Cystatin C as risk factor for cardiovascular events and all-cause mortality in the general population. The Tromso Study

Background Glomerular filtration rate <60 mL/min/1.73m2 is associated with increased cardiovascular risk. Cystatin C is believed to be a better tool than creatinine for detection of mild renal dysfunction (>60 mL/min/1.73m2) and possibly a more sensitive marker for cardiovascular risk and all-...

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Bibliographic Details
Published in:Nephrology Dialysis Transplantation
Main Authors: Toft, Ingrid, Solbu, Marit, Kronborg, Jens, Mathisen, Ulla D., Eriksen, Bjørn O., Storhaug, Hilde, Melsom, Toralf, Løchen, Maja-Lisa, Mathiesen, Ellisiv B., Njølstad, Inger, Wilsgaard, Tom, Brox, Jan
Format: Text
Language:English
Published: Oxford University Press 2012
Subjects:
Chronic Kidney Disease
Tromsø
Tromso
Online Access:http://ndt.oxfordjournals.org/cgi/content/short/27/7/2780
https://doi.org/10.1093/ndt/gfr751
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Summary:Background Glomerular filtration rate <60 mL/min/1.73m2 is associated with increased cardiovascular risk. Cystatin C is believed to be a better tool than creatinine for detection of mild renal dysfunction (>60 mL/min/1.73m2) and possibly a more sensitive marker for cardiovascular risk and all-cause mortality. We examined the association of cystatin C with cardiovascular morbidity and all-cause mortality in a prospective population-based study. Methods Cystatin C was measured in 2852 men and 3153 women in the Tromsø Study 1994/95. Gender-specific associations during 12 years of follow-up for all-cause mortality and 9.5 years for myocardial infarction (MI) and ischaemic stroke were assessed (Cox proportional hazard ratios, HRs). Results During follow-up, 591 MIs, 293 ischaemic strokes and 1262 deaths occurred. In women, HR for all-cause mortality was increased in the upper cystatin C quartile (≥0.93 mg/L) compared with the lowest quartile (≤0.73 mg/L); 1.38, 95% confidence interval 1.04–1.84. A significant interaction with gender was observed. One SD (0.17 mg/L) increase in cystatin C was associated with 9% higher risk of death in women, also when persons with a cancer history were excluded. Crude HRs for MI and ischaemic stroke were increased in both genders, but the associations did not persist after multivariable adjustments. No independent associations with end points were observed in non-gender-specific analyses. Conclusions Cystatin C was not independently associated with fatal and non-fatal MI or ischaemic stroke in the general population. However, cystatin C was a risk factor for all-cause mortality in women.

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