|R||Reductase inhibitors (HMG-CoA). Decreasing modified LDL-cholesterol, i.e., oxidized, acetylated LDL-cholesterol. Decreasing triglycerides and increasing HDL-cholesterol. Improving endothelial cell dysfunction. Restoring the abnormal Lipoprotein fractions. Thus, decreasing the redox and oxidative stress to the arterial vessel wall and myocardium.|
AngII inhibition or receptor blockade:|
ACEi-prils. ARBs-sartans. Both inhibiting the effect of angiotensin-II locally as well as systemically. Affecting hemodynamic stress through their antihypertensive effect as well as the deleterious effects of angiotensin II on cells at the local level – decreasing the stimulus for O2. production. The positive effects on microalbuminuia and delaying the progression to end stage renal disease. Plus the antioxidant effects within the arterial vessel wall and capillary. Antioxidant effects.
Aspirin antiplatelet, anti-inflammatory effect on the diabetic hyperactive platelet.
Adrenergic (non-selective blockade) in addition to its blockade of prorenin → renin conversion.
Non dihydropyridine calcium channel blocker – antagonists are preferred over dihydropyridine calcium channel blockers – antagonists in CKD.
Aggressive control of diabetes to HbA1c of less than 7. This usually requires combination therapy with the use of insulin secretagogues, insulin sensitizers (PPAR-gamma agonists), biguanides, alpha-glucosidase inhibitors, and ultimately exogenous insulin.|
Decreasing modified LDL cholesterol, i.e., glycated-glycoxidated LDL cholesterol. Improving endothelial cell dysfunction. Also decreasing glucotoxicity and the oxidative-redox stress to the intima and pancreatic islet.
Aggressive control of blood pressure, which usually requires combination therapy.
Aggressive control of homocysteine with folic acid with its associated additional positive effect on re-coupling the eNOS enzyme reaction by restoring the activity of the BH4 cofactor to run the eNOS reaction via a folate shuttle mechanism and once again produce eNO.
Aggressive control of uric acid levels with xanthine oxidase inhibitors (allopurinol and oxypurinol) should be strongly considered in view of the prevailing literature in order to achieve more complete Global Risk Reduction
Aggressive control of hyperphosphatemia and elevated PTH and control intake of oral calcium while limiting vitamin D. Calcium carbonate should no longer be used as a phosphate binder in patients with calciphylaxis or patients at very high risk for developing calciphylaxis.
Statins. Improving plaque stability (pleiotropic effects) independent of cholesterol lowering. Improving endothelial cell dysfunction. Moreover, the indirect antioxidant anti-inflammatory effects within the islet and the arterial vessel wall promoting stabilization of the unstable, vulnerable islet and the arterial vessel wall.|
Style. Lifestyle modification (weight loss, exercise, and change eating habits).
Statins: Emerging information: Positive effect on the Quality of HDL-C is emerging. i.e. prevents ox HDL-C and increases HDL-C 5–10 percent.