Strategies to help clinicians talk with patients about chronic kidney disease staging and what to expect in terms of prognosis.
Neil B. Minkoff, MD: One of the things I’m trying to understand and get from you guys, is you’ve already talked about this a little with the map and sharing it with your patients and PCPs [primary care physicians]. But how do you explain to them, or even somebody like me, the relationship between where the patient is with their CKD [chronic kidney disease] staging and what their prognosis is, the risk of severity, progression, and so on? Dr Agarwal, could you take a stab at that for me, please?
Rajiv Agarwal, MD: Yes, Neil. I’ll build on what Gene and George have said. George is ahead of the curve; he’s showing people the heat map. But since we don’t have the heat map on the screen, I’ll try to explain it. People who have a GFR [glomerular filtration rate] between 45 and 60 mL/min, for instance, have what we call stage 3 CKD. There’s a very large number of people in that stratum. You can imagine that you can have 3 categories of albuminuria in this group of 45 to 60 mL/min GFR. If you have no albuminuria, you’re not in the green zone, you’re in the yellow zone. If you have moderate albuminuria—what we used to call microalbuminuria—you’re in the orange zone. And if you have very high albuminuria, you’re in the red zone.
If a patient comes to you and says, “Doctor, you’re saying I have moderate kidney disease, yet you’re telling me I have very high risk,” I’d say, “Yes, congratulations, Mr Smith. We have identified you as very high risk, but we now have therapies to reduce your risk. If I move you from very high albuminuria to normal albuminuria, I’ve moved you from the red zone to the orange zone. I have reduced your risk. There’s opportunity to intervene while your kidney function is still fairly preserved.” That’s how you can relay it to patients.
Eugene Wright Jr., MD: If I can just add on to that….
Neil B. Minkoff, MD: Please.
Eugene Wright Jr., MD: From a primary care clinician’s perspective, one of the things that we notice when we go in the room is that the patients have a couple of interests, particularly those with diabetes. Long term, their interests rest on death or dialysis. If there’s anything that you can do to help reduce their risk for death or dialysis, many of them are all ears. They want to know about that. Part of the reason people haven’t been as engaged in the past is because of the sense of futility, that even when they do all these things, their road to death or dialysis isn’t changed much. That’s one of the exciting things now in terms of the conversations we can have with patients and our colleagues, that we have an opportunity to change that trajectory.
George L. Bakris, MD: Let me just add on to this, because this is a good flow. The analogy for the patient, and for the physician for that matter, is to look at somebody with a GFR of let’s say 45 or 50 mL/min, and the clinician will say, “There’s no way I can fix this, so forget it.” That’s not true. I’ll give you the analogy that I give the patients of a piece of metal that’s partially rusted. Are you going to reverse the rust? Well, no, you’re not going to reverse the rust, but you can protect that piece of metal from further rusting, and that’s what your job is and what you’re supposed to be doing. That’s what both Gene and Rajiv have been saying.
Neil B. Minkoff, MD: Let me push on that a little. What are the things you do to prevent further rusting? You have the patient in front of you, you say you’ve got partial rust, and we’re trying to prevent the rest of the rusting from happening. What are you recommending that they do and how do you manage that?
George L. Bakris, MD: My approach to that is the holy trinity of protecting the kidney. What is the holy trinity of protecting the kidney? No. 1, you have to get your sugar controlled. What are we talking about? We’re talking about getting the glycated hemoglobin well below 7%. If you can get the glycated hemoglobin well below 7%, you’ll have markedly reduced a lot of the inflammatory changes and a lot of the osmotic and physiologic changes that are causing injury to the small vessels. The kidney is a huge microvasculature, so you have to think about it like that. Sugar control is critical.
No. 2 is blood pressure control. You have to have the patient below 130 mm Hg. You don’t need to be below 120 mm Hg, but you do need to be around 128 or 130 mm Hg. And let me be clear that it’s a range of blood pressures. If you’re anywhere between 125 and 132 or 133 mm Hg, you’re fine. You just don’t want to be above that. That will also slow progression of kidney disease. That’s been well established.
Lastly, look at things that affect inflammation and things that can lead to fibrosis if inflammation is not checked. One of the big factors, especially in early kidney disease, is lipids and cholesterol control. That will slow kidney disease progression. That triad does not cover 100% of the factors, but it does cover about 75% to 80% of them.
Gene mentioned obesity. Weight loss also helps. That hasn’t been proven to slow kidney disease, but there are a lot of factors in the body, in adipocytes, fat cells, that are produced and actually increase inflammation. This has been seen post-bypass surgery in obese patients that removal of these cells causes a dramatic reduction in inflammation. So that’s what you need to do.
Transcript edited for clarity.