Background and Purpose Diabetic ketoacidosis (DKA) 5-year periods (i.e, 1991-1995, 1996-2000, 2001-2005 2001-2005 (2.65% and 11.63% in DKA and HHS, respectively

Background:The protective effect of +45T >G polymorphism in the adiponectin gene (ADIPOQ) on coronary artery disease (CAD) has been demonstrated in European populations, so this study investigated the effect of +45T >G polymorphism on the risk of CAD and its interactions with other metabolic risk factors in a Chinese population. Methods and Results:The +45T >G polymorphism (rs2241766) of ADIPOQ was genotyped in 600 patients with angiographically diagnosed CAD and in 718 controls. The G allele at the +45T >G polymorphism was associated with a lower risk of CAD (odds ratio (OR), 0.76; 95% confidence interval (CI), 0.64-0.89; P=0.001). The protective effect of the G allele at +45T >G polymorphism was magnified at blood pressure <140/90 mmHg (OR, 0.65; 95%CI, 0.51-0.82; P=0.0004), but disappeared at blood pressure ≥140/90 mmHg (OR, 0.98; 95%CI, 0.76-1.28; P=0.93), indicating an interaction between +45T >G polymorphism and blood pressure on CAD risk (P=0.02 for interaction). A similar interaction was also observed between plasma cholesterol level and the +45T >G polymorphism. Conclusions: An association of ADIPOQ genetic polymorphism with CAD risk is modified by traditional risk factors, such as blood pressure and plasma cholesterol level. (Circ J 2009; 73: 1934 -1938

Background Type 2 diabetes is an important challenge given the worldwide epidemic and is the most important cause of end-stage renal disease (ESRD) in developed countries. It is known that patients with ESRD and advanced renal failure suffer from immunosenescence and premature T cell aging, but whether such changes develop in patients with less severe chronic kidney disease (CKD) is unclear. Method 523 adult patients with type 2 diabetes were recruited for this study. Demographic data and clinical information were obtained from medical chart review. Immunosenescence, or aging of the immune system was assessed by staining freshly-obtained peripheral blood with immunophenotyping panels and analyzing cells using multicolor flow cytometry. Result Consistent with previously observed in the general population, both T and monocyte immunosenescence in diabetic patients positively correlate with age. When compared to diabetic patients with preserved renal function (estimated glomerular filtration rate > 60 ml/min), patients with impaired renal function exhibit a significant decrease of total CD3+ and CD4+ T cells, but not CD8+ T cell and monocyte numbers. Immunosenescence was observed in patients with CKD stage 3 and in patients with more severe renal failure, especially of CD8+ T cells. However, immunosenescence was not associated with level of proteinuria level or glucose control. In age, sex and glucose level-adjusted regression models, stage 3 CKD patients exhibited significantly elevated percentages of CD28−, CD127−, and CD57+ cells among CD8+ T cells when compared to patients with preserved renal function. In contrast, no change was detected in monocyte subpopulations as renal function declined. In addition, higher body mass index (BMI) is associated with enhanced immunosenescence irrespective of CKD status. Conclusion The extent of immunosenescence is not significantly associated with proteinuria or glucose control in type 2 diabetic patients. T cells, especially the CD8+ subsets, exhibit aggravated characteristics of immunosenescence during renal function decline as early as stage 3 CKD. In addition, inflammation increases since stage 3 CKD and higher BMI drives the accumulation of CD8+CD57+ T cells. Our study indicates that therapeutic approaches such as weight loss may be used to prevent the emergence of immunosenescence in diabetes before stage 3 CKD.

OBJECTIVE Finerenone significantly improved cardiorenal outcomes in patients with chronic kidney disease (CKD) and type 2 diabetes (T2D) in the Finerenone in Reducing Kidney Failure and Disease Progression in Diabetic Kidney Disease trial. We explored whether baseline HbA1c level and insulin treatment influenced outcomes. RESEARCH DESIGN AND METHODS Patients with T2D, urine albumin-to-creatinine ratio (UACR) of 30–5,000 mg/g, estimated glomerular filtration rate (eGFR) of 25 to &lt;75 mL/min/1.73 m2, and treated with optimized renin–angiotensin system blockade were randomly assigned to receive finerenone or placebo. Efficacy outcomes included kidney (kidney failure, sustained decrease ≥40% in eGFR from baseline, or renal death) and cardiovascular (cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure) composite endpoints. Patients were analyzed by baseline insulin use and by baseline HbA1c &lt;7.5% (58 mmol/mol) or ≥7.5%. RESULTS Of 5,674 patients, 3,637 (64.1%) received insulin at baseline. Overall, 5,663 patients were included in the analysis for HbA1c; 2,794 (49.3%) had baseline HbA1c &lt;7.5% (58 mmol/mol). Finerenone significantly reduced risk of the kidney composite outcome independent of baseline HbA1c level and insulin use (Pinteraction = 0.41 and 0.56, respectively). Cardiovascular composite outcome incidence was reduced with finerenone irrespective of baseline HbA1c level and insulin use (Pinteraction = 0.70 and 0.33, respectively). Although baseline HbA1c level did not affect kidney event risk, cardiovascular risk increased with higher HbA1c level. UACR reduction was consistent across subgroups. Adverse events were similar between groups regardless of baseline HbA1c level and insulin use; few finerenone-treated patients discontinued treatment because of hyperkalemia. CONCLUSIONS Finerenone reduces kidney and cardiovascular outcome risk in patients with CKD and T2D, and risks appear consistent irrespective of HbA1c levels or insulin use.

Although nearly half of asymptomatic DM patients had rectal carriage of K. pneumoniae and one-third of them colonized by isolates belonging to the seven serotypes related to PLA, none of them subsequently developed PLA and colonized patients did not have higher risk of microbiologically confirmed bacterial infections.