Abstract
Diabetic nephropathy (DN) contributes to nearly 50% of chronic kidney disease and end-stage renal disease cases in the United States (1). Despite clinical trials that have affirmed the importance of glycemic control and the provision of inhibitors of the renin-angiotensin-aldosterone system for slowing progression of DN, the burden of disease continues to increase (2). Therefore further mechanistic studies are needed to understand the pathogenesis of DN. One of the earliest histologic changes in glomeruli from patients with DN is mesangial extracellular matrix (ECM) deposition (3). Ultrastructural studies also demonstrate increased glomerular basement membrane (GBM) thickness and podocyte foot process effacement (3). These lesions are associated with the development of albuminuria, but three fundamental questions remain: 1 ) Although transforming growth factor (TGF)-β signaling is an important mediator of these early lesions, why does treatment with an anti-TGF-β neutralizing antibody not reduce albuminuria (4)? 2 ) What is the contribution of each glomerular cell type to these lesions and to albuminuria? 3 ) What is the role of albuminuria in mediating further glomerular and tubular damage in DN? The article by Fan et al. (5) in this issue of Diabetes represents an important step forward in addressing these gaps in our knowledge of DN. How TGF-β induces albuminuria has been debated for more than a decade. In a now classic article, Ziyadeh et al. …
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