Myocardial Fibrosis Assessment in Hypertensive Individuals with Chronic Kidney Disease

Location

Science Center: Bent Corridor

Document Type

Poster - Open Access

Start Date

4-28-2023 12:00 PM

End Date

4-28-2023 2:00 PM

Abstract

Background:
Chronic kidney disease (CKD) is associated with an increased risk of myocardial fibrosis which is a substrate for arrhythmia and heart failure. Myocardial fibrosis can be assessed non-invasively by cardiac magnetic resonance (CMR) T1 mapping or by circulating biomarkers; however, the performance of such biomarkers in the setting of impaired kidney function has not been rigorously tested.

Methods:
The Systolic Blood Pressure Intervention Trial (SPRINT) enrolled 9,361 US participants aged ≥50 years, at increased cardiovascular risk, and randomized them to intensive (<120mmHg) or standard (<140mmHg) systolic blood pressure lowering. A subgroup of 337 SPRINT participants with and without CKD had CMR T1 mapping, and measured plasma biomarkers of myocardial fibrosis: C-terminal propeptide of procollagen type I (CICP), N-terminal propeptide of procollagen type 3 (P3NP), and Galectin 3 (Gal-3) at study baseline.

Results:
Study participants had a mean age of 64.3 [SD 8.9] years, 44.8% were women, and 21% had CKD. The levels of Gal-3, PICP, and PIIINP were found inversely correlated with estimated glomerular filtration rate (eGFR) and positively correlated with log-transformed spot albumin/creatinine (p-value < 0.001 for all). No correlation was found between the level of the three biomarkers and the CMR T1 times, a more precise measure of myocardial fibrosis.

Conclusion:
In individuals with and without CKD, Gal-3, PICP, and PIIINP levels were not associated with CMR T1 times. Elevated plasma biomarkers level in the context of CKD should be interpreted with caution as it may reflect their decreased urinary clearance, rather than true pathologic processes.

Keywords:

Nephrology, Myocardial fibrosis, Biomarkers

Major

Biology

Project Mentor(s)

Dr. Monica Mantano, Department of Medicine, Division of Nephrology and Hypertension, University Hospitals Cleveland Medical Center

Dr. Mirela Dobre, Department of Medicine, Division of Nephrology and Hypertension, University Hospitals Cleveland Medical Center

2023

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Apr 28th, 12:00 PM Apr 28th, 2:00 PM

Myocardial Fibrosis Assessment in Hypertensive Individuals with Chronic Kidney Disease

Science Center: Bent Corridor

Background:
Chronic kidney disease (CKD) is associated with an increased risk of myocardial fibrosis which is a substrate for arrhythmia and heart failure. Myocardial fibrosis can be assessed non-invasively by cardiac magnetic resonance (CMR) T1 mapping or by circulating biomarkers; however, the performance of such biomarkers in the setting of impaired kidney function has not been rigorously tested.

Methods:
The Systolic Blood Pressure Intervention Trial (SPRINT) enrolled 9,361 US participants aged ≥50 years, at increased cardiovascular risk, and randomized them to intensive (<120mmHg) or standard (<140mmHg) systolic blood pressure lowering. A subgroup of 337 SPRINT participants with and without CKD had CMR T1 mapping, and measured plasma biomarkers of myocardial fibrosis: C-terminal propeptide of procollagen type I (CICP), N-terminal propeptide of procollagen type 3 (P3NP), and Galectin 3 (Gal-3) at study baseline.

Results:
Study participants had a mean age of 64.3 [SD 8.9] years, 44.8% were women, and 21% had CKD. The levels of Gal-3, PICP, and PIIINP were found inversely correlated with estimated glomerular filtration rate (eGFR) and positively correlated with log-transformed spot albumin/creatinine (p-value < 0.001 for all). No correlation was found between the level of the three biomarkers and the CMR T1 times, a more precise measure of myocardial fibrosis.

Conclusion:
In individuals with and without CKD, Gal-3, PICP, and PIIINP levels were not associated with CMR T1 times. Elevated plasma biomarkers level in the context of CKD should be interpreted with caution as it may reflect their decreased urinary clearance, rather than true pathologic processes.