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Chronic Kidney Disease in Type 2 Diabetes: Patient Selection and Education for Improved Outcomes

  • Authors: George Bakris, MD
  • CME / CE Released: 9/22/2022
  • Valid for credit through: 9/22/2023
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  • Credits Available

    Physicians - maximum of 0.25 AMA PRA Category 1 Credit(s)™

    Nurses - 0.25 ANCC Contact Hour(s) (0.25 contact hours are in the area of pharmacology)

    Pharmacists - 0.25 Knowledge-based ACPE (0.025 CEUs)

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Target Audience and Goal Statement

This activity is intended for diabetologists, endocrinologists, nephrologists, and primary care physicians.

The goal of this activity is for learners to be better able to screen and diagnose patients who have type 2 diabetes (T2D) for kidney disease and initiate appropriate treatment.

Upon completion of this activity, participants will:

  • Have greater competence related to
    • Management of CKD in patients with T2D
    • Patient education related to the management of CKD in T2D


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  • George Bakris, MD

    Professor of Medicine
    Director, ASH Comprehensive Hypertension Center
    University of Chicago Medicine
    Chicago, Illinois


    George Bakris, MD, has the following relevant financial relationships:
    Consultant or advisor for: Alnylam; AstraZeneca; Bayer; DiaMedica Therapeutics; Horizon Pharma; Ionis Pharmaceuticals; KBP BioSciences; Merck; Novo Nordisk; Quantum Genomics
    Research funding from: Bayer


  • Anne G. Le, PharmD

    Senior Medical Education Director, Medscape, LLC


    Anne G. Le, PharmD, has no relevant financial relationships.

  • Gina Montanero, PharmD, RPh

    Associate Medical Writer, Medscape, LLC


    Gina Montanero, PharmD, RPh, has no relevant financial relationships.

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  • Leigh Schmidt, MSN, RN, CNE, CHCP

    Associate Director, Accreditation and Compliance, Medscape, LLC


    Leigh Schmidt, MSN, RN, CNE, CHCP, has no relevant financial relationships.

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Chronic Kidney Disease in Type 2 Diabetes: Patient Selection and Education for Improved Outcomes

Authors: George Bakris, MDFaculty and Disclosures

CME / CE Released: 9/22/2022

Valid for credit through: 9/22/2023


Activity Transcript

Clinician: Hello Josephine.I’m Dr Harrington. It’s so nice to meet you.

Patient: Hi Dr Harrington. Nice to meet you too.

Clinician:I see we have your records with your recent labs from Dr Johnson’s office and you got the additional tests done that I recommended prior to this appointment. Thank you for doing that. I would like to go through the test results with you, but first, what brings you in today?

Patient: My primary care doctor, Dr Johnson, just retired. He’s been taking care of my family since I moved here in my 30’s. So I’ll be honest, I’ve been feeling uneasy about finding a new primary care doctor. But my good friend Betty recommended me to you. She has great things to say about your office.

Clinician: I understand that it can be hard starting over with a new doctor. I appreciate you sharing that your friend recommended here and I’ll do all that I can to live up to our reputation. Do you have any specific concerns you want to discuss with me today?

Patient: Well, I’ve had diabetes now going on 10 years. I do my best to avoid sugary foods and I take my medications religiously. I was told if I don’t do things right, I’ll get kidney disease and that really worries me. Even though I do my best, whenever I test my blood sugar, it’s higher than it should be. Usually above 150. Or even higher than 200 after I eat. And I know my blood pressure is still too high even though I don’t use extra salt. I just don’t know what else I can do?

Clinician: I agree, managing diabetes is frustrating. You’re right that your blood sugar and blood pressure are not at the levels they need to be. Especially when we are trying to protect your kidneys. Let’s go over all your test results and see if there are things we can do to change what you are experiencing and improve your health.

Patient: Ok.

Hello. I'm Dr George Bakris, Professor of Medicine at the University of Chicago Medicine in Chicago, Illinois. Welcome to this program titled “Chronic Kidney Disease in Type 2 Diabetes: Patient Selection and Education for Improved Outcomes.” The scene we just saw between Josephine and her primary care doctor is very common. She's concerned that she will get kidney disease due to longstanding diabetes. She has a 10-year history of type 2 diabetes, obesity, hypertension, and dyslipidemia so the next step is to identify if she has kidney disease. How do we do this? Well, first of all, let's take a look at the unappreciated epidemiology of kidney disease. 37 million people, adults in the US, have kidney disease. Diabetes is by far the number 1 cause of chronic kidney disease. And chronic kidney disease in diabetes exerts a significant toll on quality of life, cardiovascular events, and death. Lower GFR, defined as an estimated GFR of less than 60, is associated with increased cardiovascular events and death. It's very important that you have not just the estimated GFR, but also a spot albumin-creatinine ratio. Both of those are needed to make a proper diagnosis of stages of kidney disease. Josephine's eGFR was 50. Her serum creatinine was 1.5. But we also need to know what her urine albumin-creatinine ratio is. Why is this important? Well, this table, which I actually encourage all of you to show patients, basically tells you what stage of kidney disease the patient is in. On the left, you see all of the estimated GFRs and the respective stage of kidney disease. And across the top, you have 3 different categories of albuminuria excretion. If they see they're in red or in orange, they know they're in trouble and they know they really need to get with the program. So let's return now to the scene, as Dr Johnson reviews Josephine's test results with her.

Clinician: I had you get a spot urine test because I needed to see how much protein is in your urine, in addition to your glomerular filtration rate from Dr Johnson’s labs, to properly assess your kidneys. I’m going to be direct with you. You do have kidney disease, but you are far from needing dialysis.

Patient: Oh no! How bad are my kidneys?

Clinician: I’ll show you where you stand on this chart and explain what it all means. There are 2 main levels that tell us how well your kidneys are working. Your glomerular filtration rate is 50 which puts you here on the chart and your albuminuria or the protein in your urine, is 650 which puts you in the red section of the chart. Now, I know you see red and that seems scary. What it means is that you've lost about half of your kidney function, but the other half is working and it is still doing a good job.

Patient: Are there medicines that can get my kidneys fully working again?

Clinicians: The kidney function you’ve lost can’t be regained, but there are ways to prevent you from losing more. I would like you to start a new medication called an SGLT2 inhibitor. It was originally made to lower blood sugar, but it also protects the kidneys and heart and lowers blood pressure, and weight. Many of the things that can improve your health including keeping your kidney disease from getting worse.

Patient: Ok, are there any side effects?

Clinician: You have to maintain good personal hygiene and drink lots of water to prevent urinary tract infections. And it’s important to really dry your under-area after urinating to prevent yeast infections. Also, if you’re sick and are not eating much, you may need to stop taking this medication for a few days.In addition to this new medicine, I would also like to switch a few of your other medications and increase the dose of some of them to get the most benefit.

Patient: This sounds like a lot of changes.

Clinician: I know it feels overwhelming. I assure you these adjustments are all needed to improve your health. You are sick and we need to do all we can to protect your kidneys. I’ll have our nurse come in and go over the changes with you thoroughly.

Patient: Great. That will help.

As we saw in this scene, based on Josephine's uACR and eGFR, she clearly has kidney disease. For many patients. I also use the KDIGO heat map to show them where they stand, as I mentioned earlier. Then, I discuss medication adjustments, options, and other things that she needs to know, such as dietary changes. So, what are we going to do here? Well, we're going to increase the lisinopril to at least 20 mg once a day, and possibly 40 mg if needed. The diuretic should be changed from hydrochlorothiazide to indapamide, 1.25 mg, because it is a different type of thiazide diuretic. We can also use chlorthalidone, 12.5 mg, and leave amlodipine alone. We're going to increase the atorvastatin to 20 mg daily, and also change the glyburide to pioglitazone 7.5 mg daily. At this dose, there's very little edema and very few side effects compared to the much higher doses. We're also going to add a low dose of an SGLT2 inhibitor per guidelines. Now, I think it's important that we summarize some of these things.

First of all, SGLT2 inhibitors, this meta-analysis clearly looks at cardiovascular outcomes as well as kidney outcomes in people with high cardiovascular risk that have diabetes. The data are abundantly clear that the reduction in heart failure and heart failure hospitalizations with SGLT2 inhibitors. And in fact, they are part of the 2022 American Diabetes Clinical Practice guidelines as mandatory therapy in patients with kidney disease and or heart failure. Additionally, it has positive effects on other cardiovascular outcomes. From a safety standpoint, it's important to understand that SGLT2 inhibitors are going to increase the risk of vulvovaginitis, and in people on insulin or taking sulfonylureas that develop GI problems, if they stop the insulin or sulfonylurea, they need to stop the SGLT2 inhibitor, otherwise they'll have a risk for ketoacidosis. So, that's very important. The last thing, and probably, in my opinion, more important, is you're going to get a small dip in the GFR when you start these agents. Do not stop these agents. A small dip, 10%, 20% drop in GFR is temporary and does not correlate at all with outcomes, because all the data are very positive on slowing progression of kidney disease. Therefore, this is a harbinger of good, not bad. Remember, SGLT2 inhibitors are cardiorenal risk reducing drugs, irrespective of their glucose changing ability.

Finerenone, the nonsteroidal mineralocorticoid receptor antagonist is the first drug approved to slow diabetic kidney disease and reduce heart failure risk in this class of nonsteroidal MRAs. And based on a joint agreement between the American Diabetes Association and the KDIGO Diabetes Guideline Committee finerenone really needs to be part of the regimen to slow progression of diabetic kidney disease progression. So very important that everybody's on the same page here that these agents need to be used to slow diabetic kidney disease.

So, rightfully, Josephine feels overwhelmed with their new diagnosis, but it's important as clinicians to help slow Josephine's renal function decline. Josephine agrees to try an SGLT2 inhibitor, so let's return to the scene one last time. It's now 1 month later.

Clinician: Hello again, Josephine. Glad to see you back!

Patient: Hello. Nice to see you again doctor.

Clinician: How have you been doing taking the dapagliflozin? Any adverse effects?

Patient: I don’t think so. I was worried about feeling dizzy, even though you said the new drug won’t cause blood sugar drops. I guess you were right, because I feel fine! I think I even lost a few pounds. And no urine problems.

Clinician: Great news. You may see more weight loss as time goes on, especially if you are sticking with your nutrition plan from our dietitian.

Patient: Yes, I am. I learned so much from her. I’ve even noticed my blood sugar has been in the low 100’s.

Clinician: You’re right. Your fasting blood sugar from your follow-up labs was 110. So that is good news! Your blood pressure has also improved. It’s now 144/82.

Patient: What about my kidneys?

Clinician: The medication is moving your kidney function in the right direction too. There is less protein in your urine with your new labs. Which we expected and hoped would happen. But, even though your kidney labs are improving, you still have too much protein in your urine. Your albuminuria is 550. So, it’s best if we add another new medication to protect your kidneys even more.

Patient: Really?

Clinician: There are 3 main classes of medicine that slow kidney disease progression and you are taking 2 of them, lisinopril and dapaglifozin. The third medication is finerenone. It’s in a new class that works similar to a drug called spironolactone. Have you heard of that before?

Patient: Actually yes, I have. Doesn’t it have a lot of side effects though?

Clinician: Well, finerenone is like a third cousin to spironolactone. Even though finerenone works on the same body system, it works differently than spironolactone and is much safer with less adverse effects. There are other drugs in clinical trials, coming down the pipeline, but this one has recently been FDA approved first.

Patient: I see.

Clinician: Two huge clinical trials, with more than 13,000 people in each, were just finished. These trials showed that finerenone protects the kidneys and keeps kidney disease from getting worse. And it does this by reducing inflammation in the kidney, not by reducing blood sugar or blood pressure. Taking it along with the dapagliflozin will give you added protection for your kidneys.

Patient: Well, I trust you. The last medication helped, so I will give this one a try too.

Again, the goal is 2-fold for Josephine. We have to slow her GFR decline and we have to reduce her cardiovascular risk. To slow progression of chronic kidney disease in type 2 diabetes and reduce cardiovascular risk, we need to follow the 3 pillars of therapy, a concept borrowed from our heart failure cardiology friends. RAS blockade needs to be there at maximally tolerated doses, a SGLT2 inhibitor needs to be given, and the nonsteroidal MRAs, finerenone, as I just discussed with you. This is to show you that this is really kind of the way things are holding up the building, and we're adding support as we go.

Nonsteroidal MRAs, finerenone specifically, is the only drug approved to slow diabetic kidney disease progression, and is very different from spironolactone. First of all, it's a nonsteroidal. Spironolactone is a steroidal molecule. It has much less hyperkalemia than spironolactone, and it was approved by the FDA in July of 2021. Basically, it's based on 2 very large complementary trials, one with a cardiovascular outcome primarily, and that's the FIGARO-DKD. And one with a renal outcome primarily, and that was the FIDELIO-DKD. And together, because the protocols were virtually identical with different inclusion criteria, we have the FIDELITY-DKD individual patient analysis of over 13,000 patients with type 2 diabetes and a variety spectrum of cardiovascular and kidney diseases. And together, it is the largest database done to date looking at progression of diabetic kidney disease with a single molecule.

The FIDELITY-DKD trial was 5,734 patients and the FIGARO trial was 7,437 patients. Both these trials used finerenone 10 mg a day as a starting dose. And if the GFR was less than 60, you got 10 mg. If it was greater than 60, you got 20 mg a day. Both studies included a run in period of 4 to 16 weeks to make sure that everybody was on maximally tolerated doses of an ACE or an ARB, because that's the dose that was shown in the clinical trials with ACEs and ARBs to protect the kidney, not homeopathic doses of lisinopril of 5 or 10 mg.

Both trials, FIGARO and FIDELIO, showed significant reduction with finerenone in the primary cardiovascular and renal endpoints in the respective trials. The purpose of the FIDELITY analysis is, as I told you earlier, was to really look at the entire spectrum of kidney disease. And in FIDELITY, the individual patient analysis, finerenone showed significantly reduced risk for the composite cardiovascular outcome by 14% vs placebo. And, time to dialysis and doubling of creatinine by 23% risk reduction, very significant outcomes. Across both trials, there was a modest reduction in blood pressure of about 2 to 3 mmHg. There was no significant effect on HbA1c, and there were no significant sexual side effects.

Hyperkalemia was increased with hyperkalemia vs placebo. However, the rates of hyperkalemia with clinical consequences were quite low. Permanent discontinuation of the steady drug in hospitalization due to hyperkalemia was very uncommon in the finerenone group - 1.7% of the 6,500 plus patients had that problem, and 0.6% of the placebo group, so the rates were very low. So, what to monitor when starting a nonsteroidal MRA? Potassium. And for Josephine, the potassium was monitored in 1 month and then every 6 months, which is what was actually done in the trials. Success is also increased with a team-based integrated care approach, which is critical in all of these patients. The dietitian, the pharmacist, the diabetes care educator, the nephrologist, and the cardiologist all need to be part of this team to basically make sure that the same message is communicated to the patient in a different way.

We've come to a close of our program. The key take home messages are, number 1, in order to make a diagnosis of kidney disease, you need both the estimated GFR and the urine albumin-creatinine ratio, critical. Number 2, to really maximize therapy, especially in people with high levels of albuminuria, you not only need maximally dosed ACEs or ARBs, but you need an SGLT2 inhibitor and you need a nonsteroidal MRA. And if you take that approach and explain to the patient why you're doing what you're doing and what the reasons are, you'll have a much higher success rate than just doling out the medications. I think this is very important.

Thank you for participating in this activity. Please also continue on to answer the questions that follow and complete the evaluation. Thank you for your time.

This transcript has not been copyedited.

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