Abstract

Diabetic nephropathy is the major cause of ESRD in the United States.1 Unfortunately, only angiotensin-converting enzyme inhibitors or angiotensin type 1 receptor blockers are registered for slowing the progression of diabetic nephropathy—but they do not halt progression.2–5 Given that diabetic nephropathy costs the health care system close to $30 billion per year,6 one would hope to see a flurry of active clinical trials aimed at registering new therapies to slow progression. Instead, the sad truth is that only 31 interventional phase 2 or 3 trials are currently listed on ClinicalTrials.gov and most only study various angiotensin-converting enzyme inhibitor/angiotensin type 1 receptor blocker and renin inhibitor combinations. In striking contrast, there are 757 breast cancer and 989 lung cancer interventional survival trials and 175 interventional major adverse cardiac event outcomes trials in the same database.7 Numerous hurdles exist to closing this gap for diabetic nephropathy, including the identification of dynamic biomarkers that reflect not just the presence of disease but also the rate of loss of kidney function.8,9 Discovery of these biomarkers and novel therapies will require a deeper understanding of the pathophysiology of diabetic nephropathy. Because of limited access to diseased human kidney tissues, validated and clinically relevant animal models of diabetic nephropathy would significantly facilitate these …

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