Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
A reduced ratio of cystatin C to creatinine-based estimated glomerular filtration rate (eGFRcys/eGFRcr-ratio <0.7), indicative of Selective Glomerular Hypofiltration Syndromes (SGHS), predicts adverse outcomes independent of kidney function. However, the relationship between SGHS and glucometabolic disturbances in the general population remains insufficiently explored.
We analyzed 29,246 participants (age 50–64 years) from the population-based Swedish CArdioPulmonary bioImage Study (SCAPIS). Glycaemic status was categorized as normoglycaemia, prediabetes, or diabetes using fasting P-glucose and HbA1c. eGFRcr was estimated with Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) 2021 equation and eGFRcys with CKD-EPI 2012; SGHS was defined as eGFRcys/eGFRcr-ratio <0.7. Associations of glycaemia and insulin resistance (HOMA-IR) with continuous ratio and SGHS were examined using multivariable regression with sequential adjustment for age, sex, site, BMI, smoking, blood pressure, antihypertensive therapy, LDL, and lipid-lowering therapy. Sensitivity analyses employed the revised Lund–Malmö (LMrev) creatinine equation and the Caucasian–Asian–Pediatric–Adult (CAPA) cystatin C equation. Kernel density plots of the eGFRcys/eGFRcr-ratio were generated by glycaemic status
The mean eGFRcys/eGFRcr-ratio declined stepwise from 0.95 in normoglycaemia to 0.90 in prediabetes and 0.85 in diabetes (p<0.001). As shown in figure 1, ratio distributions were progressively shifted leftward with worsening glycaemia SGHS prevalence increased from 6.6% to 10.6% and 18.7%, respectively (p<0.001). Both HbA1c (per 10 mmol/mol) (β –0.015, 95% CI –0.018 to –0.012) and fasting P-glucose (per 1 mmol/L) (β –0.007, 95% CI –0.009 to –0.005) were inversely associated with the ratio, and independently predicted SGHS (OR HbA1c 1.27, 95% CI 1.19–1.35; OR glucose 1.11, 95% CI 1.06–1.15). Logistic regression confirmed higher odds of SGHS in prediabetes (OR 1.31, 95% CI 1.17–1.46) and diabetes (OR 2.69, 95% CI 2.37–3.05) versus normoglycaemia. Insulin resistance was strongly associated with SGHS, even among normoglycaemic individuals (OR 1.30, 95% CI 1.26–1.35). Findings were consistent across alternative equations in sensitivity analysis.
In this large population-based cohort, SGHS and a lower eGFRcys/eGFRcr-ratio were consistently associated with worsening glycaemic status. Insulin resistance was related to SGHS even among individuals without diabetes, highlighting metabolic stress as a potential early driver of selective hypofiltration. These findings suggest that SGHS may serve as a novel and sensitive marker of subclinical kidney injury in metabolic dysregulation, with implications for early risk stratification and prevention.
