Elevations of inflammatory and procoagulant biomarkers in elderly persons with renal insufficiency.
BACKGROUND
Renal insufficiency has been associated with cardiovascular disease events and mortality in several prospective studies, but the mechanisms for the elevated risk are not clear. Little is known about the association of renal insufficiency with inflammatory and procoagulant markers, which are potential mediators for the cardiovascular risk of kidney disease.


RESULTS
The cross-sectional association of renal insufficiency with 8 inflammatory and procoagulant factors was evaluated using baseline data from the Cardiovascular Health Study, a population-based cohort study of 5888 subjects aged > or =65 years. C-reactive protein, fibrinogen, factor VIIc, and factor VIIIc levels were measured in nearly all participants; interleukin-6, intercellular adhesion molecule-1, plasmin-antiplasmin complex, and D-dimer levels were measured in nearly half of participants. Renal insufficiency was defined as a serum creatinine level > or =1.3 mg/dL in women and > or =1.5 mg/dL in men. Multivariate linear regression was used to compare adjusted mean levels of each biomarker in persons with and without renal insufficiency after adjustment for other baseline characteristics. Renal insufficiency was present in 647 (11%) of Cardiovascular Health Study participants. After adjustment for baseline differences, levels of C-reactive protein, fibrinogen, interleukin-6, factor VIIc, factor VIIIc, plasmin-antiplasmin complex, and D-dimer were significantly greater among persons with renal insufficiency (P<0.001). In participants with clinical, subclinical, and no cardiovascular disease at baseline, the positive associations of renal insufficiency with these inflammatory and procoagulant markers were similar.


CONCLUSIONS
Renal insufficiency was independently associated with elevations in inflammatory and procoagulant biomarkers. These pathways may be important mediators leading to the increased cardiovascular risk of persons with kidney disease.
Shlipak
Michael G
MG
Department of Medicine, University of California, San Francisco, and the Veterans Affairs Medical Center, San Francisco 94121, USA. shlip@itsa.ucsf.edu
Fried
Linda F
LF
Crump
Casey
C
Bleyer
Anthony J
AJ
Manolio
Teri A
TA
Tracy
Russell P
RP
Furberg
Curt D
CD
Psaty
Bruce M
BM
D000368:Aged; D015415:Biomarkers / Q000032:analysis; D001779:Blood Coagulation Factors / Q000032:analysis*; D002097:C-Reactive Protein / Q000032:analysis; D002318:Cardiovascular Diseases / Q000209:etiology; D015331:Cohort Studies; D003404:Creatinine / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005340:Fibrinogen / Q000032:analysis; D005341:Fibrinolysin / Q000032:analysis; D006801:Humans; D007249:Inflammation / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D011446:Prospective Studies; D051437:Renal Insufficiency / Q000097:blood* / Q000150:complications / Q000175:diagnosis; D012307:Risk Factors; D000979:alpha-2-Antiplasmin / Q000032:analysis
D015415:Biomarkers; D001779:Blood Coagulation Factors; D005338:Fibrin Fibrinogen Degradation Products; D015850:Interleukin-6; D000979:alpha-2-Antiplasmin; C036309:fibrin fragment D; D005340:Fibrinogen; D002097:C-Reactive Protein; D003404:Creatinine; D005341:Fibrinolysin