Diabetic Kidney Disease

Abstract

Chronic kidney disease (CKD) is increasing at epidemic rates worldwide. This increase in CKD is principally due to the worldwide rise in type 2 diabetes mellitus. Development and progression of CKD not only may lead to end-stage kidney disease but also is associated with significant increases in cardiovascular disease and cardiovascular death. Elevated blood glucose is the main inciting cause for the development of diabetic kidney disease (DKD). Elevated blood glucose leads to activation of mechanisms in the kidney such as increases in glomerular filtration, in reactive oxygen species, in protein kinase C isoforms, in transforming growth factor β, and others. Prevention is achieved by blood sugar control (hemoglobin A1c of <7%) and blood pressure control (<130/80). Treatment is achieved by aiming for similar goals as prevention and by lowering urine albumin levels principally by using medications that prevent the actions of angiotensin II. Early diagnosis and intervention is key. Only 20–40% of all people with diabetes will develop DKD. Current screening and monitoring methods (calculating the estimated glomerular filtration rate and measuring the urine albumin level) are good but not fully adequate. New markers for risk for monitoring for development and progression of DKD have been discovered that may be useful. Knowing who will develop DKD and who will progress is critical so that patients can be treated as early as possible and so that research studies can be done to determine which treatments optimally prevent development and progression of DKD.