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Shrunken Pore Syndrome Is Associated With Increased Levels of Atherosclerosis-Promoting Proteins

Sällman Almén, Markus ; Björk, Jonas LU ; Nyman, Ulf LU ; Lindström, Veronica LU orcid ; Jonsson, Magnus LU orcid ; Abrahamson, Magnus LU ; Schiller Vestergren, AnnaLotta ; Lindhe, Örjan ; Franklin, Gary and Christensson, Anders LU , et al. (2019) In Kidney International Reports 4(1). p.67-79
Abstract

Introduction: Shrunken pore syndrome (SPS), originally defined by cystatin C-based estimated glomerular filtration rate (eGFRcystatin C) being less than 60% of creatinine-based estimated glomerular filtration rate (eGFRcreatinine) in the absence of extrarenal influences on the plasma levels of cystatin C or creatinine, is associated with a high increase in mortality, even in the absence of reduced glomerular filtration rate (GFR). The objective of the present study was to determine whether the proteome of patients with SPS shows differences from that of patients with normal or reduced measured GFR (mGFR) without SPS.

Methods: Four patient cohorts were included: 1 cohort with normal mGFR without SPS, 1 with normal mGFR with SPS, 1... (More)

Introduction: Shrunken pore syndrome (SPS), originally defined by cystatin C-based estimated glomerular filtration rate (eGFRcystatin C) being less than 60% of creatinine-based estimated glomerular filtration rate (eGFRcreatinine) in the absence of extrarenal influences on the plasma levels of cystatin C or creatinine, is associated with a high increase in mortality, even in the absence of reduced glomerular filtration rate (GFR). The objective of the present study was to determine whether the proteome of patients with SPS shows differences from that of patients with normal or reduced measured GFR (mGFR) without SPS.

Methods: Four patient cohorts were included: 1 cohort with normal mGFR without SPS, 1 with normal mGFR with SPS, 1 with reduced mGFR without SPS, and 1 with reduced mGFR with SPS. The plasma levels of 177 selected proteins were analyzed.

Results: Differences in the levels of 30 proteins were specific for SPS; 31 differences were specific for patients with both SPS and reduced mGFR; and 27 were specific for reduced mGFR. Eighteen of the differences specific for SPS concerned proteins described as promoting, or being associated with, atherosclerosis. Twelve of the differences specific for patients with both SPS and reduced mGFR and 10 of the differences specific for reduced mGFR also concerned proteins described as promoting, or being associated with, atherosclerosis. Almost all (82 of 88) of the concentration differences represented increased levels. For SPS, but not for reduced mGFR, a correlation between protein size and increase in level was observed, with smaller proteins being associated with higher levels.

Conclusion: The high mortality in shrunken pore syndrome might be caused by the accumulation of atherosclerosis-promoting proteins in this condition.

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organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
cystatin C, Shrunken Pore Syndrome, creatinine, mortality, GFR
in
Kidney International Reports
volume
4
issue
1
pages
67 - 79
publisher
Elsevier
external identifiers
  • pmid:30596170
  • scopus:85055732913
  • pmid:30596170
ISSN
2468-0249
DOI
10.1016/j.ekir.2018.09.002
project
Shrunken Pore Syndrome (SPS) - morbidity and mortality in a population with measured glomerular filtration rate (GFR)
language
English
LU publication?
yes
id
bb9e584f-9218-4109-82f7-31bbc6367b5d
date added to LUP
2018-11-15 19:13:27
date last changed
2024-04-15 17:10:28
@article{bb9e584f-9218-4109-82f7-31bbc6367b5d,
  abstract     = {{<p>Introduction: Shrunken pore syndrome (SPS), originally defined by cystatin C-based estimated glomerular filtration rate (eGFRcystatin C) being less than 60% of creatinine-based estimated glomerular filtration rate (eGFRcreatinine) in the absence of extrarenal influences on the plasma levels of cystatin C or creatinine, is associated with a high increase in mortality, even in the absence of reduced glomerular filtration rate (GFR). The objective of the present study was to determine whether the proteome of patients with SPS shows differences from that of patients with normal or reduced measured GFR (mGFR) without SPS.</p><p>Methods: Four patient cohorts were included: 1 cohort with normal mGFR without SPS, 1 with normal mGFR with SPS, 1 with reduced mGFR without SPS, and 1 with reduced mGFR with SPS. The plasma levels of 177 selected proteins were analyzed.</p><p>Results: Differences in the levels of 30 proteins were specific for SPS; 31 differences were specific for patients with both SPS and reduced mGFR; and 27 were specific for reduced mGFR. Eighteen of the differences specific for SPS concerned proteins described as promoting, or being associated with, atherosclerosis. Twelve of the differences specific for patients with both SPS and reduced mGFR and 10 of the differences specific for reduced mGFR also concerned proteins described as promoting, or being associated with, atherosclerosis. Almost all (82 of 88) of the concentration differences represented increased levels. For SPS, but not for reduced mGFR, a correlation between protein size and increase in level was observed, with smaller proteins being associated with higher levels.</p><p>Conclusion: The high mortality in shrunken pore syndrome might be caused by the accumulation of atherosclerosis-promoting proteins in this condition.</p>}},
  author       = {{Sällman Almén, Markus and Björk, Jonas and Nyman, Ulf and Lindström, Veronica and Jonsson, Magnus and Abrahamson, Magnus and Schiller Vestergren, AnnaLotta and Lindhe, Örjan and Franklin, Gary and Christensson, Anders and Grubb, Anders}},
  issn         = {{2468-0249}},
  keywords     = {{cystatin C; Shrunken Pore Syndrome; creatinine; mortality; GFR}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{67--79}},
  publisher    = {{Elsevier}},
  series       = {{Kidney International Reports}},
  title        = {{Shrunken Pore Syndrome Is Associated With Increased Levels of Atherosclerosis-Promoting Proteins}},
  url          = {{http://dx.doi.org/10.1016/j.ekir.2018.09.002}},
  doi          = {{10.1016/j.ekir.2018.09.002}},
  volume       = {{4}},
  year         = {{2019}},
}