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Peripheral arterial disease is a common clinical condition in chronic kidney disease patients, especially the elderly, diabetics, and arteriopathies, causing morbidity and mortality, associated with occlusive cardiovascular events, such as stroke, ICO and PAD. In the general population, the main triggering and perpetuating factor is atherosclerosis, but in chronic kidney patients, it is added to uremic toxins, a state of endothelial pro-inflammation, and disorders of bone mineral metabolism. In the early and intermediate stages, parathyroid hormone, calcium, phosphorus, and vitamin D levels may still be within normal limits but are altered as the glomerular filtration rate decreases. This study aims to verify whether there is clinical clarity with the interruptions of bone mineral metabolism dysfunction with subclinical peripheral arterial disease verified by the ankle-brachial index in patients with non-dialysis chronic kidney disease.
This investigation is a continuation of a cohort study involving patients with chronic kidney disease who were not undergoing dialysis. The study was conducted over a span of three years and involved 134 patients in a cross-sectional analysis. Throughout the study, clinical and laboratory data were collected and analyzed. To determine differences in independent variables, either the t-test or Mann-Whitney test was employed, while the Chi-square test was used to obtain categorical variables. Correlations were assessed using Spearman's coefficient.
The study revealed that 14.1% of patients had an altered ankle-brachial index (ABI) <0.9. Among this group, there was a higher occurrence of diabetics (p<0.02), patients with higher mean systolic and diastolic blood pressure (SBP p<0.009 DBP p<0.04), and patients with higher albumin/creatinine ratio (p<0.04). However, there was no connection found with lipid profile, blood glucose, or estimated glomerular filtration rate. The bone mineral profile indicated that subclinical arterial disease was linked to increased phosphorus and decreased vitamin D. These results were further validated by the observed correlations of ABI with phosphorus (r=-0.3 p=0.001), vitamin D (r=0.2 p=0.007), albumin/creatinine ratio (ACR)( r=-0.18 p=0.03) and systolic blood pressure ( r=-0.4 p<0.001
It is concluded that higher phosphorus and lower vitamin D in non-dialytic chronic kidney disease patients correlate with subclinical arterial disease, indicating important therapeutic targets.