Perioperative Iloprost and Endothelial Progenitor Cells in Uremic Patients With Severe Limb Ischemia Undergoing Peripheral Revascularization

Coppolino, Giuseppe; Buemi, Antoine; Bolignano, Davide; Lacquaniti, Antonio; Spada, Michele La; Stilo, Francesco; Caridi, Giovanni De; Benedetto, Filippo; Loddo, Saverio; Buemi, Michele; Spinelli, Francesco

doi:10.1016/j.jss.2008.07.017

Cited by 18 publications

(10 citation statements)

References 46 publications

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“…Indeed, the leakage of albumin in the vessel-wall may trigger an inflammatory response, thus accelerating the atherosclerotic process. More recently, multiple experimental and clinical studies elucidated that the presence of albuminuria witnesses abnormalities in endothelial glycocalyx, as well as other endothelial structures (Stehouwer et al, 1992;Coppolino et al, 2009;Perticone et al, 2016). Perticone et al (2015) have also found a significant inverse relationship between alkaline phosphatase and endothelium-dependent vasodilation, which can be mediated by an increase in fibroblast growth factor-23, an early marker of endothelial dysfunction in CKD patients.…”

Section: Link Between Kidney Measures and Cardiovascular Damagementioning

confidence: 99%

Unraveling Cardiovascular Risk in Renal Patients: A New Take on Old Tale

Provenzano

Coppolino

Nicola

et al. 2019

Front. Cell Dev. Biol.

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Chronic kidney disease (CKD), defined by an estimated glomerular filtration rate <60 ml/min/1.73 m 2 and/or an increase in urine protein excretion (i.e., albuminuria), is an important public health problem. Prevalence and incidence of CKD have risen by 87 and 89%, worldwide, over the last three decades. The onset of either albuminuria and eGFR reduction has found to predict higher cardiovascular (CV) risk, being this association strong, independent from traditional CV risk factors and reproducible across different setting of patients. Indeed, this relationship is present not only in high risk cohorts of CKD patients under regular nephrology care and in those with hypertension or type 2 diabetes, but also in general, otherwise healthy population. As underlying mechanisms of damage, it has hypothesized and partially proved that eGFR reduction and albuminuria can directly promote endothelial dysfunction, accelerate atherosclerosis and the deleterious effects of hypertension. Moreover, the predictive accuracy of risk prediction models was consistently improved when eGFR and albuminuria have been added to the traditional CV risk factors (i.e., Framingham risk score). These important findings led to consider CKD as an equivalent CV risk. Although it is hard to accept this definition in absence of additional reports from scientific Literature, a great effort has been done to reduce the CV risk in CKD patients. A large number of clinical trials have tested the effect of drugs on CV risk reduction. The targets used in these trials were different, including blood pressure, lipids, albuminuria, inflammation, and glucose. All these trials have determined an overall better control of CV risk, performed by clinicians. However, a non-negligible residual risk is still present and has been attributed to: (1) missed response to study treatment in a consistent portion of patients, (2) role of many CV risk factors in CKD patients not yet completely investigated. These combined observations provide a strong argument that kidney measures should be regularly included in individual prediction models for improving CV risk stratification. Further studies are needed to identify high risk patients and novel therapeutic targets to improve CV protection in CKD patients.

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Section: Link Between Kidney Measures and Cardiovascular Damagementioning

confidence: 99%

Unraveling Cardiovascular Risk in Renal Patients: A New Take on Old Tale

Provenzano

Coppolino

Nicola

et al. 2019

Front. Cell Dev. Biol.

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“…18 In recent times, we showed that revascularization performed on HD patients affected by critical peripheral artery disease stimulated release of progenitor cells from the bone marrow, and prostanoids improved this mechanism. 19 In addition, a physiologic hemodynamic stress, such as dipping hands in icy water (named cold pressor test), was able to rapidly increase progenitor cells. 20 Furthermore, we found elevated numbers of EPCs in patients undergoing HD, reflecting the direct response of bone marrow to hemodynamic stress on vessels.…”

Section: Discussionmentioning

confidence: 99%

Parathyroid Hormone and Mobilization of Circulating Bone Marrow-Derived Cells in Uremic Patients

Coppolino

Bolignano²,

Paola³

et al. 2011

Journal of Investigative Medicine

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“…Endothelial stem cells (also called endothelial progenitor cells) are multipotent cells usually derived from the bone marrow and identified by cell markers CD133 and VEGFR2 [86][87][88][89][90][91][92][93][94][95][96]. Nonmarrow source of endothelial stem cells has also been identified circulating in blood with the ability to differentiate into endothelial cells for blood vessels formation in a process called vasculogenesis [88].…”

Section: Endothelial Stem Cellsmentioning

confidence: 99%

“…However, recruitment and incorporation of these cells require a complicated sequence of events including adhesion, migration, chemoattraction, and the ultimate differentiation into endothelial cells. These cells have also been studied in leg ischemia caused by peripheral artery disease [92]. These cells have also been studied in leg ischemia caused by peripheral artery disease [92].…”

Section: Endothelial Stem Cellsmentioning

confidence: 99%