Screening for albuminuria in diabetes:the need to do more

Aims: To reassess the utilisation rate of urinary albumin to creatinine ratio (ACR) screening in our centre; and the rate of repeat testing, where appropriate. To look at risk factors for albuminuria in our outpatient population. Methods: All patients attending one of our two weekly diabetes outpatient clinics in 2011–2012 were enrolled in this study. Demographic and relevant clinical data were extracted from electronic care records and analysed using SPSS 21. Results: Our study cohort comprised 998 people (51.4% men;59.6% White, 30.5% Southeast Asian, 9.9% Afro-Caribbean),most of whom had Type 2 diabetes (82.6%). The ACR testing rate in our centre was 62.8% (2012–2013 data; previously 62.4%). The incidence of initial albuminuria was 32.2% in women vs42.8% in men. Just 48.7% of patients (44.4% of women, 51.8% of men) with initial albuminuria were retested: 36.4% of women and 19.7% of men with initial albuminuria had no evidence of this on follow-up. Logistic regression modelling confirmed an association of high systolic blood pressure with albuminuria [odds ratio1.92 (1.01–3.70 in women, 1.08–3.57 in men)]. Treatment with anangiotens in converting enzyme inhibitor (ACEi) or angiotens in 2 receptor blocker (A2RB) was negatively associated with albuminuria in men [odds ratio 0.42 (0.20–0.89)], but not in women. Conclusions: A relatively high, albeit suboptimal, albuminuria screening rate in our outpatient population has been sustained.High systolic blood pressure was confirmed as a risk factor foralbuminuria. The incidence of albuminuria was higher in men, who had a lower rate of negative repeat testing and appeared to benefit more from ACEi/A2RB therapy. More rigorous screening for albuminuria is warranted to identify at-risk individuals.

Transglutaminase inhibition ameliorates experimental diabetic nephropathy

Diabetic nephropathy is characterized by excessive extracellular matrix accumulation resulting in renal scarring and end-stage renal disease. Previous studies have suggested that transglutaminase type 2, by formation of its protein crosslink product epsilon-(gamma-glutamyl)lysine, alters extracellular matrix homeostasis, causing basement membrane thickening and expansion of the mesangium and interstitium. To determine whether transglutaminase inhibition can slow the progression of chronic experimental diabetic nephropathy over an extended treatment period, the inhibitor NTU281 was given to uninephrectomized streptozotocin-induced diabetic rats for up to 8 months. Effective transglutaminase inhibition significantly reversed the increased serum creatinine and albuminuria in the diabetic rats. These improvements were accompanied by a fivefold decrease in glomerulosclerosis and a sixfold reduction in tubulointerstitial scarring. This was associated with reductions in collagen IV accumulation by 4 months, along with reductions in collagens I and III by 8 months. This inhibition also decreased the number of myofibroblasts, suggesting that tissue transglutaminase may play a role in myofibroblast transformation. Our study suggests that transglutaminase inhibition ameliorates the progression of experimental diabetic nephropathy and can be considered for clinical application.