In chronic kidney disease (CKD), metabolic derangements resulting from the interplay between decreasing renal excretory capacity and impaired gut function contribute to accelerating disease progression and enhancing the risk of complications. To protect residual kidney function and improve quality of life in conservatively managed predialysis CKD patients, current guidelines recommend protein-restricted diets supplemented with essential amino acids (EAAs) and their ketoanalogues (KAs). In clinical studies, such an approach improved nitrogen balance and other secondary metabolic disturbances, translating to clinical benefits, mainly the delayed initiation of dialysis. There is also increasing evidence that a protein-restricted diet supplemented with KAs slows down disease progression. In the present review article, recent insights into the role of KA/EAA-supplemented protein-restricted diets in delaying CKD progression are summarized, and possible mechanistic underpinnings, such as protein carbamylation and gut dysbiosis, are elucidated. Emerging evidence suggests that lowering urea levels may reduce protein carbamylation, which might contribute to decreased morbidity and mortality. Protein restriction, alone or in combination with KA/EAA supplementation, modulates gut dysbiosis and decreases the generation of gut-derived uremic toxins associated, e.g., with cardiovascular disease, inflammation, protein energy wasting, and disease progression. Future studies are warranted to assess the effects on the gut microbiome, the generation of uremic toxins, as well as markers of carbamylation.
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http://dx.doi.org/10.3390/nu15163503 | DOI Listing |
Clin Exp Rheumatol
December 2024
Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, and Clinical Institute of Inflammation and Immunology (CIII), Frontiers Science Centre for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
This review comprehensively discusses the cross-reactivity of autoantibodies against modified proteins (AMPAs), the hallmark of rheumatoid arthritis (RA). We found that regardless of tissue sources, subtypes, or isotypes of B cells, AMPAs show high cross-reactivity within and across antigens undergoing citrullination, carbamylation, lysine-acetylation or ornithine-acetylation. The cross-reactive patterns of AMPAs display clonal and individual heterogeneity.
View Article and Find Full Text PDFIntroduction: The processes of atherosclerosis, inflammation, and carbamylation are closely linked in cardiovascular (CV) disease, but the potential of carbamylation burden as a CV mortality predictor is unclear, especially in patients with no or mild chronic kidney disease (CKD). This study aimed to investigate whether elevated carbamylated albumin (C-Alb), as a surrogate marker for carbamylation burden, is associated with mortality and arterial stiffness/atherosclerotic burden in patients with no or mild CKD, using pulse pressure (PP) as a marker for arterial stiffness.
Methods: We measured C-Alb in 3,193 participants of the Ludwigshafen Risk and Cardiovascular Health study who had been referred for coronary angiography and followed up for 10 years.
Mol Biomed
October 2024
Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Firenze, Firenze, Italy.
RMD Open
October 2024
Univ Rouen Normandie, Inserm, Normandie Univ, PANTHER UMR 1234, CHU Rouen, Department of Rheumatology & CIC-CRB 1404, F-76000 Rouen, France.
Exp Ther Med
November 2024
Department of Nephrology, Nanjing Second Hospital, Nanjing Hospital Affiliated to Nanjing University of Traditional Chinese Medicine, Nanjing, Jiangsu 210037, P.R. China.
Vascular calcification is closely associated with morbidity and mortality in patients with chronic kidney disease, atherosclerosis and diabetes. In the past few decades, vascular calcification has been studied extensively and the findings have shown that the mechanism of vascular calcification is not merely a consequence of a high-phosphorus and high-calcium environment but also an active process characterized by abnormal calcium phosphate deposition on blood vessel walls that involves various molecular mechanisms. Recent advances in bioinformatics approaches have led to increasing recognition that aberrant post-translational modifications (PTMs) play important roles in vascular calcification.
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