Alkali Reactive Carbonate Rocks: Is it Alkali Silica Reaction (ASR) or Alkali Carbonate Reaction (ACR)?

The root cause of distress in two different concrete structures made from carbonate coarse aggregates that fit the textural and compositional criteria cited for ACR was found to be caused by ASR, not ACR. Stereo-optical examination and transmitted polarized light microscopy (PLM) analysis showed that the concretes contain some dark gray, fine-grained argillaceous dolomitic coarse aggregates in which secondary white deposit filling the cracks extending from these aggregates into the paste (as well as lining air voids) is ASR gel. Back scattered electron (BSE) imaging with EDS spectra and x-ray elemental mappings, clearly confirm that the white secondary deposits consist of ASR gel. BSE images with EDS spectra and X-ray maps of different samples for each element within areas occupied by the gel showed typical ASR gel. High magnification PLM examination showed the presence of cryptocrystalline to microcrystalline quartz in pockets in the matrix of the rock. The presence of Si-rich phases as finely divided interstitial cryptocrystalline silica minerals intermixed with the matrix and locally in pockets in the matrix of the rocks is confirmed by X-ray mapping, and these silica minerals are the source of silica for ASR. The uniform Mg concentration as reflected by the scan across the dolomite rhombs indicates no sign of dedolomitization, and there was no evidence of brucite formation. While the aggregates have the classic texture often cited for ACR, there is no evidence of the deterioration of the dolomite rhombs or migration of Mg into the rims/peripheries of the dolomite rhombs. Instead, in these cases there is compelling evidence that the concrete distress was caused by ASR and not ACR

Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy

BACKGROUND Type 2 diabetes mellitus is the leading cause of kidney failure worldwide, but few effective long-term treatments are available. In cardiovascular trials of inhibitors of sodium–glucose cotransporter 2 (SGLT2), exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes. METHODS In this double-blind, randomized trial, we assigned patients with type 2 diabetes and albuminuric chronic kidney disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo. All the patients had an estimated glomerular filtration rate (GFR) of 30 to 300 to 5000) and were treated with renin–angiotensin system blockade. The primary outcome was a composite of end-stage kidney disease (dialysis, transplantation, or a sustained estimated GFR of <15 ml per minute per 1.73 m 2), a doubling of the serum creatinine level, or death from renal or cardiovascular causes. Prespecified secondary outcomes were tested hierarchically. RESULTS The trial was stopped early after a planned interim analysis on the recommendation of the data and safety monitoring committee. At that time, 4401 patients had undergone randomization, with a median follow-up of 2.62 years. The relative risk of the primary outcome was 30% lower in the canagliflozin group than in the placebo group, with event rates of 43.2 and 61.2 per 1000 patient-years, respectively (hazard ratio, 0.70; 95% confidence interval [CI], 0.59 to 0.82; P=0.00001). The relative risk of the renal-specific composite of end-stage kidney disease, a doubling of the creatinine level, or death from renal causes was lower by 34% (hazard ratio, 0.66; 95% CI, 0.53 to 0.81; P<0.001), and the relative risk of end-stage kidney disease was lower by 32% (hazard ratio, 0.68; 95% CI, 0.54 to 0.86; P=0.002). The canagliflozin group also had a lower risk of cardiovascular death, myocardial infarction, or stroke (hazard ratio, 0.80; 95% CI, 0.67 to 0.95; P=0.01) and hospitalization for heart failure (hazard ratio, 0.61; 95% CI, 0.47 to 0.80; P<0.001). There were no significant differences in rates of amputation or fracture. CONCLUSIONS In patients with type 2 diabetes and kidney disease, the risk of kidney failure and cardiovascular events was lower in the canagliflozin group than in the placebo group at a median follow-up of 2.62 years