ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2021 and some content may be unavailable. To unlock all content for 2021, please visit the archives.

Abstract: PO2301

Shrunken Pore Syndrome Is Associated with a Rise in Mortality in a Community-Based Population of Middle-Aged Individuals

Session Information

Category: CKD (Non-Dialysis)

  • 2101 CKD (Non-Dialysis): Epidemiology, Risk Factors, and Prevention

Authors

  • Xhakollari, Liana, Dept of Nephrology, Skåne University Hospital, Malmö, Skåne, Sweden
  • Åkesson, Anna, Dept of Clinical Sciences, Lund University, Malmö, Skåne, Sweden
  • Björk, Jonas, Dept of Clinical Sciences, Lund University, Malmö, Skåne, Sweden
  • Christensson, Anders, Dept of Nephrology, Skåne University Hospital, Malmö, Skåne, Sweden
Background

Chronic kidney disease (CKD) is a risk factor for increased mortality mainly due to cardiovascular disease (CVD). Glomerular filtration rate (GFR) is the best way to estimate kidney function, but it cannot be measured. Creatinine and cystatin C are two molecules that are used in clinical practice to estimate GFR (eGFR). The lower eGFR, the higher is the mortality. CKD staging is therefore a good marker of mortality and development of CVD. However, there are patients who have the same CKD stage and risk factors for development of CVD but different outcome in mortality. Shrunken pore syndrome (SPS) has shown to be a marker of increased mortality in different patients groups regardless of their measured GFR. The theory behind SPS is supposed to be a difference in the renal filtration of small molecules like creatinine compared to middle sized molecules like cystatin C. Little is known about the prevalence of SPS and the effect on mortality in the general population. The aim of our study is to investigate this.

Methods

The study population consisted of 5061 individuals from the Malmö Diet and Cancer Cardiovascular cohort community-based study that was gathered during 1991 and 1996 in Malmö, Sweden. The individuals were 44-64 years old. Blood samples, anthropometric measurement and a questionnaire about life style etc was available. CAPACYC formula was used for eGFR based on cystatin C and LMRCR formula was used for eGFR based on creatinine. SPS was defined as eGFRCYS ≤ 70% of eGFRCR. Generalized propensity score was used to match individuals with SPS and those without. Kaplan–Meier estimates were used to present survival probabilities in four eGFRCYS/eGFRCR-ratio intervals. To account for within quartet correlation, or frailty, Cox proportional hazard models with shared frailty was employed. Results are presented as hazard ratios (HR) with 95 % confidence intervals (CI).

Results

405 individuals (8%) fulfilled the criterion for SPS. Median (2.5-97.5 percentiles) eGFRcys was 63 (38-97) and median eGFRcr was 70 (49-92) mL/min/1.73m2. HR for mortality in individuals with SPS in the matched data was 2.43 (1.15 - 5.14).

Conclusion

Healthy middle age individuals with SPS have a doubled risk of all-cause mortality. Further studies are needed to explore the mechanisms behind the association between SPS and mortality.