2020
DOI: 10.3390/toxins12030140
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Should We Consider the Cardiovascular System While Evaluating CKD-MBD?

Abstract: Cardiovascular (CV) disease is highly prevalent in the population with chronic kidney disease (CKD), where the risk of CV death in early stages far exceeds the risk of progression to dialysis. The presence of chronic kidney disease-mineral and bone disorder (CKD-MBD) has shown a strong correlation with CV events and mortality. As a non-atheromatous process, it could be partially explained why standard CV disease-modifying drugs do not provide such an impact on CV mortality in CKD as observed in the general pop… Show more

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Cited by 7 publications
(5 citation statements)
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“…Renal transplantation also improved cardiac structure and function, with significant improvements in LVEF, left ventricular mass, left ventricular end‐diastolic size and right ventricular systolic pressure 49 . Of note, in the presence of severe LV systolic dysfunction even mild renal impairment is independently associated with increased risk for all‐cause mortality 50 …”
Section: Discussionmentioning
confidence: 98%
“…Renal transplantation also improved cardiac structure and function, with significant improvements in LVEF, left ventricular mass, left ventricular end‐diastolic size and right ventricular systolic pressure 49 . Of note, in the presence of severe LV systolic dysfunction even mild renal impairment is independently associated with increased risk for all‐cause mortality 50 …”
Section: Discussionmentioning
confidence: 98%
“…In addition, abnormal calcium-phosphorus metabolism is often observed in CKD patients. It has been suggested that disturbances in bone and mineral metabolism contribute to the excessively high CVD morbidity and mortality among CKD patients ( 27 ). The KDIGO guidelines for CKD-MBD ( 6 ) suggest restricting the dose of calcium containing phosphate binders in the presence of arterial calcification in patients with CKD stages 3–5D and hyperphosphatemia.…”
Section: Discussionmentioning
confidence: 99%
“…Elevated PTH levels are also expected in uremic patients much earlier than hyperphosphatemia. PTH stimulates calcitriol synthesis that further contributes to increased serum calcium [41]. In contrast with the physiologic state where FGF23 acts on the parathyroid gland by diminishing gene expression and secretion in CKD in the absence of Klotho, the parathyroid gland shows resistance to FGF23, enhancing PTH secretion.…”
Section: Phosphate Homeostasis In the Physiological Milieu And Ckdmentioning
confidence: 99%