Role of Advanced Glycation Endproducts and Potential Therapeutic Interventions in Dialysis Patients

Mallipattu, Sandeep K.; He, John Cijiang; Uribarri, Jaime

doi:10.1111/j.1525-139x.2012.01081.x

Cited by 26 publications

(18 citation statements)

References 140 publications

(167 reference statements)

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“…In addition, patients who were carriers of this risk allele had increased albuminuria and worsened renal function by the end of the 84-month follow-up period [13■■]. The significant role of AGEs in contributing to end-organ damage in patients on chronic renal replacement therapy, hemodialysis or peritoneal dialysis was the focus of a recent review [14]. …”

Section: Excess Advanced Glycation End Products Contribute To End-orgmentioning

confidence: 99%

“…Several reviews have discussed in detail the deleterious role of AGEs in contributing to end-organ damage [14–19]. The accumulation of AGEs contributes to tissue injury by protein-crosslinking, thereby leading to alteration of protein structure and function and by activating proinflammatory and prooxidative cellular signaling pathways [20].…”

Section: Excess Advanced Glycation End Products Contribute To End-orgmentioning

confidence: 99%

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Advanced glycation end product accumulation

Mallipattu

Uribarri

2014

Current Opinion in Nephrology and Hypertension

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Purpose of review The critical role of advanced glycation end products (AGEs) in the progression of chronic diseases and their complications has recently become more apparent. This review summarizes the recent contributions to the field of AGEs in chronic kidney disease (CKD). Recent findings Over the past 3 decades, AGEs have been implicated in the progression of CKD, and specifically diabetic nephropathy. Although numerous in-vitro and in-vivo studies highlight the detrimental role of AGEs accumulation in tissue injury, few prospective human studies or clinical trials show that inhibiting this process ameliorates disease. Nonetheless, recent studies have focused on the novel mechanisms that contribute to end-organ injury as a result of AGEs accumulation, as well as novel targets of therapy in kidney disease. Summary As the prevalence and the incidence of CKD rises in the United States, it is essential to identify therapeutic strategies that either delay the progression of CKD or improve mortality in this population. The focus of this review is on highlighting the recent studies that advance our current understanding of the mechanisms mediating AGEs-induced CKD progression, as well as novel treatment strategies that have the potential to abrogate this disease process. Video abstract http://links.lww.com/CONH/A12

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Section: Excess Advanced Glycation End Products Contribute To End-orgmentioning

confidence: 99%

Section: Excess Advanced Glycation End Products Contribute To End-orgmentioning

confidence: 99%

Advanced glycation end product accumulation

Mallipattu

Uribarri

2014

Current Opinion in Nephrology and Hypertension

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“…AGEs constitutes a large group of heterogeneous molecules formed by the non enzymatic reactions of sugar with free amino groups of proteins, lipids, peptides and nucleic acids within the so-called "Maillard reaction", a tribute to the French scientist Louis Camille Maillard (1878-1936) (21) .…”

Section: Discussionmentioning

confidence: 99%

Assessment of Advanced Glycation Endproducts in Offspring of Type 2 Diabetes

2015

IJSR

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Abstract:Background: Diabetes is a group of metabolic diseases characterized by hyperglycemia, There are several, well researched theories of how chronic hyperglycemia can lead to micro or macrovascular disease in diabetes including the advanced glycation end products (AGEs) theory.pentosidine is one of the best chemically characterized AGEs in humanspentosidine levels were significantly increased in diabetic patients with retinopathy and in diabetic patients with nephropathy. Aim of the work: This study is designed to identify any changes of the level of AGEs in offspring of type 2 diabetes with and without impaired glucose tolerance and its relation to age, body mass index and various metabolic parameters in those subjects. Subjects: Case control study was carried out On 66 volunteers subjects. And were divided into two main groupswhich were age, sex matched:Group A Control group, includes 33 apparently healthy subjects. Group B: Includes 33 non diabetic offspring of type 2 diabetic patientsof whom one or both parents are diabetic which were further subdivided into 2 subgroups according to oral glucose tolerance test into: i) Subgroup B1:Non diabetic normal glucose tolerant offspring, includes 16 healthy subjects. ii)Subgroup B2:Non diabetic impaired glucose tolerant offspring, includes 17 healthy offspring subjects. Methods: all subjects of study were subjected to full history and thorough clinical examination, routine investigation as urine analysis, complete blood picture, liver and renal function tests oral glucose tolerance test, lipid profile .And specific investigation included measurement of fasting insulin and serum pentosidineby ELISA technique, and calculation of insulin resistance by HOMA index. Results: There is significant increase in serum pentosidinelevel in group B2 in comparison to group A and group B1while there is no significant difference in this risk factor between Group A and Group B1. There is significant positive correlation between serum pentosidine level and each of fasting insulin level and HOMA-IR in group B2. While there was no significant correlation between pentosidine and each of age, Smoking status, BMI, waist circumference, cholesterol, triglycerides, FBG and 2hr postprandial blood glucose in group B1and groupB2. Conclusion:the high level of serum pentosidine as an advanced glycation end product (AGE) in offspring of type 2 diabetes with impaired glucose tolerancemay play a role in many vascular complications that occur before development of diabetes. Therefore we recommend screening offspring of type 2 diabetes for AGEs and early management to guard against vascular complications that may occur in the pre diabetic state.

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“…A dvanced glycation end products (AGEs) are a heterogeneous group of molecules that result from the nonenzymatic glycation of proteins, lipids, and nucleic acids. 1 Moreover, AGEs are uremic toxins that are markedly increased in persons with chronic kidney disease (CKD), particularly on dialysis, owing to increased production, impaired excretion, and inefficient removal. 2,3 AGEs are rapidly formed either endogenously during hyperglycemia and oxidative stress or through exogenous sources such as cigarette smoke and food.…”

mentioning

confidence: 99%

“…2,3 AGEs are rapidly formed either endogenously during hyperglycemia and oxidative stress or through exogenous sources such as cigarette smoke and food. 1 AGEs form crosslinks between tissue protein molecules and interact with specific AGE receptors, resulting in systemic inflammation and, consequently, exacerbation of tissue damage. 4 Tissue AGE accumulation can be assessed noninvasively, using SAF.…”

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confidence: 99%

Factors Associated With Change in Skin Autofluorescence, a Measure of Advanced Glycation End Products, in Persons Receiving Dialysis

Hörner

Selby

2020

Kidney International Reports

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Introduction: An increase over time in skin autofluorescence (SAF), a measure of accumulation of advanced glycation end products (AGE), predicts higher mortality on hemodialysis (HD). However, evidence is lacking regarding factors that contribute to changes in SAF over time in populations on dialysis. We investigated the rate of change in SAF over 1 year and the factors associated with these changes. Methods: We enrolled 109 patients on HD and 28 on peritoneal dialysis in a prospective study. SAF was measured at baseline, 3, 6, 9, and 12 months. Rate of change in SAF was calculated using the SLOPE function in Microsoft Excel (Microsoft, Redmond, WA). Participants were then grouped into those with stable SAF or increasing SAF. Dietary AGE intake and nutritional assessments were performed at baseline, 6, and 12 months. Results: The mean SAF trend observed was an increase of 0.30 AE 0.63 arbitrary units (AU) per year, but this varied from a decrease of 0.15 AE 0.44 to an increase of 0.76 AE 0.42 AU per year in stable and increasing SAF groups, respectively. Increasing SAF was more common in participants who developed malnutrition during the observation period, whereas those who became well-nourished were more likely to have stable SAF (8 [80%] vs. 14 [42%]; P ¼ 0.02). Development/prevalence of malnutrition over 1 year, HD as first dialysis modality, and current smoking were independent predictors of increasing SAF. Conclusion: SAF increases over time in most persons on dialysis. Independent determinants of increasing SAF were development/prevalence of malnutrition, HD as first dialysis modality, and current smoking. Strategies to reduce/prevent the rise in SAF, including prevention/correction of malnutrition, should be investigated in prospective studies.

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Role of Advanced Glycation Endproducts and Potential Therapeutic Interventions in Dialysis Patients

Cited by 26 publications

References 140 publications

Advanced glycation end product accumulation

Advanced glycation end product accumulation

Assessment of Advanced Glycation Endproducts in Offspring of Type 2 Diabetes

Factors Associated With Change in Skin Autofluorescence, a Measure of Advanced Glycation End Products, in Persons Receiving Dialysis

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