Elevated WBC count, even within the normal range, is associated with both macro- and microvascular complications in type 2 diabetes. Chronic inflammation, as indicated by a higher WBC count, may play a linkage role in the development of macro- and microvascular complications in diabetes.

OBJECTIVE -Chronic kidney disease (CKD) predicts cardiovascular disease (CVD) in the general population. We investigated the effects of stages of renal function using the estimated glomerular filtration rate (eGFR) on all-cause mortality and cardiovascular end points in a prospective cohort of Chinese type 2 diabetic patients. -Between 1995 and 2000, 4,421 patients without macrovascular disease or end-stage renal disease were recruited. Renal function was assessed by eGFR, as calculated by the abbreviated Modification of Diet in Renal Disease Study Group formula. Clinical end points included all-cause mortality, cardiovascular end point (cardiovascular death, new admissions due to angina, myocardial infarction, stroke, revascularization, or heart failure), and renal end point (reduction in eGFR by Ͼ50%, progression of eGFR to stage 5, or dialysis or renal death). RESEARCH DESIGN AND METHODS RESULTS-After a median follow-up period of 39.4 months (interquartile range 20.3-55), all-cause mortality rate increased from 1.2% (95% CI 0.8 -1.7) to 18.3% (9.1-27.5) (P for trend Ͻ0.001) as renal function deteriorated from stage 1 (eGFR Ն90 ml/min per 1.73 m 2 ) to stage 4 (15-29 ml/min per 1.73 m 2 ). The respective rate of new cardiovascular end points also increased from 2.6% (2.0 -3.3) to 25.3% (15.0 -35.7) (P for trend Ͻ0.001). After adjustment for covariates (age, sex, albuminuria, use of renin-angiotensin-aldosterone system [RAAS] inhibitors, lipids, blood pressure, and glycemic control), hazard ratios across different stages of eGFR (Ն90, 60 -89, 30 -59, and 15-29 ml/min per 1.73 m 2 ) for all-cause mortality were 1.00, 1.27, 2.34, and 9.82 (P for trend Ͻ0.001), for cardiovascular end points were 1.00, 1.04, 1.05, and 3.23 (P for trend Ͻ0.001), and for renal end points were 1.00, 1.36, 3.34, and 27.3 (P for trend Ͻ0.001), respectively. CONCLUSIONS -Chinese type 2 diabetic patients with reduced eGFR were at high risk of developing cardiovascular end points and all-cause mortality, independent of albuminuria and metabolic control. Diabetes Care 29:2046 -2052, 2006I n the general population, chronic kidney disease (CKD) predicts occurrence of cardiovascular disease (CVD), but similar information in the diabetic population is limited (1-3). Diabetes is the most common cause of end-stage renal disease, accounting for nearly 50% of all new cases of renal replacement therapy in most developed countries (3,4). Asians have a high risk of developing nephropathy, which affects 60% of hypertensive type 2 diabetic patients (5). In the World Health Organization Multinational Study of Vascular Disease in Diabetes (4), 10 -15% of diabetic patients in China and Japan died from end-stage renal disease in contrast to Ͻ5% in North America and Europe, possibly due to genetic influence (6), environmental factors yet to be identified, and limited access to renal replacement therapy. Although large-scale studies have suggested that Asians might have a lower risk of developing CVDs compared with Caucasians (7), given their predilection for...

The effect of biphosphonate therapy on bone mineral density (BMD) in patients with primary hyperparathyroidism (PHP) is unknown. Forty postmenopausal women (mean age, 70 yr) with PHP were randomized to receive alendronate 10 mg/d or placebo for 48 wk, followed by treatment withdrawal for 24 wk. The mean (+/-SD) changes in BMD at femoral neck (+4.17 +/- 6.01% vs. -0.25 +/- 3.3%; P = 0.011) and lumbar spine (+3.79 +/- 4.04% vs. 0.19 +/- 2.80%; P = 0.016) were significantly higher with alendronate at 48 wk. Serum calcium was reduced with alendronate but not placebo (-0.09 vs. +0.01 mmol/liter; P = 0.018). Serum bone-specific alkaline phosphatase activity was lower with alendronate from 12 wk onward and increased 24 wk after treatment withdrawal (21.1 +/- 12.8 to 7.3 +/- 4.9 IU/liter at 48 wk, and 15.0 +/- 14.8 IU/liter 24 wk after withdrawal; P = 0.002 for trend). Osteocalcin concentration decreased at 48 wk and increased 24 wk after alendronate withdrawal (P = 0.019 for trend of change over time) but not with placebo. Urinary N-telopeptide/creatinine ratio decreased with alendronate at 48 wk and increased 24 wk after treatment withdrawal (P = 0.008 for trend). N-telopeptide/creatinine ratio did not change with placebo. Alendronate improves BMD and reduces bone turnover markers in postmenopausal women with PHP.

Background-Herpesvirus infection is a possible risk factor for atherogenesis, and diabetics may be at particular risk.Endothelial dysfunction is an early marker for atherosclerosis, and the present study tests the hypotheses that (1) prior infection with cytomegalovirus (CMV) and herpes simplex virus (HSV) is associated with endothelial dysfunction and (2) this may be more marked in diabetics. Methods and Results-Serum samples were tested for anti-IgG antibodies to CMV and HSV from 400 subjects (mean age for diabetics and nondiabetics, 37.8Ϯ4.3 and 37.9Ϯ3.7 [SD]). We also assessed Helicobacter pylori and Chlamydia pneumoniae serology. Coronary atheroma was quantified by means of electron beam computed tomography. Subjects (nϭ157) underwent venous occlusion plethysmography with acetylcholine, bradykinin, glyceryl trinitrate, norepinephrine, and L-N G -monomethyl-L-arginine. Individuals who were seropositive for CMV had reduced responses to bradykinin (Pϭ0.005) and glyceryl trinitrate (Pϭ0.006). The reduced response to bradykinin remained significant (Pϭ0.045) after adjusting for the response to glyceryl trinitrate and was independent of conventional risk factors. Positive serology for the other organisms did not have an independent effect on reactivity. There was a weaker association between CMV and coronary artery calcification (Pϭ0.09). Positive serology for each of the other pathogens did not affect reactivity, but there was a relation between total pathogen burden and impaired vascular reactivity. No significant differences were found between diabetics and nondiabetics. Conclusions-This