Diabetes and nephropathy.
OBJECTIVE
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.


RESULTS
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.


CONCLUSIONS
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.
Caramori
M Luiza
ML
Endocrine Division, Universidade Federal do Rio Grande do Sul, Brazil and bDepartment of Pediatrics, University of Minnesota, Minneapolis, Minnesota 55455, USA.
Mauer
Michael
M
D000419:Albuminuria / Q000209:etiology / Q000628:therapy; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D016207:Cytokines / Q000502:physiology; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D003928:Diabetic Nephropathies / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006133:Growth Substances / Q000502:physiology; D006439:Hemodynamics; D006801:Humans; D018384:Oxidative Stress; D011110:Polymorphism, Genetic; D011507:Proteinuria / Q000209:etiology / Q000628:therapy
D001786:Blood Glucose; D016207:Cytokines; D017127:Glycation End Products, Advanced; D006133:Growth Substances