English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

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