<abstract xmlns="http://www.w3.org/1999/xhtml"><p>Premature loss of functional integrity of the nervous system in chronic renal failure (CRF) as a consequence of persistent biological activities of the general uremic milieu is almost identical to its structural and functional involution during the process of physiological ageing, but disproportionate and independent of chronological age. In the hyperuremic status of CRF (urea - carbamide), forced carbamylation, as a non-enzymatic post-translational modification (NEPTM) of proteins and amino acids, by changing their biological properties and decreasing proteolysis capacity, represents pathogenetic potential of intensified molecular ageing and accelerated, pathological involution. Physiological predisposition and the exposure of neuropathy before complications of other organs and organ systems in CRF, due to the simultaneous and mutually pathogenetically related uremic lesion and the tissue and vascular segment of the nervous system, direct interest towards proteomic analytical techniques of quantification of carbamylated products as biomarkers of uremic neurotoxicity. Hypothetically, identical to the already established applications of other NEPTM products in practice, they have the potential of clinical methodology in the evaluation of uremic neuropathy and its contribution to the general prediction, but also to the change of the conventional CRF classification. In addition, the identification and therapeutic control of the substrate of accelerated involution, responsible for the amplification of not only neurological but also general degenerative processes in CRF, is attractive in the context of the well-known attitude towards aging.</p></abstract>

Premature loss of functional integrity of the nervous system in chronic renal failure (CRF) as a consequence of persistent biological activities of the general uremic milieu is almost identical to its structural and functional involution during the process of physiological ageing, but disproportionate and independent of chronological age. In the hyperuremic status of CRF (urea - carbamide), forced carbamylation, as a non-enzymatic post-translational modification (NEPTM) of proteins and amino acids, by changing their biological properties and decreasing proteolysis capacity, represents pathogenetic potential of intensified molecular ageing and accelerated, pathological involution. Physiological predisposition and the exposure of neuropathy before complications of other organs and organ systems in CRF, due to the simultaneous and mutually pathogenetically related uremic lesion and the tissue and vascular segment of the nervous system, direct interest towards proteomic analytical techniques of quantification of carbamylated products as biomarkers of uremic neurotoxicity. Hypothetically, identical to the already established applications of other NEPTM products in practice, they have the potential of clinical methodology in the evaluation of uremic neuropathy and its contribution to the general prediction, but also to the change of the conventional CRF classification. In addition, the identification and therapeutic control of the substrate of accelerated involution, responsible for the amplification of not only neurological but also general degenerative processes in CRF, is attractive in the context of the well-known attitude towards aging.

Neuropathy - Exponent of Accelerated Involution in Uremia: The Role of Carbamylation

Faculty of Medical Sciences, Department of Internal medicine

Experimental and Applied Biomedical Research (EABR)

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Premature loss of functional integrity of the nervous system in chronic renal failure (CRF) as a consequence of persistent biological activities of the general...

Neuropathy - Exponent of Accelerated Involution in Uremia: The Role of Carbamylation

Data publikacji: 27 wrz 2021

Zakres stron: -

Otrzymano: 22 lut 2021

Przyjęty: 06 mar 2021

DOI: https://doi.org/10.2478/sjecr-2021-0013

Słowa kluczowe
chronic renal failure, neuropathy, carbamylation, pathological involution

© 2021 Tatjana Lazarevic et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Neuropathy - Exponent of Accelerated Involution in Uremia: The Role of Carbamylation

Data publikacji: 27 wrz 2021

Zakres stron: -

Otrzymano: 22 lut 2021

Przyjęty: 06 mar 2021

DOI: https://doi.org/10.2478/sjecr-2021-0013

Słowa kluczowechronic renal failure, neuropathy, carbamylation, pathological involution

© 2021 Tatjana Lazarevic et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Słowa kluczowe
chronic renal failure, neuropathy, carbamylation, pathological involution