Why the study?
Does the etiology of chronic kidney disease (PKD vs. IgAN) differentially affect arterial stiffness?
Does the etiology of chronic kidney disease (PKD vs. IgAN) differentially affect arterial stiffness?
Arterial stiffness is more pronounced in patients with polycystic kidney disease compared to those with IgA nephropathy, highlighting that vascular function alteration in CKD depends on the underlying etiology.
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Greater arterial stiffness in PKD versus IgAN; supports etiology-specific vascular effects in CKD but leaves causal and prognostic implications open.
BACKGROUND: Renal function is a major predictor of vascular function and cardiovascular diseases. Little information exists about the effect of specific renal diseases on vascular function in chronic kidney diseases (CKD). METHODS: One hundred and twenty patients (60 with IgA nephropathy, IgAN, and 60 with polycystic kidney disease, PKD) with CKD stages 1-4 were studied and compared. Pulse-wave velocity was measured by the digital volume pulse (DVP) method and stiffness index (SI(DVP)) was derived. RESULTS: All CKD (IgAN and PKD) patients had increased SI(DVP) compared to controls (10.39 vs. 8.87 ± 1.79 m/s, p = 0.008). PKD patients had increased SI(DVP) compared to IgAN and controls (11.14 ± 2.19, 9.66 ± 2.02 and 8.87 ± 1.79 m/s, respectively, p < 0.001). An inverse correlation was found between SI(DVP) and glomerular filtration rate in all CKD (IgAN and PKD) patients (p = 0.001) and in IgAN alone (p < 0.01), but not in PKD. With multivariate regression analysis, only age and 24-hour systolic blood pressure exerted independent effects on SI(DVP). CONCLUSIONS: Compared to controls, arterial stiffness was increased in CKD patients. However, arterial stiffening was more pronounced in PKD than in IgAN, suggesting that vascular function is not similarly altered in etiologically different CKD groups. The fact that blood pressure was an independent risk factor underscores a therapeutic opportunity.
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Késői et al. (2011) studied this question.
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