Purpose of review Diabetic nephropathy
is the single most common disorder leading to renal failure. Its annual incidence has more than doubled in the past decade to reach 44% of all end-stage renal disease, despite recent therapeutic advances. Thus, research into diabetic nephropathy pathophysiology
that could lead to new treatment
approaches is urgently needed and this review aims to summarize the work performed in this area in the past year.
There have been advances in the understanding of diabetic nephropathy pathology
. Clearly, structural changes may be advanced before any clinical findings are apparent. Not all functional consequences of the condition are explained by current structural analyses. Genetic studies have connected the disorder risk to multiple candidate genes and a few genetic loci, but the exact genetic predisposition or protectors are not fully described. Perturbations in multiple metabolic pathways are associated with diabetic nephropathy
in animals and humans, but their relative importance requires further work. Glycemia and blood pressure control are crucial for diabetic nephropathy
prevention and treatment
, but new modalities are needed.
Recent advances in molecular biology and genetics will bring new insights to the mechanisms involved in diabetic nephropathy
development. This will allow early identification of patients at risk of, or safe from, diabetic nephropathy
and will hopefully lead to preventive strategies, based on the understanding of the pathophysiology
of the disorder. Meanwhile, aggressive implementation of proven therapies to prevent (glycemic control) and slow (antihypertensive therapy, especially with renin-angiotensin system blockers) the progression of diabetic nephropathy
are strongly recommended.