Key result
Diabetic nephropathy linked to impaired aortic function independent of mean arterial pressure.
Why the study?
The study aimed to assess the potential impacts of mean arterial pressure and its determinants (cardiac output and systemic vascular resistance) on diabetic nephropathy-associated impaired aortic function.
Does mean arterial pressure mediate diabetic nephropathy-associated impaired aortic function in patients with chronic kidney disease?
Observational (n=115)
Does mean arterial pressure mediate diabetic nephropathy-associated impaired aortic function in patients with chronic kidney disease?
Impaired aortic function in diabetic nephropathy is not mediated by mean arterial pressure, suggesting that blood pressure lowering alone may not improve aortic stiffness in this specific subgroup.
Answers are grounded in this paper and cite their sources.
Impaired aortic function in diabetic nephropathy appears independent of mean arterial pressure; cross-sectional data leave open whether BP-independent therapies are needed.
Objective: The study aimed to assess the potential impacts of mean arterial pressure (MAP) and its determinants (cardiac output and systemic vascular resistance) on diabetic nephropathy (DNP)-associated impaired aortic function. Methods: This multi-ethnic study included 115 chronic kidney disease (CKD) patients (67 non-dialysis and 48 dialysis). Six aortic function measures were evaluated by SpygmoCor. The stroke volume was determined by echocardiography. Results: Hypertensive nephropathy (HNP) (53.9%), DNP (32.2%), glomerulonephritis (19.1%), and HIV-associated nephropathy (7.8%) composed the major CKD etiologies. Concurrent HNP and DNP were present in 31.1% of the patients. Participants with compared with those without concurrent HNP and DNP experienced more frequent established cardiovascular disease (43.2% versus 14.9%, p = 0.01), a faster pulse wave velocity (p = 0.001), and smaller total arterial compliance as an indicator of proximal aortic stiffness (p = 0.03). DNP was associated with each aortic function measure (p < 0.001–0.02) independent of potential confounders and MAP, as well as its determinants. HNP was not related to aortic function (p > 0.05 for all relationships). MAP and its determinants did not mediate the potential impact of DNP on aortic function (−4.1–6.4% contribution). Covariates that were associated with impaired aortic function measures included MAP and its determinants (p < 0.001–0.01). Conclusions: Mean or distending arterial pressure and its determinants were associated with impaired aortic function in the overall CKD population. However, these hemodynamic factors did not mediate DNP-associated impaired aortic function. Our results suggest that blood pressure lowering can be anticipated to improve impaired aortic function in the overall CKD population but not when it is solely induced by DNP.
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Hsu et al. (2024) conducted an observational in Chronic kidney disease (n=115). Diabetic nephropathy vs. Without diabetic nephropathy was evaluated on Aortic function measures (p=<0.001–0.02). Diabetic nephropathy was associated with impaired aortic function independent of mean arterial pressure and its determinants, which did not mediate this relationship (-4.1-6.4% contribution).
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