Background: The value of carotid‐femoral pulse wave velocity (cfPWV) as risk factor for development of complications in type 1 diabetes mellitus remains to be determined. We investigated associations between cfPWV and renal outcomes, cardiovascular events, and all‐cause mortality in people with type 1 diabetes mellitus. Methods and Results: cfPWV was measured with SphygmoCor in 633 people with type 1 diabetes mellitus. Median (interquartile range) follow‐up was 6.2 (5.8−6.7) years. End points included progression in albuminuria group, decline in estimated glomerular filtration rate (eGFR) ≥30%, end‐stage kidney disease, cardiovascular event, mortality, and a composite renal end point. Hazard ratios (HRs) were calculated per 1‐SD increase in cfPWV. Adjustments included age, sex, hemoglobin A1c, mean arterial pressure, body mass index, low‐density lipoprotein cholesterol, smoking, urine albumin excretion rate, and eGFR. The cohort included 45% women, mean (SD) age was 54 (13) years, mean (SD) eGFR was 83.2 (27.9) mL/min per 1.73 m ² , and mean (SD) cfPWV was 10.4 (3.3) m/s. Median (interquartile range) albumin excretion rate was 17 (17‐63) mg/24 h. After adjustment, higher cfPWV was associated with increased hazard of progression in albuminuria (HR, 1.59; 95% CI, 1.10−2.32); decline in eGFR ≥30% (HR, 1.38; 95% CI, 1.06−1.79); cardiovascular event (HR, 1.31; 95% CI, 1.01−1.70); mortality (HR, 1.36; 95% CI, 1.00−1.85); and the composite renal end point (HR, 1.30; 95% CI, 1.04−1.63), but not with end‐stage kidney disease (HR, 1.18; 95% CI, 0.62−2.26). Higher cfPWV was associated with steeper yearly increase in albumin excretion and steeper yearly decline in eGFR after adjustment ( P =0.002 and P =0.01, respectively). Conclusions: cfPWV was associated with increased hazard of renal outcomes, cardiovascular event, and mortality. cfPWV may be suited for risk stratification in type 1 diabetes mellitus.

Type 1 diabetes is associated with increased intestinal inflammation and decreased abundance of butyrate-producing bacteria. We investigated the effect of butyrate on inflammation, kidney parameters, HbA1c, serum metabolites and gastrointestinal symptoms in persons with type 1 diabetes, albuminuria and intestinal inflammation. We conducted a randomized placebo-controlled, double-blind, parallel clinical study involving 53 participants randomized to 3.6 g sodium butyrate daily or placebo for 12 weeks. The primary endpoint was the change in fecal calprotectin. Additional endpoints were the change in fecal short chain fatty acids, intestinal alkaline phosphatase activity and immunoglobulins, serum lipopolysaccharide, CRP, albuminuria, kidney function, HbA1c, metabolites and gastrointestinal symptoms. The mean age was 54 ± 13 years, and the median [Q1:Q3] urinary albumin excretion was 46 [14:121] mg/g. The median fecal calprotectin in the butyrate group was 48 [26:100] μg/g at baseline, and the change was −1.0 [−20:10] μg/g; the median in the placebo group was 61 [25:139] μg/g at baseline, and the change was −12 [−95:1] μg/g. The difference between the groups was not significant (p = 0.24); neither did we find an effect of butyrate compared to placebo on the other inflammatory markers, kidney parameters, HbA1c, metabolites nor gastrointestinal symptoms. Twelve weeks of butyrate supplementation did not reduce intestinal inflammation in persons with type 1 diabetes, albuminuria and intestinal inflammation.

OBJECTIVE: We investigated endotrophin, a profibrotic signaling molecule reflecting collagen VI formation, in serum and urine as risk marker for complications to type 2 diabetes. RESEARCH DESIGN AND METHODS: Endotrophin was measured in 774 individuals with type 2 diabetes. Outcomes included a composite kidney end point, first major adverse cardiovascular event (MACE), mortality, progression of albuminuria, incident heart failure, and sight-threatening eye disease. Adjusted Cox proportional hazards models were applied. RESULTS: Doubling of serum endotrophin was associated with the kidney end point (n = 49; hazard ratio 1.80 [95% CI 1.13–2.87]), first MACE (n = 66; 1.54 [1.04–2.28]), mortality (n = 156; 1.69 (1.31–2.19]), and incident heart failure (n = 42; 1.63 [1.02–2.60]). A doubling of urine endotrophin was associated with progression of albuminuria (n = 85; 1.20 [1.04–1.39]). CONCLUSIONS: Serum endotrophin was a risk marker for mortality and kidney and cardiovascular complications in type 2 diabetes. Urine endotrophin was a marker for albuminuria progression.

Diabetic euglycaemic ketoacidosis is a possible adverse effect of sodium–glucose co-transporter-2 inhibitors (SGLT2i). We report a case in which the combination of SGLT2i and a strict very low-carbohydrate diet led to severe diabetic ketoacidosis in a young Caucasian man with type 2 diabetes.

Objectives: The aim of this study was to adjust the default white blood cell (WBC) differential count flag settings on the Sysmex XN‐9100 haematology analyser to reduce unnecessary additional leukocyte differential counts without compromising diagnostic sensitivity. Methods: Data from 4554 routine blood samples flagged on Sysmex XN‐9100 and corresponding additional leukocyte differential counts performed on the Sysmex XF‐1600 flow cytometer were used to optimise the WBC flagging rules. Results: A total of 1148 samples had scattergram‐related flags, which are non‐adjustable. Optimal cut points for Q‐flags were established based on Youden's Index for the remaining 3406 samples, while the diagnostic sensitivity of the new flagging rules for acute leukaemia was assessed in a validation cohort. The optimal cut points for Q‐flags were 120 for ‘Atypical Lymphocytes’, 170 for ‘Abnormal Lymphocytes’ and 160 for ‘Blasts’, while the Q‐flag ‘Left shift’ offered no diagnostic value in our cohort. The count flags ‘eosinophilia’, ‘basophilia’ and ‘monocytopenia’ were deactivated, as the results from Sysmex XN were comparable to the flow cytometric reference method. By implementing the new flagging rules, 1709 (37.5%) of the samples would have been processed without need for additional leukocyte differential count. When evaluated in a separate validation cohort of 90 samples from patients with newly diagnosed acute leukaemia, the new rules showed similar diagnostic sensitivity to the default flagging system. Conclusion: Optimisation of Sysmex flagging rules for leukocyte differential counts was feasible and significantly reduced unnecessary reflex testing, while maintaining analytical accuracy and diagnostic safety.