Details

Autor(en) / Beteiligte

• Vágvölgyi, Anna

Titel

Assessment of Neuronal Dysfunction in Young Patients with Type 1 Diabetes Mellitus and in Patients After Kidney Transplantation

Ort / Verlag

ProQuest Dissertations & Theses

Erscheinungsjahr

2022

Link zum Volltext

• ProQuest

Quelle

ProQuest Dissertations & Theses A&I

Beschreibungen/Notizen

• Neuropathy is one of the most detrimental and diversified neurological conditions that upsets several physiological processes. It considerably impairs patients’ quality of life and it is also associated with increased morbidity and mortality (1). Neuropathy is usually not an independent disease, but a symptom or group of symptoms associated with other diseases. The number of diseases leading to the development of nerve damage is several hundreds, and the majority of them are rare diseases. The diseases that can lead to the development of neuropathy include metabolic disorders, chronic alcoholic and non-alcoholic liver, chronic kidney diseases, haematological pathologies, exogenous intoxications, infections, systemic diseases, polyneuropathies arising from allergic reactions, and diseases with a genetic background. Regarding its prognostic and clinical significance, diabetic neuropathy must be highlighted (2). Cardiovascular autonomic neuropathy and peripheral sensory neuropathy were investigated in two delicate patient groups: one group at a designated time-period of their disease and the other group with multiple risk factors.The high rate of cardiovascular mortality among CKD patients can be attributable to orthostatic and intradialytic hypotension, reduced heart rate variability or impaired spontaneous baroreflex sensitivity as well as cardiovascular autonomic dysfunction due to resistant hypertension, which are all complications of kidney dysfunction (54). The impaired baroreceptor, cardiopulmonary and chemoreceptor reflex function, activation of the renal afferents, accelerated renin-angiotensin-aldosterone system activity (54) and cardiovascular structural remodelling may also be held responsible for the high mortality rate in CKD. Krishnan and Kiernan reviewed the potential neurologic dysfunctions induced by uremic toxins such as urea, creatinine, parathyroid hormone, myoinositol and β2-microglobulin. As a result of these toxins, hydroelectrolytic changes in small nerve fibres elicit expansion or shrinkage of the endoneurial space, but further studies are needed to shed light on the exact pathogenesis of neuronal damage. Some studies have found a significant improvement in some neuropathic symptoms and electrophysiological indices in pancreas and kidney transplant patients, mostly in case of advanced neuropathy. The goal of our study was to broaden the knowledge we have of cardiovascular autonomic and sensory peripheral neuropathy, as well as cardiac repolarization abnormalities after KTx, and to compare the data we collected to that of age- and gender-matched healthy controls.