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Inflammatory depression is associated with selective glomerular hypofiltration

Söderberg Veibäck, Gustav LU ; Malmgren, Linnea LU orcid ; Asp, Marie LU ; Ventorp, Filip LU ; Suneson, Klara LU ; Grudet, Cécile LU orcid ; Westrin, Åsa LU and Lindqvist, Daniel LU (2024) In Journal of Affective Disorders 356. p.80-87
Abstract

Background: Systemic low-grade inflammation may be a pathophysiological mechanism in a subtype of depression. In this study we investigate a novel candidate mechanism of inflammatory depression - Selective Glomerular Hypofiltration Syndromes (SGHS) - which are characterized by a reduced estimated glomerular filtration rate (eGFR) based on cystatin C (cysC) relative to eGFR based on creatinine (crea). SGHS have been associated with increased blood levels of pro-inflammatory markers, but have never been investigated in a sample of depressed individuals. Method: The prevalence of SGHS was compared between 313 patients with difficult-to-treat depression and 73 controls. Since there is no single established... (More)

Background: Systemic low-grade inflammation may be a pathophysiological mechanism in a subtype of depression. In this study we investigate a novel candidate mechanism of inflammatory depression - Selective Glomerular Hypofiltration Syndromes (SGHS) - which are characterized by a reduced estimated glomerular filtration rate (eGFR) based on cystatin C (cysC) relative to eGFR based on creatinine (crea). SGHS have been associated with increased blood levels of pro-inflammatory markers, but have never been investigated in a sample of depressed individuals. Method: The prevalence of SGHS was compared between 313 patients with difficult-to-treat depression and 73 controls. Since there is no single established eGFRcysC/eGFRcrea-ratio cut-off to define SGHS, several cut-offs were investigated in relation to a depression diagnosis, inflammation, and symptom severity. Plasma inflammatory markers tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), interleukin (IL)-6, IL-8, and IL-10 were available from 276 depressed patients. We examined mediation effects of IL-6 on the relationship between SGHS and depression. Results: Depressed patients were more likely to have SGHS compared to controls defining SGHS as either eGFRcysC/eGFRcrea-ratio < 0.9 (33.2 % vs 20.5 %, p = 0.035) or < 0.8 (15.7 % vs 5.5 %, p = 0.023). Lower eGFRcysC/eGFRcrea-ratio was associated with higher levels of inflammatory markers in depressed patients. IL-6 partly mediated the relationship between SGHS and depression. Conclusion: This is the first study to demonstrate a link between SGHS and inflammatory depression. If replicated in independent and longitudinal cohorts, this may prove to be a relevant pathophysiological mechanism in some cases of depression that could be targeted in future intervention and prevention studies.

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author
; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Cystatin C, Depression, Glomerular filtration rate, Inflammation
in
Journal of Affective Disorders
volume
356
pages
8 pages
publisher
Elsevier
external identifiers
  • pmid:38574872
  • scopus:85189973676
ISSN
0165-0327
DOI
10.1016/j.jad.2024.04.007
project
GEN-DS Part II, Follow-up and Further Substudies
language
English
LU publication?
yes
id
c111cefc-55c1-4703-99c0-49cda3c1ddde
date added to LUP
2024-04-23 13:26:41
date last changed
2025-10-23 16:49:54
@article{c111cefc-55c1-4703-99c0-49cda3c1ddde,
  abstract     = {{<p>Background: Systemic low-grade inflammation may be a pathophysiological mechanism in a subtype of depression. In this study we investigate a novel candidate mechanism of inflammatory depression - Selective Glomerular Hypofiltration Syndromes (SGHS) - which are characterized by a reduced estimated glomerular filtration rate (eGFR) based on cystatin C (cysC) relative to eGFR based on creatinine (crea). SGHS have been associated with increased blood levels of pro-inflammatory markers, but have never been investigated in a sample of depressed individuals. Method: The prevalence of SGHS was compared between 313 patients with difficult-to-treat depression and 73 controls. Since there is no single established eGFR<sub>cysC</sub>/eGFR<sub>crea</sub>-ratio cut-off to define SGHS, several cut-offs were investigated in relation to a depression diagnosis, inflammation, and symptom severity. Plasma inflammatory markers tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), interleukin (IL)-6, IL-8, and IL-10 were available from 276 depressed patients. We examined mediation effects of IL-6 on the relationship between SGHS and depression. Results: Depressed patients were more likely to have SGHS compared to controls defining SGHS as either eGFR<sub>cysC</sub>/eGFR<sub>crea</sub>-ratio &lt; 0.9 (33.2 % vs 20.5 %, p = 0.035) or &lt; 0.8 (15.7 % vs 5.5 %, p = 0.023). Lower eGFR<sub>cysC</sub>/eGFR<sub>crea</sub>-ratio was associated with higher levels of inflammatory markers in depressed patients. IL-6 partly mediated the relationship between SGHS and depression. Conclusion: This is the first study to demonstrate a link between SGHS and inflammatory depression. If replicated in independent and longitudinal cohorts, this may prove to be a relevant pathophysiological mechanism in some cases of depression that could be targeted in future intervention and prevention studies.</p>}},
  author       = {{Söderberg Veibäck, Gustav and Malmgren, Linnea and Asp, Marie and Ventorp, Filip and Suneson, Klara and Grudet, Cécile and Westrin, Åsa and Lindqvist, Daniel}},
  issn         = {{0165-0327}},
  keywords     = {{Cystatin C; Depression; Glomerular filtration rate; Inflammation}},
  language     = {{eng}},
  month        = {{07}},
  pages        = {{80--87}},
  publisher    = {{Elsevier}},
  series       = {{Journal of Affective Disorders}},
  title        = {{Inflammatory depression is associated with selective glomerular hypofiltration}},
  url          = {{http://dx.doi.org/10.1016/j.jad.2024.04.007}},
  doi          = {{10.1016/j.jad.2024.04.007}},
  volume       = {{356}},
  year         = {{2024}},
}