Hypertension and nephrology

[The significance of depressive disorders in patients with chronic kidney diseases]

ZALAI Dóra Márta1, SZEIFERT Lilla1,2, NOVÁK Márta1,2,3

JUNE 20, 2010

Hypertension and nephrology - 2010;14(03)

[In this article a practice-oriented narrative review of the depressive disorders in chronic kidney disease is provided. Depressive disorders affect approximately one fourth of the chronic kidney disease population. These mental disorders interfere with physical, cognitive and social functioning and are associated with poor prognosis of patients with chronic kidney disease. Bio-psycho-social factors, including immuno-inflammatory processes, disturbance in glucose- insulin homeostasis, sleep disorders, chronic pain, sexual difficulties, changes in social roles, losses in multiple areas of life and low social support increase the risk for the development of depression. Routine, regular screening of depression in the chronic kidney disease population seems to be warranted. Only limited published evidence is available on the therapeutic possibilities of depression in chronic kidney disease. Preliminary evidence indicates that short, structured psychotherapy may be effective for acute treatment and prevention of psychological distress. Some antidepressants can be applied without the need for dose adjustments. On the other hand, some of the psychotropic medications require dose reduction or should be avoided.]


  1. Psychonephrology Unit, Department of Psychiatry, University Health Network, University of Toronto, Toronto, Canada
  2. Pszichonefrológia Munkacsoport, Semmelweis Egyetem, Magatartástudományi Intézet, Budapest
  3. Semmelweis Egyetem, I. Sz. Belgyógyászati Klinika, Budapest



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[Endothelial nitric oxide synthase enzyme is regulated through the phosphorylation of the Ser(1177) and the Thr(495) sites, which influence the biological availabilaty of nitric oxide. We examined the acute effect of cigarette smoke, which decreases nitric oxide production. Endothelial cells were treated with different concentrations and for different times with cigarette smoke buffer, then with reduced glutathione or different protein kinase inhibitors. We determined the total and the phosphorylated nitric oxide synthase levels with Western blot. Cigarette smoke increased phosphorylation in a concentration- and time dependent manner at the Ser(1177) site and more pronounced at the Thr(495) site. Besides, it also led to the dissociation of the active dimer form of the enzyme. Reduced glutathione inhibited these phosphorylations and prevented the dissociation of endothelial nitric oxide synthase enzyme. The inhibition of protein kinase A or B did not influence the effect of cigarette smoke. However, protein kinase C inhibitors increased the phosphorylation caused by cigarette smoke at Ser(1177), but decreased it at Thr(495) sites. Summarized, cigarette smoke shifts the phosphorylation of the enzyme towards an inhibitory state, further on, it leads to the dissociation of the enzymatically active form. This results in the decreased biological availabilaty of nitric oxide, in which protein kinase C may play an important role.]

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