Size-selective glomerular filtration as a hallmark of premature kidney ageing in nondiabetic individuals
(2025) In Clinical Kidney Journal 18(8). p.1-12- Abstract
Background During the last decade, evidence has emerged on selective glomerular hypofiltration syndromes (SGHS), defined by selectively reduced filtration of middle-sized molecules irrespective of kidney function and resulting in a low ratio between cystatin C- and creatinine-based estimated glomerular filtration rates (eGFRcys/eGFRcr). We aimed to examine whether SGHS is a hallmark of premature kidney ageing manifested by accumulation of advanced glycation end-products (AGEs) and endothelial dysfunction in a population free from chronic kidney disease and diabetes. Methods A total of 3804 participants of The Malmö Offspring Study (MOS) underwent AGE (skin autofluorescence acquired), eGFRcys and eGFRcr measurements. AGEs ≥1.6 were... (More)
Background During the last decade, evidence has emerged on selective glomerular hypofiltration syndromes (SGHS), defined by selectively reduced filtration of middle-sized molecules irrespective of kidney function and resulting in a low ratio between cystatin C- and creatinine-based estimated glomerular filtration rates (eGFRcys/eGFRcr). We aimed to examine whether SGHS is a hallmark of premature kidney ageing manifested by accumulation of advanced glycation end-products (AGEs) and endothelial dysfunction in a population free from chronic kidney disease and diabetes. Methods A total of 3804 participants of The Malmö Offspring Study (MOS) underwent AGE (skin autofluorescence acquired), eGFRcys and eGFRcr measurements. AGEs ≥1.6 were categorized as high, and AGEs <1.6 as normal. Reactive hyperemia index (RHI) was available in 2204 participants; RHI <1.67 indicated endothelial dysfunction (ED), and RHI ≥1.67 normal endothelial function (EF). Combining AGEs and RHI, four groups were compared: (group 1) AGEs <1.6 and EF, (group 2) AGEs <1.6 and ED, (group 3) AGEs ≥1.6 and EF, and (group 4) AGEs ≥1.6 and ED. Results Lower eGFRcys/eGFRcr ratio was associated with an increase in AGEs in men and women. After adjusting for cardiovascular factors, lower eGFRcys/eGFRcr ratio was associated with AGE accumulation in men older than 30 years. The 'AGEs ≥1.6 and ED' and 'AGEs ≥1.6 and EF' groups showed the highest prevalence of eGFRcys/eGFRcr under 0.9 (in men, 22% vs 19.7%, in women 19.5% vs 16%, respectively). Conclusions Accumulation of AGEs resulting from SGHS leads to age dependent changes in glomerular basement membrane and increased selectivity for middle-sized molecules. Presence of these findings in younger individuals supports the hypothesis that SGHS is a model of early kidney ageing, occurring before decline in kidney function.
(Less)
- author
- Laucyte-Cibulskiene, Agne
LU
; Nilsson, Christopher LU
; Jujic, Amra LU
; Holm, Hannes LU and Christensson, Anders LU
- organization
- publishing date
- 2025-08-01
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- advanced glycation end products, cystatin C, estimated glomerular filtration rate, kidney ageing, size-selective kidney filtration
- in
- Clinical Kidney Journal
- volume
- 18
- issue
- 8
- article number
- sfaf208
- pages
- 1 - 12
- publisher
- Oxford University Press
- external identifiers
-
- scopus:105012539079
- ISSN
- 2048-8505
- DOI
- 10.1093/ckj/sfaf208
- language
- English
- LU publication?
- yes
- additional info
- Publisher Copyright: © 2025 The Author(s). Published by Oxford University Press on behalf of the ERA.
- id
- 7d20c247-7ddc-45e4-a09c-4fdc26a2da9e
- date added to LUP
- 2025-09-15 14:44:28
- date last changed
- 2025-09-15 15:07:05
@article{7d20c247-7ddc-45e4-a09c-4fdc26a2da9e, abstract = {{<p>Background During the last decade, evidence has emerged on selective glomerular hypofiltration syndromes (SGHS), defined by selectively reduced filtration of middle-sized molecules irrespective of kidney function and resulting in a low ratio between cystatin C- and creatinine-based estimated glomerular filtration rates (eGFRcys/eGFRcr). We aimed to examine whether SGHS is a hallmark of premature kidney ageing manifested by accumulation of advanced glycation end-products (AGEs) and endothelial dysfunction in a population free from chronic kidney disease and diabetes. Methods A total of 3804 participants of The Malmö Offspring Study (MOS) underwent AGE (skin autofluorescence acquired), eGFRcys and eGFRcr measurements. AGEs ≥1.6 were categorized as high, and AGEs <1.6 as normal. Reactive hyperemia index (RHI) was available in 2204 participants; RHI <1.67 indicated endothelial dysfunction (ED), and RHI ≥1.67 normal endothelial function (EF). Combining AGEs and RHI, four groups were compared: (group 1) AGEs <1.6 and EF, (group 2) AGEs <1.6 and ED, (group 3) AGEs ≥1.6 and EF, and (group 4) AGEs ≥1.6 and ED. Results Lower eGFRcys/eGFRcr ratio was associated with an increase in AGEs in men and women. After adjusting for cardiovascular factors, lower eGFRcys/eGFRcr ratio was associated with AGE accumulation in men older than 30 years. The 'AGEs ≥1.6 and ED' and 'AGEs ≥1.6 and EF' groups showed the highest prevalence of eGFRcys/eGFRcr under 0.9 (in men, 22% vs 19.7%, in women 19.5% vs 16%, respectively). Conclusions Accumulation of AGEs resulting from SGHS leads to age dependent changes in glomerular basement membrane and increased selectivity for middle-sized molecules. Presence of these findings in younger individuals supports the hypothesis that SGHS is a model of early kidney ageing, occurring before decline in kidney function.</p>}}, author = {{Laucyte-Cibulskiene, Agne and Nilsson, Christopher and Jujic, Amra and Holm, Hannes and Christensson, Anders}}, issn = {{2048-8505}}, keywords = {{advanced glycation end products; cystatin C; estimated glomerular filtration rate; kidney ageing; size-selective kidney filtration}}, language = {{eng}}, month = {{08}}, number = {{8}}, pages = {{1--12}}, publisher = {{Oxford University Press}}, series = {{Clinical Kidney Journal}}, title = {{Size-selective glomerular filtration as a hallmark of premature kidney ageing in nondiabetic individuals}}, url = {{http://dx.doi.org/10.1093/ckj/sfaf208}}, doi = {{10.1093/ckj/sfaf208}}, volume = {{18}}, year = {{2025}}, }