Abstract. Inflammatory and prothrombotic markers are elevated in individuals with mild to moderate renal disease. It was hypothesized that these markers may also be determinants of the progression of renal disease. The association of six markers-serum C-reactive protein (CRP), white blood cell (WBC) count, fibrinogen, factor VII, albumin, and hemoglobin-with subsequent elevations of creatinine and decline in estimated GFR in the Cardiovascular Health Study, a community-based cohort of elderly individuals, was analyzed. Linear regression was used to determine predictors of an annualized change in serum creatinine as the main outcome. Duration of follow-up was 7 yr for the original cohort and 4 yr for the more recently recruited black cohort. A total of 588 (12.7%) individuals had a decline in estimated GFR of at least 3 ml/min per yr per 1.73 m 2 . Higher CRP (P Ͻ 0.001), WBC count (P Ͻ 0.001), fibrinogen (P Ͻ 0.001), and factor VII (P Ͻ 0.001) levels and lower albumin (P Ͻ 0.001) and hemoglobin levels (P Ͻ 0.001) were associated with a rise in creatinine, after adjusting for age. With additional adjustments for race, gender, baseline creatinine, systolic and diastolic BP, lipid levels, weight, and packyears smoking, higher CRP, factor VII, fibrinogen, WBC count, and lower albumin and hemoglobin levels remained associated with a rise in creatinine. Similar results were found for decline in estimated GFR. The decline in GFR was greater with increasing number of inflammatory or prothrombotic markers that were above the median (below for hemoglobin and albumin). Inflammatory and prothrombotic markers are predictors for a change in kidney function in elderly individuals. Interventions that reduce inflammation might confer significant cardiovascular and renal benefits.Patients with renal failure have a high prevalence of cardiovascular disease, and it has been proposed that atherosclerosis may promote the progression of renal disease in older individuals (1). Diamond et al. (2) proposed that mechanisms that result in atherosclerosis also cause glomerulosclerosis and that renal disease in atherosclerosis is not simply the result of ischemia from renal artery disease. In his model, glomerulosclerosis results from the influx and accumulation of inflammatory cells (monocytes and macrophages), with mesangial cells responding in a similar manner to vascular smooth muscle cells. If this hypothesis is correct, then renal disease and cardiovascular disease should share similar risk factors. In particular, inflammatory and prothrombotic factors, which are risk factors for atherosclerosis (3), might be important factors in the progression of renal disease. The relationship of inflammation to a subsequent loss of renal function has not been previously examined in a population-based sample.We have previously found that inflammatory and prothrombotic markers are elevated in elderly individuals with mild to moderate renal insufficiency, a relationship that persisted after adjusting for the greater extent of atherosclerosis that is ...