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17th World Summit on Positive Psychology, Psychotherapy & Cognitive Behavioral Sciences

Toronto, Canada

Nigar Sekercioglu

Nigar Sekercioglu

Mc Master University, Canada

Title: Depression in patients with chronic kidney disease

Biography

Biography: Nigar Sekercioglu

Abstract

Recurrent depressive disorder or major depressive disorder (henceforth referred to as depression) is a clinical syndrome that persists at least two weeks. Patients with depression may have suicidal thoughts, depressed mood as well as diminished appetite, sleep and no interest in usual activities. The prevalence of depression ranges from 2 to 9% in the general population. The presence of comorbid conditions, high body-mass index and lower socio-economic status, all have been associated with depression. Chronic kidney disease (CKD) is described as irreversible loss of kidney functions. The prevalence of depression has been shown to be high in CKD patients and has been linked to mortality. Depression management include pharmacotherapy, psychotherapy and electroconvulsive therapy. Neurochemical imbalance in the central nervous system is the root of the problem in depression. The disease process involves several alterations in the brain and in the peripheral nervous system, including reduced serotonin and increased sympathetic tone. The sympathetic nervous system is governed by the hypothalamic-pituitary-adrenal (HPA) axis. Corticotrophin Releasing Hormone (CRH) is one of the substances that is released by the HPA axis and stimulates the secretion of adrenocorticotropic hormone (ACTH) which stimulates the adrenal cortex and medulla, and increases epinephrine and norepinephrine levels. Previous research showed that the volume of space occupied by CRH neurons increased in depression. The HPA is inhibited by Gamma Amino Butyric acid (GABA) and cortisol feedback. Overall, the underlying pathophysiology of depression is complex, and involves several substances. Due to lack of negative feedback of GABA and/or alpha 2 adrenergic systems, the HPA becomes overactive with elevated CRH levels. CRH stimulates corticotrophs and ACTH is secreted. As a result, a sympathovagal imbalance is established, contributing to the disease process.