Neil B. Minkoff, MD: Let me turn my question to Dr Wright. There’s this new breakthrough, right? There’s this new drug. It’s been described here by our colleagues as the designer molecule and so on, and it’s shown significant improvement, or at least slowing kidney disease progression and so on. Where do you see that entering your practice?
Eugene Wright Jr., MD: That’s a great question. I’d like to pick up on where my colleagues left off. I thought they gave a great basic science lecture. But often when I’m talking about these kinds of discoveries with my colleagues, both in medicine and sometimes with patients who are at the higher end of understanding, is this a distinction without a difference? I go back to one of the lessons that we learned early in biochemistry, that molecular anatomy determines molecular structure, and structure determines function.
It’s like the difference between ultralente insulin and a rapid-acting insulin. They’re both insulins, but they work very differently. Understanding this difference, where do I see that it fits? Based on the data that we have from the trials, this is a therapy that can be used early in the course of diabetic kidney disease, or chronic kidney disease in patients with type 2 diabetes, as soon as we detect that they’re crossing that threshold, irrespective of their eGFR [estimated glomerular filtration rate].
I tell this story because I had a patient several years ago who came in with type 2 diabetes he’d had for a while, with many of the complications, but his eGFR calculated at 130 mL/min. At first, you’d look at that and say, “Oh my gosh, I’ve got lots of room with this kidney.” But when you check the urine protein, this guy’s spilling 2 or 3 g a day. You start to figure that this isn’t good. He’s in the hyperfiltration phase. So irrespective of that eGFR, this is the point that George and Rajiv made earlier, that you’ve got to look at the urine albumin-to-creatinine ratio, and once that becomes abnormal, you need to treat.
Transcript edited for clarity.