Diabetic Nephropathy and Diabetic Kidney Disease

Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease (CKD) and end-stage kidney disease (ESKD) in the United States and worldwide. Alterations in glomerular hemodynamics, inflammation, and fibrosis are primary mediators of kidney tissue damage, although the relative contribution of these mechanisms likely varies between individuals and over the course of the natural history of diabetic kidney disease. The presence of DKD is also strongly associated with cardiovascular morbidity/mortality and has a major influence on survival. Clinical presentation and prognosis of DKD are heterogeneous and vary between individuals, although the severity of albuminuria, particularly when combined with elevated blood pressure, remains an important marker of those at higher risk of progression. Management of DKD requires a holistic approach that combines cardiovascular risk reduction with elements to slow the progression of kidney disease, namely glycemic control, RAAS inhibition and blood pressure lowering. Effective delivery of these interventions in combination reduces the risks of DKD progression, as well as other microvascular complications, cardiovascular events, and mortality. Several international groups have issued clinical guidelines that largely agree on recommended targets, and in clinical practice these should be tailored for each individual patient. SGLT2 inhibitors are exciting new options now available to slow the progression of diabetic nephropathy.