Content - Navigating the CKM Axis Module 1

Introduction

In this module, 3 experts across cardiology, endocrinology, and nephrology discuss how the CKM axis bridges the pathophysiology of CKD, heart failure (HF), and T2D (or CKM syndrome).

Decera Clinical Education plans to measure the educational impact of this activity. Some questions will be asked twice: once at the beginning of the activity and then once again after the discussion that informs the best choice. Your responses will be aggregated for analysis, and your specific responses will not be shared.

Before continuing with this educational activity, please take a moment to answer the following questions.

A 64-year-old man with type 2 diabetes (T2D), stage 3b/A2 chronic kidney disease (CKD), and heart failure with reduced ejection fraction (HFrEF; ejection fraction: 30%) presents with worsening exertional dyspnea and mild ankle edema. He has a history of prostatic hypertrophy and a mild delay in voiding. His medications include sacubitril/valsartan, empagliflozin, furosemide, and metoprolol succinate. His laboratory values include: K⁺ 4.7 mEq/L, creatinine 1.8 mg/dL, estimated glomerular filtration rate (eGFR) 40 mL/min/1.73m², and urine–albumin-to-creatinine ratio (UACR) 60 mg/g. Which of the following is the best next management step to target aldosterone’s role in worsening cardiovascular–kidney–metabolic (CKM) conditions?

A.
Increase loop diuretic dose to further lower volume and reduce risk of hyperkalemia
B.
Discontinue angiotensin receptor-neprilysin inhibitor to prevent hyperkalemia and substitute with hydralazine/isosorbide dinitrate
C.
Stop sodium-glucose cotransporter-2 (SGLT2) inhibitor due to risk of genitourinary infections
D.
Add spironolactone to reduce mortality risk and closely monitor potassium and eGFR

A 68-year-old man with HFrEF and stage 3a/A2 CKD (eGFR 55 mL/min/1.73m² and UACR 120 mg/g) is being considered for enrollment in a clinical trial evaluating an investigational aldosterone synthase inhibitor (ASI). Which of the following statements best reflects a potential advantage of ASIs over MRAs in the management of patients with CKM conditions?

A.
ASIs inhibit aldosterone binding to mineralocorticoid receptors, preventing downstream gene transcription in the distal tubule and cortical collecting ducts
B.
ASIs block aldosterone production at its enzymatic source, potentially reducing both genomic and nongenomic effects
C.
ASIs enhance potassium excretion by competitively inhibiting epithelial sodium channels in the distal nephron
D.
ASIs increase cortisol synthesis, which competitively antagonizes aldosterone at mineralocorticoid receptors

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Navigating the CKM Axis: Understanding the Pathophysiologic Connection Between CKD and HF

Stefano Del Prato, MD

Michelle Kittleson, MD, PhD

Katherine R. Tuttle, MD, FASN, FACP, FNKF

Activity

Introduction

How confident are you in your understanding of the underlying pathophysiology of cardio-kidney-metabolic syndrome?

How many patients do you see each week with a cardio-kidney-metabolic disorder?

Please select the option that best describes your primary practice setting: