Background: Pediatric patients with chronic kidney disease (CKD) are at increased risk of early cardiovascular disease and premature death. Abnormalities in microvascular structure and function may presage end-organ damage including vascular calcification and myocardial ischemia associated with disordered mineral metabolism. Early detection of microvascular rarefaction (reduced density of capillaries) may identify at-risk patients and prompt timely therapeutic interventions. Our objective was to study capillary rarefaction in pediatric hemodialysis (HD) patients and to determine possible associations with mineral metabolism and cardiac risk biomarkers.
Methods: Capillary density (CD) was measured by nailfold capillaroscopy in 19 pediatric HD patients and 20 healthy controls. Demographic and biochemical markers were collected at entry and 6-month follow-up.
Results: CD was significantly decreased in HD patients compared with controls with a deficit of 24 and 31% at baseline and subsequent follow-up. Maximal CD correlated significantly with intact parathyroid hormone (iPTH) (r = -0.45; P = 0.005), serum calcium (r = -0.38; P = 0.02) and 25(OH) vitamin D levels (r = +0.36; P = 0.03) in HD patients. Capillary functional measures were similar to controls. By multivariate analysis, the primary negative determinants of CD were African American race and hyperparathyroidism; whereas, glomerular disease had a positive influence on capillary rarefaction (R (2) = 64.2% variance; P = 0.001).
Conclusion: Pediatric HD patients demonstrate a 'structural deficit' in CD but show preserved 'functional integrity'. Capillary rarefaction, an early risk factor of incipient vascular calcification, was strongly associated with biomarkers of altered mineral metabolism. Further studies are warranted to determine the impact of optimizing blood pressure and metabolic control on changes in capillary rarefaction in young CKD patients.
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http://dx.doi.org/10.1093/ckj/sfu106 | DOI Listing |
High Blood Press Cardiovasc Prev
December 2024
First Department of Cardiology, School of Medicine, National and Kapodistrian University of Athens, Hippokration Hospital, Vas. Sofias 114, 11527, Athens, Greece.
Introduction: Hypertension is associated with changes in microcirculation, while increased blood pressure (BP) during exercise stress testing has been correlated with adverse outcomes.
Aim: To evaluate the relationship of microcirculation with exercise BP response in hypertensive individuals.
Methods: 105 hypertensive individuals underwent exercise stress testing and nail-fold videocapillaroscopy assessment, in order to evaluate the relationship of BP response to exercise with capillary density.
Front Physiol
November 2024
Department of Cardiovascular and Respiratory Physiology in Extreme Environments, Institute of Biomedical Problems of the Russian Academy of Sciences, Moscow, Russia.
Cell Rep
December 2024
Division of Medical Sciences, University of Victoria, Victoria, BC V8W 2Y2, Canada; Department of Psychiatry, University of British Columbia, Vancouver, BC V6T 1Z4, Canada. Electronic address:
Cerebral angiogenesis is well appreciated in development and after injury, but the extent to which it occurs across cortical regions in normal adult mice and the underlying mechanisms are incompletely understood. Using in vivo imaging, we show that angiogenesis in anterior-medial cortical regions (retrosplenial and sensorimotor cortex) was exceptionally rare. By contrast, angiogenesis was significantly elevated in posterior-lateral regions such as visual cortex, primarily within 200 μm of the cortical surface.
View Article and Find Full Text PDFJACC CardioOncol
October 2024
Interdisciplinary Center for Health Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.
Basic Res Cardiol
December 2024
The Hatter Cardiovascular Institute, University College London & UCL Hospital, 67 Chenies Mews, London, WC1E 6HX, UK.
Myocardial ischemia-reperfusion (IR) injury is a major cause of morbidity and mortality in patients with chronic kidney disease (CKD). The most frequently used and representative experimental model is the rat dietary adenine-induced CKD, which leads to CKD-associated CVD. However, the continued intake of adenine is a potential confounding factor.
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