable CKD (Stage G2A1) secondary to IgA nephropathy. She has a strong family history of premature ASCVD and confirmed statin intolerance (significant muscle symptoms with 3 different statins, including rechallenges).

Medications: • Dapagliflozin 10 mg daily • Ezetimibe 10 mg daily • Lisinopril 40 mg daily • Metformin 1000 mg twice daily

Vitals: • BP 126/72 mmHg; HR 72 beats/min • BMI: 32.1 kg/m2

Social history: • Has never used tobacco • ~3 hours of moderate-intensity exercise/week

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Guided by Inflammation: Applying New Insights to CKD and ASCVD Care

Supported by an educational grant from Novo Nordisk.

Index

Pre-test

Learning Objectives

Faculty Disclosures

The interconnectedness of CKD, systemic inflammation, and ASCVD

Overlapping Risk Factors for CKD and ASCVD

Systemic Inflammation and High-Sensitivity C-Reactive Protein (hs-CRP)

Anti-inflammatory effects of current & emerging treatment options

Recommended Further Reading

Patient Case Vignettes

References

Claim CME/CE Credit

Learning Objectives

Faculty Disclosures

Pre-test

Pre-test, Question 1

Pre-test, Question 2

Pre-test, Question 3

Pre-test, Question 4

The Interconnectedness of CKD, Systemic Inflammation, and ASCVD

Figure 1. Association Between eGFR/uACR and Cardiovascular Mortality

The Interconnectedness of CKD, Systemic Inflammation, and ASCVD

Figure 2. KDIGO CKD Heat Map

A1

A2

A3

Normal to mildly increased

Moderately increased

Severely increased

<30 mg/g <3 mg/mmol

30-300 mg/g3-30 mg/mmol

>300 mg/g>30 mg/mmol

Normal or high

≥90

G1

G2

60-89

Mildly decreased

Mildly to moderately decreased

G3a

45-59

Moderately to severely decreased

30-44

G3b

Severely decreased

G4

15-29

G5

<15

Kidney Failure

Overlapping Risk Factors for CKD and ASCVD

Table 1. Overlapping Risk Factors for CKD and ASCVD

Overlapping Risk Factors for CKD and ASCVD

Figure 3. The Impact of Social Determinants of Health on Systemic Inflammation and CVD

Systemic Inflammation and High-Sensitivity C-Reactive Protein (hs-CRP)

Figure 4. Inflammatory pathways involved in atherosclerosis

Systemic Inflammation and High-Sensitivity C-Reactive Protein (hs-CRP)

Table 2. Summary of guideline recommendations regarding hs-CRP and primary ASCVD risk prevention

Systemic Inflammation and High-Sensitivity C-Reactive Protein (hs-CRP)

Figure 5. Relationship of increasing quartiles of baseline hsCRP to associated cardiovascular and mortality risks for individuals with eGFR < 60 mL/min/1.73m2 in CANTOS trial

Anti-inflammatory Effects of Current & Emerging Treatment Options