AFRICA Cardiovascular Journal of Africa • SAHS Biennial Congress 2024 10 Submission ID: 1629 Introduction Impaired aortic function is a core mechanism in the development of uremic cardiomyopathy. We recently documented in a large cohort of chronic kidney disease (CKD) patients (n=743) that mean arterial pressure (MAP) can fully account for the potential impact of presumed hypertensive nephropathy (HNP) (103.9-115.7%) but not diabetic nephropathy (DNP), (-2.0%-(-)7.5%) on pulsatile pressures including peripheral pulse pressure (PP) and systolic blood pressure (SBP). This suggests that impaired aortic function may be improved by volume control and/or reducing systemic vascular resistance (SVR) in patients with HNP but not those with DNP. Herein, we address this hypothesis. Methods The current multi-ethnic study (black 40.0%; white 24.4%; mixed race 7.8%; Asian 27.8%) included 115 CKD patients (67 non-dialysis and 48 dialysis). Their mean (SD) age was 57.7 (14.0) years, 37.4% were women and CKD duration was 5.4 (4.5) years. HNP (53.9%), DNP (32.2%), glomerulonephritis (19.1%) and HIV associated nephropathy (7.8%) comprised the major CKD etiologies. Concurrent HNP and DNP was present in 31.1% of the patients. Aortic function measures comprised PP, SBP, central pulse pressure, central systolic blood pressure, proximal aortic stiffness as estimated by the inverse of total arterial compliance (invTAC), carotid-femoral pulse wave velocity, backward wave pressure and forward wave pressure. The potential mutually independent impact of presumed HNP and DNP on aortic function was assessed in confounder and mediator adjusted multiple regression models. The contribution of MAP and the interaction between cardiac output (CO) and SVR to CKD etiology-aortic function relationships was assessed in adjusted product of coefficient mediation analysis. The calculated power of the study was 0.997 based on α=0.05. Results Patients with compared to without concurrent HNP and DNP experienced more frequent cardiovascular disease (43.2% versus 14.9%, p=0.01) and impaired aortic function (p=0.006-0.05 for 5 of the measures). DNP was independently associated with each aortic function measure (p<0.001-0.02). HNP was not directly related to aortic function (p>0.05). Other covariates that were consistently associated with impaired aortic function measures except for invTAC, included MAP (p<0.001-0.01) and its determinants. MAP and CO x SVR did not account for the potential effect of DNP on any aortic function measure (0.02-(-)7.3%). Dialysis status did not impact any of the identified relationships (interaction p>0.05). Conclusion This study validates our previously reported findings. Our results suggest that reducing MAP by decreasing volume overload and/or SVR through fluid intake restriction, diuretic therapy and antihypertensive agents or vasodilators may improve aortic function in the overall CKD population. However, these interventions are unlikely to reverse impaired aortic function that is induced by DNP. The potential impact of MAP and its determinants as well as DNP on aortic function is similar in non-dialysis and dialysis patients. Whether increased arterial medial calcification associated with diabetes and DNP explain our findings merits further study. Name: Presenting Author Information Article Category Abstract Title Cardiovascular Pathophysiology and Genomics Research Unit, Faculty of Health Sciences, School of Physiology, University of the Witwatersrand, Johannesburg, South Africa. oluwatosin.tade@wits.ac.za English Abstract Researchers/Clinicians - Early, mid & senior career Diabetic nephropathy induced impaired aortic function is not mediated by mean arterial pressure and its determinants Author Affiliation: Email: Grace Tade Science Theme Clinical continued on next page ORAL PRESENTATION
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