Skin autofluorescence as a marker of cardiovascular risk in children with chronic kidney disease

Makulska, Irena; Szczepańska, Maria; Drożdż, Dorota; Polak−Jonkisz, Dorota; Zwołińska, Danuta

doi:10.1007/s00467-012-2280-z

Cited by 20 publications

(20 citation statements)

References 49 publications

(57 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It has been reported that endothelial progenitor cells have the ability to repair cardiovascular damage [30]. In CKD children, tissue accumulation of AGE was observed, aggravated as eGFR declined and related to early cardiovascular changes and some biochemical CVD risk markers [31].…”

Section: Skin Autofluorescence Is a Strong Predictor Of Cardiovasculamentioning

confidence: 99%

Advanced glycation end-products and skin autofluorescence in end-stage renal disease: a review

Arsov¹,

Graaff

Oeveren

et al. 2014

Clinical Chemistry and Laboratory Medicine

View full text Add to dashboard Cite

Chronic kidney disease (CKD), especially in its end stage, is marked by extremely high cardiovascular rates of morbidity and mortality; hemodialysis patients have a five-fold shorter life expectancy than healthy subjects of the same age. In CKD the metabolic products that accumulate in the body are so-called uremic toxins. These include advanced glycation end-products (AGE). AGE levels are markedly increased in CKD patients not only because of impaired excretion but also because of increased production. AGE formation has initially been described as a non-enzymatic reaction between proteins and glucose in the so-called Maillard reaction, but they are also more rapidly formed during oxidative stress and subsequent formation of reactive carbonyl compounds like (methyl)glyoxal. AGE accumulate in tissue where they cross-link with proteins, e.g., collagen, inducing tissue stiffening of blood vessels and skin. They may also interact with receptor of AGE (RAGE) and other receptors, which lead to activation of intracellular transduction mechanisms resulting in cytokine release and further tissue damage in CKD. The accumulation of AGE in the skin can be measured non-invasively using autofluorescence. The skin autofluorescence is a strong marker of cardiovascular mortality in CKD. The focus of this review is on the role of tissue and plasma AGE, and of skin autofluorescence as a proxy of tissue AGE accumulation, in the increase in cardiovascular disease in end stage renal disease (ESRD). This review will also present the possibility of reducing the AGE accumulation in ESRD patients using the following five methods: 1) use of low AGE peritoneal dialysis solutions; 2) use of advanced hemodialysis techniques; 3) use of AGE reducing drugs; 4) optimizing the nutrition of hemodialysis patients; and 5) renal transplantation.

show abstract

Section: Skin Autofluorescence Is a Strong Predictor Of Cardiovasculamentioning

confidence: 99%

Advanced glycation end-products and skin autofluorescence in end-stage renal disease: a review

Arsov¹,

Graaff

Oeveren

et al. 2014

Clinical Chemistry and Laboratory Medicine

View full text Add to dashboard Cite

show abstract

“…Beyond bone health, there is interest in understanding the role of AGEs in the cardiovascular and metabolic manifestations that often accompany obesity and diabetes. Earlier studies in children and adults have shown that AGEs are associated with higher blood pressure, lipids, vascular stiffness, and coronary artery calcification . Though we did not perform a comprehensive assessment of metabolic outcomes and did not collect data on cardiovascular health, pentosidine was associated with measures of insulin resistance, including QUICKI, HOMA‐IR, and fasting insulin.…”

Section: Discussionmentioning

confidence: 90%

“…Earlier studies in children and adults have shown that AGEs are associated with higher blood pressure, lipids, vascular stiffness, and coronary artery calcification. (20)(21)(22)(23) Though we did not perform a comprehensive assessment of metabolic outcomes and did not collect data on cardiovascular health, pentosidine was associated with measures of insulin resistance, including QUICKI, HOMA-IR, and fasting insulin. That most, but not all, relationships between pentosidine and cortical bone geometric measures were attenuated after controlling for QUICKI is suggestive of a potential intermediary role of insulin resistance in these relationships.…”

Section: Journal Of Bone and Mineral Researchmentioning

confidence: 99%

Pentosidine Is Associated With Cortical Bone Geometry and Insulin Resistance in Otherwise Healthy Children

Kindler

Laing

Liu

et al. 2019

Journal of Bone and Mineral Research

View full text Add to dashboard Cite

Pentosidine is an advanced glycation end product (AGE) associated with fracture in adults with diabetes. AGE accumulation in bone collagen contributes to bone fragility but might also adversely influence bone turnover and, consequently, bone geometry. The relationships between AGEs and bone health have yet to be studied in children. Thus, the objective of this study was to assess relationships between pentosidine and cortical bone volumetric density, geometry, and estimated strength in children. Participants were otherwise healthy black and white boys and girls, ages 9 to 13 years, who were at sexual maturation stage 2 or 3 (N = 160). Tibia and radius cortical bone and muscle area (66% site) were assessed via pQCT. In fasting sera, insulin, glucose, and pentosidine were measured. The Quantitative Insulin Sensitivity Check Index (QUICKI), a measure of insulin sensitivity, was calculated. While controlling for race, sex, maturation, and height, pentosidine negatively correlated with QUICKI (P < 0.05). In unadjusted analyses, pentosidine was associated with lower radius and tibia cortical volumetric bone mineral density, bone mineral content (Ct.BMC), area (Ct.Ar), and thickness (Ct.Th); a larger radius endosteal circumference (Endo.Circ); and lower tibia polar strength strain index (all P < 0.05). While controlling for race, sex, maturation, height, and muscle area, pentosidine was negatively associated with tibia Ct.BMC, Ct.Ar, and Ct.Th but positively associated with Endo.Circ (all P < 0.05). Linear regression revealed a significant interaction between pentosidine and QUICKI in relation to tibia Ct.Th (pinteraction = 0.049), indicating that the negative relationship between pentosidine and Ct.Th was stronger in those with lower QUICKI (ie, greater insulin resistance). This is the first study to report evidence of a potentially adverse influence of AGEs on bone strength in otherwise healthy children. This relationship was strongest in children with the greatest insulin resistance, supporting further work in youth with chronic metabolic health conditions. © 2019 American Society for Bone and Mineral Research.

show abstract

“…This may be reflected by the worse skin autofluorescence (SAF) findings in PD versus HD patients, when adjusted for age and dialysis vintage in adults [59], but not different in children [60]. Besides cardiovascular morbidity and increased mortality, high SAF was related to a greater risk for sepsis-related mortality in PD patients [61].…”

Section: Carbohydrates and Hemodialysismentioning

confidence: 99%

Dialysis Procedures Alter Metabolic Conditions

Stegmayr

2017

Nutrients

View full text Add to dashboard Cite

A progressive chronic kidney disease results in retention of various substances that more or less contribute to dysfunction of various metabolic systems. The accumulated substances are denominated uremic toxins. Although many toxins remain undetected, numerous newly defined toxins participate in the disturbance of food breakdown. In addition, toxic effects may downregulate other pathways, resulting in a reduced ability of free fatty acid breakdown by lipoprotein lipase (LPL) and hepatic lipase (HL). Dialysis may even worsen metabolic functions. For LPL and HL, the use of heparin and low molecular weight heparin as anticoagulation during hemodialysis (HD) initiate a loss of these enzymes from their binding sites and degradation, causing a temporary dysregulation in triglyceride breakdown. This lack of function will cause retention of the triglyceride containing lipids for at least 8 h. In parallel, the breakdown into free fatty acids is limited, as is the energy supply by them. This is repeated thrice a week for a normal HD patient. In addition, dialysis will cause a loss of amino acids and disturb glucose metabolism depending on the dialysates used. The addition of glucose in the dialysate may support oxidation of carbohydrate and the retention of Amadori products and subsequent tissue alterations. To avoid these effects, it seems necessary to further study the effects of anticoagulation in HD, the extent of use of glucose in the dialysate, and the supplementation of amino acids.

show abstract

Skin autofluorescence as a marker of cardiovascular risk in children with chronic kidney disease

Cited by 20 publications

References 49 publications

Advanced glycation end-products and skin autofluorescence in end-stage renal disease: a review

Advanced glycation end-products and skin autofluorescence in end-stage renal disease: a review

Pentosidine Is Associated With Cortical Bone Geometry and Insulin Resistance in Otherwise Healthy Children

Dialysis Procedures Alter Metabolic Conditions

Contact Info

Product

Resources

About