Background and Purpose-Recent studies have attributed the increased infection vulnerability of patients with stroke to stroke-induced immunosuppression. We have therefore explored the immunological changes in patients with ischemic stroke. Methods-Blood from 46 patients with stroke was analyzed by fluorescent-activated cell sorter to determine leukocyte subsets. To identify changes that represent clinically relevant immunosuppression, we compared patients who developed infection within 14 days after stroke with those who did not. Results-Stroke induced a dramatic and immediate loss of T-lymphocytes, most pronounced within 12 hours after stroke onset. Only patients with subsequent infection exhibited a delay in the recovery of CD4ϩ T-lymphocyte counts. Conclusions-Our data suggest that a loss of CD4ϩ T cell function contributes to the stroke-induced immunosuppression.The CD4ϩ T cell count on the day after stroke may emerge as a predictive marker for poststroke infection allowing, early identification of patients at risk. (Stroke. 2008;39:237-241.)

Galectin-3 has been linked to incident renal disease, experimental renal fibrosis, and nephropathy. However, the association among galectin-3, renal function, and adverse outcomes has not been described. We studied this association in two large cohorts of patients over a broad range of renal function. We measured galectin-3 concentrations in baseline samples from the German Diabetes mellitus Dialysis (4D) study (1168 dialysis patients with type 2 diabetes mellitus) and the Ludwigshafen Risk and Cardiovascular Health (LURIC) study (2579 patients with coronary angiograms). Patients were stratified into three groups: eGFR of $90 ml/min per 1.73 m 2 , 60-89 ml/min per 1.73 m 2 , and ,60 ml/min per 1.73 m 2 . We correlated galectin-3 concentrations with demographic, clinical, and biochemical parameters. The association of galectin-3 with clinical end points was assessed by Cox proportional hazards regression within 10 years (LURIC) or 4 years (4D) of follow-up. Mean6SD galectin-3 concentrations were 12.864.0 ng/ml (eGFR$90 ml/min per 1.73 m 2 ), 15.665.4 ng/ml (eGFR 60-89 ml/min per 1.73 m 2 ), 23.169.9 ng/ml (eGFR,60 ml/min per 1.73 m 2 ), and 54.1619.6 ng/ml (dialysis patients of the 4D study). Galectin-3 concentration was significantly associated with clinical end points in participants with impaired kidney function, but not in participants with normal kidney function. Per SD increase in log-transformed galectin-3 concentration, the risks of all-cause mortality, cardiovascular mortality, and fatal infection increased significantly. In dialysis patients, galectin-3 was associated with the combined end point of cardiovascular events. In conclusion, galectin-3 concentrations increased with progressive renal impairment and independently associated with cardiovascular end points, infections, and all-cause death in patients with impaired renal function. 26: 221326: -222126: , 201526: . doi: 10.1681 Galectin-3, also known as 35-kD lectin, IgE-binding protein, laminin-binding protein, and Mac-2, is a 250 amino-acid galactose-specific lectin with a high affinity for b-galactosides and IgE. It is a member of the multifunctional galectin family 1,2 and is ubiquitously expressed, for instance in the heart, the kidney, blood vessels, and macrophages. 3 Alternative splicing results in multiple transcript variants. Galectin-3 is a so-called chimera-type galectin, with a J Am Soc Nephrol