How do genetic and environmental factors interact in diabetic kidney disease?

361 ISSN 1758-1907 10.2217/DMT.12.44 © 2012 Future Medicine Ltd Diabetes Manage. (2012) 2(5), 361–364 Diabetic kidney disease (DKD), also known as diabetic nephropathy, is one of the most serious complications of diabetes and results from a complex interplay of metabolic and hemodynamic disturbances in genetically predisposed individuals. Classically, DKD is characterized by persistent proteinuria, elevated arterial blood pressure, and progressive decline in renal function. In recent years, a subset of patients with diabetes and progressive loss of renal function without significant proteinuria either treated or untreated with renin–angiotensin–aldosterone system inhibitors have also been identified. Diabetes accounts for approximately 44% of patients on replacement therapy for endstage renal disease each year, including dialysis and renal transplantation. Despite the fact that its incidence has been declining in recent years, the current epidemic of obesity and diabetes is anticipated to reverse this trend and result in a disproportionate number of diabetics with end-stage renal disease, potentially reaching 70% by 2015 [1]. Diabetic individuals with nephropathy have a significantly increased morbidity and premature mortality primarily due to accelerated macrovascular cardiovascular disease, such as coronary heart disease and stroke. In addition to morbidity and mortality associated with DKD, the disease has major societal impact because of the enormous financial burden associated with renal replacement therapy. The increasing number of patients with end-stage renal disease and the associated socioeconomic burden necessitates the identification of cellular and molecular pathways involved in the development and progression of DKD. This should impact adequate classification, prognosis and treatment. Epidemiological studies investigating the causative factors demonstrate that