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Expert Perspectives to Recap Kidney Week: Where Are We Now With Chronic Kidney Disease Management?

  • Authors: Matthew R. Weir, MD; Katherine R. Tuttle, MD, FASN, FACP, FNKF; Christoph Wanner, MD
  • CME / ABIM MOC Released: 1/12/2023
  • Valid for credit through: 1/12/2024
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Target Audience and Goal Statement

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

The goal of this activity is that learners will be better able to use appropriate therapies to manage patients with CKD.

Upon completion of this activity, participants will:

  • Have increased knowledge regarding the
    • Relationship of cardio-renal comorbidities with poor health outcomes 
    • New data presented at ASN 2022 related to management of patients with CKD with or without comorbidities
  • Have greater competence related to
    • Using strategies for improving health outcomes in patients with CKD and comorbidities


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  • Matthew R. Weir, MD

    Professor of Medicine
    University of Maryland School of Medicine
    Director, Division of Nephrology
    Department of Medicine
    University of Maryland Hospital
    Baltimore, Maryland, United States


    Matthew R. Weir, MD, has the following relevant financial relationships:
    Consultant or advisor for: Akebia; AstraZeneca; Bayer; Boehringer Ingelheim; Fibrogen; Janssen; Merck; Novo Nordisk; Vifor


  • Katherine R. Tuttle, MD, FASN, FACP, FNKF

    Executive Director for Research
    Providence Health Care
    Professor of Medicine
    Division of Nephrology
    Co-Principal Investigator
    Institute of Translational Health Sciences
    University of Washington
    Spokane, Washington, United States


    Katherine R. Tuttle, MD, FASN, FACP, FNKF, has the following relevant financial relationships:
    Consultant or advisor for: AstraZeneca; Bayer; Boehringer Ingelheim; Eli Lilly; Gilead; Goldfinch Bio; Novo Nordisk
    Research funding from: Goldfinch Bio; Travere Therapeutics

  • Christoph Wanner, MD

    Professor of Medicine
    University Hospital Würzburg
    Department of Medicine
    Division of Nephrology
    Würzburg, Germany


    Christoph Wanner, MD, has the following relevant financial relationships:
    Consultant or advisor for: AstraZeneca; Bayer; Boehringer Ingelheim; GlaxoSmithKline
    Speaker or member of speakers bureau for: Bayer; Boehringer Ingelheim; Eli Lilly; FMC; GlaxoSmithKline


  • Anne G. Le, PharmD

    Senior Medical Education Director, Medscape, LLC


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

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    Associate Director, Accreditation and Compliance, Medscape, LLC


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Expert Perspectives to Recap Kidney Week: Where Are We Now With Chronic Kidney Disease Management?

Authors: Matthew R. Weir, MD; Katherine R. Tuttle, MD, FASN, FACP, FNKF; Christoph Wanner, MDFaculty and Disclosures

CME / ABIM MOC Released: 1/12/2023

Valid for credit through: 1/12/2024


Activity Transcript

Matthew R. Weir, MD: Good day. Welcome to MedscapeLIVE, “Expert Perspectives to Recap Kidney Week: Where Are We Now With Chronic Kidney Disease Management?” My name is Dr Matthew Weir. I'm professor of medicine and chief of nephrology at the University of Maryland School of Medicine in Baltimore, Maryland. And I'm very excited to have today 2 world experts on kidney disease and newer therapeutic opportunities. Ladies first, Katherine R. Tuttle is a physician and professor of medicine and executive director of research at Providence Health Care. She's also the co-PI for the Institute of Translational Health Sciences at the University of Washington in Spokane, Washington.

Katherine R. Tuttle, MD, FASN, FACP, FNKF: Thank you for having me.

Dr Weir: Additionally, we are lucky to have from Germany, Christoph Wanner, who is also a physician and professor of medicine at University Hospital in Wuerzburg in the Division of Nephrology and Department of Medicine in Würzburg, Germany. Welcome everybody; this is going to be a very exciting opportunity for us because we'll cover a number of interesting discussion points. First, the link between CKD, type 2 diabetes and heart failure, newer treatment strategies for CKD, as well as new data from ASN Kidney Week 2022 related to CKD management. And then we'll finish with best practices in managing CKD using a case example. At this point, I will turn the program over to Dr Tuttle. Please, take it away, Kathy.

Dr Tuttle: Thank you for the kind introduction, Dr Weir, and great to be joining all of you here today to talk about these really exciting topics and what was new at ASN Kidney Week. I want to set the stage with discussing the enormity of diabetes and chronic kidney disease. They are currently 537 million people worldwide with diabetes. 95% of them have type 2, and about 5% have type 1. And in both populations, kidney disease is still very common, about 4 in 10 of type 2 and 3 and 10 of type 1 now making diabetes responsible for half of all chronic kidney disease, making it the most common cause. And while our traditional focus in nephrology has been progression to kidney failure, a very important outcome in reality, these patients have a very high cardiovascular risk, heart failure, and atherosclerotic CVD events such that these events will actually outpace progression to kidney failure and cause many deaths. Only about 10% of people survive to end-stage kidney disease because of this enormous risk of competing cardiovascular events and death. So when we think about diabetes and CKD, we need to think holistically and think about reducing cardiovascular risk as well as kidney disease risks.

The data that I've just presented to you are prevalence data. That is how many people with the condition are currently in the population. But I'd like to show you some recent evidence on incidence; that is, where does it all start? Who are the people with diabetes who get kidney disease? Incidence means new-onset kidney disease. This is from a study in our large diabetes and CKD registry, CURE-CKD from Providence and UCLA Health, where we actually looked at a group of people who at baseline at entering the registry had diabetes, but no evidence of chronic kidney disease. And then we asked over time who developed chronic kidney disease, and this was based on guideline recommendations for measuring albuminuria and GFR. So it was a rigorous definition and not based on administrative codes. If you look over in the right panel between 2015 and 2020, we see that new onset kidney disease or the people who developed kidney disease were more often people in non-white populations, particularly American Indian, Alaskan native, black, Hispanic, or Latino. And the highest increased risk was in people who identify as being native Hawaiian or Pacific Islanders. Interestingly enough, people identified as Asians actually had a slightly lower risk. When we look over time by other demographics, whether it's by age, by race, or by sex, there are trends downward in successive 2-year periods. But the red line represents an incidence rate of about 7% per year. And you can see that despite the reduction over time in many populations, especially people over the age of 60, again, most non-white populations and in men, they're still at this threshold or higher. And if you do the math, that adds up pretty quickly, 7% per year building toward that very large prevalence number. But remember that cumulative incidence is not the same as prevalence because some people leave the population and remember why they leave, predominantly due to death, not because they're getting better. So these are very concerning statistics in terms of the number of people who are developing kidney disease along with the growing diabetes population telling us that this burden is going to continue to be a major public health issue. And it's particularly prominent in non-white populations, older adults, and men.

Now I'd like to turn it over to Dr Wanner to talk about the updated clinical practice guidelines and introduce some of the exciting new data that we heard at ASN.

Christoph Wanner, MD: Thank you, Katherine and Matt, for your kind introduction. I'll come first to the updated clinical guidelines, which has also been discussed at the American Society of Nephrology. The guidelines in nephrology are represented by KDIGO, Kidney Disease: Improving Global Outcomes and the 2022 KDIGO guidelines have been published in Kidney International and are available for free download from the website. We have the cardio kidney or kidney heart risk factor management, a comprehensive care approach, outlined here. On the bottom, we know we always do lifestyle, and then what I call foundational therapies are introduced and have received the 1a grading. So we use statins for atherosclerotic cardiovascular disease. The RAS blockers and the SGLT2 inhibitors, we use for kidney disease, preventing kidney disease progression and also cardiovascular outcomes in respect to SGTL2 inhibition, and metformin, we want to keep for glucose control. New in these updated guidelines are non-steroidal mineralocorticoid receptor antagonists, actually finerenone, which is currently on the market. And this is an additional drug for heart and kidney protection. We also use GLP-1 receptor agonists and I think we will hear more for cardiovascular protection. These guidelines have all outlined this recently.

How do we approach the patient then with all these new opportunities? We use a holistic approach to our type 2 diabetic patients with CKD. You can see on the left-hand side, type 2 diabetes patients are specifically treated first-line with an SGLT2 inhibitor once the GFR is above 20. We start treatment as long as GFR is above 20 and we do not stop the treatment until patients go into dialysis, we continue the treatment. And for eyesight, we still use metformin, best in combination with an SGLT2 inhibitor. Then, if we need additional glycemic control, the GLP-1 receptor agonist is now indicated to be added to achieve individualized glycemic target. If we have residual albuminuria, the guidelines suggest adding a non-steroidal MRA, finerenone, once we have residual urinary albumin-creatinine ratio above 30 mg/g. On the right-hand side, you see the classic standard of care treatment with RAS inhibitor, the statin treatment and more aggressive lipid lowering treatment if needed.

So, before the treatment is always the diagnosis and I want to remind you and all of you out there that glomerular filtration rate is standard when you want to see where the patients is during his career marching or driving towards the cliff, the cliff would be dialysis. The eGFR shows you where the patient currently is, but UACR, urinary albumin-creatinine ratio, shows you how fast the train is driving towards the cliff. So the question always is, how much time do you have and the patients have when you treat standard of care and additional treatments, organ protective treatments? And we will hear a little bit more about this.

I think I will continue, Matt, with the new data from ASN and the new organ protective treatments. The next slide shows you the new trial which has been presented, the EMPA-KIDNEY trial, empagliflozin in patients with chronic kidney disease. Here on the left-hand side, I jump directly into the primary endpoint. The primary endpoint was a relative reduction by 28%. The curve was opening up after 1 year and there was a significant result with a small confidence interval and a robust result. On the right-hand side, the primary endpoint is distributed into patients with diabetes and half of them also had non-diabetic kidney disease. And since the confidence intervals are overlapping, we treat this result uniform as the treatment works in patients with diabetes and without diabetes. You also see from the point estimates far left from unity and the confidence intervals in a narrow area that the intervention, in this case empagliflozin works in patient with a glomerular filtration rate below 30 mL/min and similarly in higher ranges of glomerular filtration rate. The most interesting thing was the impact on the primary endpoint in patients with different categories of urinary albumin to creatinine ratio. And since the point estimate was moving in the low albuminuria group to its unity and there was an interaction test which was significant, everybody felt that maybe the intervention had less effect in those patients with low albuminuria. However, you have to look at the slopes to get more information on this message. First of all, here you see empagliflozin dipping then crossing at 18 months and stabilizing kidney function. The group all over had a progression rate of 2.75 mL/min/1.73m2 per year and empagliflozin reduced these progression rate to 1.37 mL/min/1.73m2, so by 50% and this was highly significant result, that is, the chronic slope over time. When we then go into again the low albuminuria group in those below 30 and look at all these categories in respect to slopes, then you can see here on the next slide that the slope for those below 30 mg/g albuminuria was significant, it was reduced the mL/min/1.73m2 progression rate from 0.89 mL/min/1.73m2 per year to 0.1 mL/min/1.73m2, so a neutral slope was achieved, and the reduction was significant and reduced by 0.78 mL/min/1.73m2 per year. The trial was too short to show you a hard outcome in 2 years, but the slopes can clearly see that there is an effect, you only have to wait longer for those with low albuminuria.

Next, I will go into the CREDENCE trial, which has been presented as a poster at the American Society Nephrology Congress. And for the first time, biomarkers have been added to outcomes to get a feeling whether biomarker can help us categorize the patients in respect to outcome. And more biomarker, more points you have, and on top is the primary composite. The better is the outcome, the more the point estimate is moving away from unity. The second line or box is the renal composite. The third is hospitalization for heart failure, and cardiovascular death on the bottom. And all showing consistent results here; with biomarkers, you can predict a more intense reduction of the primary outcome.

Then, we saw a new message from dapagliflozin in patients without diabetes and with microalbuminuria, so also in the low albuminuria range. On the left-hand side, you see the effect of dapagliflozin on the rate of change in eGFR in participants of a trial with microalbuminuria. Initially with dapagliflozin, you see the nice dip on eGFR but then a stabilization and overall in mL/min/1.73m2, dapagliflozin prevented progression of kidney disease, and the difference between placebo and dapagliflozin was highly significant. On the right-hand side, you see the change in urinary albumin creatinine ratio over the study period in patients with microalbuminuria. This poster specifically focused in microalbuminuric or low albuminuric patients, and the placebo group had less reduction in albuminuria. The difference was 15% here on this log scale, so a higher impact of dapagliflozin on reduction of albuminuria in this group of patients.

Then finally, my last 2 slides come from a meta-analysis which was presented on November 6th [2022] at the same time the EMPA-KIDNEY trial came out. The meta-analysis on the impact of diabetes on the effects of sodium glucose co-transporters, or SGLT2 inhibitors on kidney outcomes. And here, you see on the next slide the totality of evidence from the 13 trials with 19,000 participants to date, we have in randomized control trials. In yellow, the trials in patients with diabetes, and in blue, the trials with patients without diabetes. You can see on the bottom, the DAPA-CKD and the EMPA-KIDNEY trial in patients with and without diabetes. The interesting thing is, irrespective whether the kidney is in the primary endpoint or in the second endpoint or what underlying pathology is present, the kidney is always protected. You see the point estimates left of unity, they nicely line up and the meta-analysis give us a 38% relative risk reduction, something we have never seen the past 20 years. And if you recall the ACE inhibitor or the ARB studies, RENAAL, received half of the benefit we get today from SGLT2 inhibitors and a similar result was in patients without diabetes, so non-diabetic kidney disease, which was a reduction by close to 30%. So this is the totality of evidence from all trials and also presented at the meetings. And with this, I stop here and hand it over to Katherine Tuttle. She will give us now the new data on other medications. Thank you.

Dr Tuttle: Thanks very much, Dr Wanner. That was a wonderful overview of the data on this growing body of evidence for SGLT2 inhibitors and important predictors of clinical outcomes. What I'd like to show you now are some new data that we heard on the GLP-1 receptor agonist class. Although the FLOW trial testing semaglutide is still in progress, it is a study of a population with type 2 diabetes and chronic kidney disease with primary kidney disease outcomes that is fully enrolled. There's great interest in the meantime to look at a number of studies that have been done with GLP-1 receptor agonists and an even newer dual agonists that includes a GIP combined with a GLP-1. So if you will, a super incretin and I will discuss these data as a prelude for the hypothesis about how GLP-1 receptor agonists and perhaps this new GIP/GLP dual incretin may go beyond glycemic control and heart protection to also possibly provide kidney protection.

These data are data on eGFR slope that we've already heard about. And just a reminder that eGFR slope we view as a surrogate that's likely to predict the effect of an intervention on clinical outcomes related to kidney disease endpoints such as kidney failure. And when we see a difference between the intervention group and control group of more than 0.75 mLl/min per year in eGFR slope, that's highly predictive of a favorable effect of the intervention. This study was a post hoc analysis that we did among studies that were originally conducted to test semaglutide vs placebo for non-alcoholic fatty liver disease. And so these people were selected for liver disease and mostly had normal kidney functions. We divided eGFR at the median, not necessarily at the typical threshold of 60 for CKD. But what you can see is those with lower eGFR compared with a GFR above 75 had a highly significant difference in eGFR slope between semaglutide treatment and placebo. A difference of 7.45, 10 times the threshold that would predict a treatment effect. Whereas we really saw no significant difference in those with preserved eGFR. And this has been a theme through all of these studies that the GLP-1 class effect on eGFR slopes or other kidney disease outcomes appears to be more pronounced in patients with lower eGFR, which is actually really important because there's a great need for interventions in people who already have established kidney disease characterized by low kidney function.

This is another study. This is a post hoc of semaglutide vs placebo on eGFR slope in SUSTAIN-6 looking at the difference between the intervention with semaglutide represented in blue vs placebo across albuminuria categories. And of course, those with the highest grade albuminuria well within the duration of a trial progressed more quickly. But you can see the estimated treatment difference here, 1.15, estimated treatment difference in those with microalbuminuria of a little over 1 and an estimated treatment difference even in the microalbuminuric group of 1.0, all exceeding that threshold of 0.75 and no interaction suggesting that the treatment responses were different by albuminuria category. So again, a strong signal that across different albuminuria states, these agents remain therapeutically effective for preserving eGFR.

So now onto tirzepatide. This is one of the newest agents. This is a combined GIP/GLP agonist, so if you will, the dual or super incretin compared with standard treatment with insulin glargine. This was in a population of people with type 2 diabetes who were selected for high cardiovascular risk, so SURPASS-4. And here again, another analysis by either microalbuminuria or more albuminuria. And whether we look at cystatin C-based GFR or creatinine-based GFR, these are the estimated differences in slope by category. And you can see most, if not all of them exceed .75. Again, highly predictive that these agents would be expected to preserve kidney function and prevent kidney disease endpoints in the long run.

But now turning back to what's happening in clinical practice based on these trials, these are data again from our CURE-CKD registry that was presented by Suzanne Nicholas at ASN Kidney Week looking at guideline directed medical therapy. The 2 classes that are now considered first-line therapy for diabetes and CKD, SGLT2 inhibitors and an ACE inhibitor or an ARB. If we first focus on the right panel on ACE or ARB use, you can see at baseline about 71% of patients were getting these agents. But when we look to see whether or not people stayed on for at least 90 days, even at that relatively early time point, only 40% were still on therapy. We know these agents are stopped frequently. So this is an important issue that we need to focus on as persistence of use. We looked at predictors of persistent use. In the green box were positive predictors in the red box, negative predictors. So not having commercial insurance or being treated in Providence, which is more of a community-based primary care system vs UCLA, which is more of a tertiary specialty based practice, was also associated with lower use of these agents. But note that race was no longer a disparity when we controlled for health system access and insurance status, although men were still more likely to receive these agents than women. So that is a persisting disparity that we need to understand better. But these give us some insights into issues that we may be able to address to increase use of these agents and keep people on them over time. Over on the left, you see SGLT2 inhibitor use much lower. Remember this is 2019, 2020 when the data were first emerging. And this is pretty consistent with other national data sets. We saw baseline use about 5.7%, and again, some fall off over time. The disparities are quite similar in that people who did not have commercial insurance or treated at Providence, were less likely to persist on these agents or have them prescribed at all as was hospitalization, which we might expect because we do have sick day rules for these agents. And again, we don't see disparity by race, but by sex we still do see a disparity in use with men more likely to get them than women. So some of the things that we can address, again, emphasizing the importance of having adequate insurance coverage so that people have access to these medicines and perhaps even working more closely with primary care partners on education and implementation efforts.

Speaking of implementation, one issue that we really do have to consider is drug pricing. This is from a paper published several months ago in CJASN looking at implementation issues where cost was identified as a major barrier. And you can see that the SGLT2 inhibitors and the GLP-1 receptor agonists are really quite expensive. These are the prices for a 1-month supply at the pharmacy, and even in people with commercial insurance, they still often have copays that are several hundred dollars per month and especially in people who are on multiple medicines; this is a very challenging situation in terms of affordability. You can also see that in other countries where that data have been available and there are more data for SGLT2 inhibitors and GLP-1s, but still in the US, we're paying several fold higher prices than in other countries. So this is an important issue that we will need to address in order to make these therapies more accessible. So with that, I'm going to turn it back to Dr Weir to take us through a case-based clinical application.

Dr Weir: Thank you both very much for your wonderful updates. Again, I couldn't think of 2 better people to give us some perspective on all the newer data as they have been clearly involved in many of these studies and this certainly provides a lot of insight. We do have a typical case here of an individual who is quite young, only 65, who has some medical comorbidities in terms of 2 different kinds of kidney disease, eGFR of 48, a uACR of 1.2 g/g, a lot of proteinuria, who’s blood pressure is not well-controlled, who's overweight, and with an HbA1c that's not well-controlled. As we heard today, there are a number of new opportunities to make a difference in this patient who is at high risk for progression to chronic kidney disease as well as let's also add cardiovascular disease, which claims many more people than anything else with chronic kidney disease. I think we can all agree that based on the newer data, there are three foundational therapy opportunities and certainly as Dr Tuttle discussed, we may have a fourth opportunity to add in there on top of all of our intensive approaches to control blood pressure, cholesterol, and glucose. I'd like to ask each one of you to provide in a sense a single overriding communication point on each of your presentations to provide perspective on a patient like this. Ladies first, Dr Tuttle, why don't you provide some thoughts about your commentary.

Dr Tuttle: I think that was a great discussion. I would just add that this person is clearly at higher risk for progression of CKD, and remember that progression has different outcomes, and of course kidney failure is one of them. We saw the analogy presented by Dr Wanner of the train on the downward slope. We know that a high level of albuminuria like this, and in the setting of type 2 diabetes combined with a primary kidney disease such as IGA nephropathy, we would expect a rapid GFR decline. But it's important to remember that on the way down, many people exit horizontally to death, especially cardiovascular death. So it's very important to consider the cardiovascular risks along with the kidney disease risks in a patient such as this one. I think that based on the guidelines and the newer data that continue to emerge that this person should receive an SGLT2 inhibitor. And with regard to other risk factors, the SGLT2 inhibitor is likely to lower the blood pressure a little bit, maybe not enough, but it would be helpful and there will be some effect to reduce weight. There'll probably be a very minimal effect on HbA1c at this level of GFR. I'll stop there because based on the residual risk of blood pressure and HbA1c, there may be some additional therapies, but I'd like to turn it to Dr Wanner to give his perspective before we go that direction.

Dr Wanner: Thank you, Kathy. Reflecting on this case and looking also on the warning the patient gave us on the right bottom, I already take 7 pills. I wonder whether you can add an SGLT2 inhibitor and finerenone which are clearly indicated. If I look at these patients, he certainly, with this amount of albuminuria, is progressing around 7 mL/min per year, and in 5 years, he is clearly in dialysis. So the question is, how much time I do have when I'm looking at other parameters? For example, blood pressure, LDL cholesterol, I could say, oh my goodness, this is so optimal treatment and I can improve my homework, I can improve lipid lowering, switch to atorvastatin 40 mg, I can increase the ramipril, I can use a polypill, adding into the polypill, maybe a diuretic to improve his blood pressure. I can do a lot, but the question is, how much time do I have? Therefore, I would agree to add immediately organ protective treatment to this patient profile and I would give him an SGLT2 inhibitor and maybe I recall the attitude of cardiologists and add all these organ protective treatments in heart failure patient as fast as possible so I would give him a non-steroidal MRA as well maybe 8 weeks later and change the profile, keep him on 7 pills if possible with a polypill. So this is my conclusion. Thank you.

Dr Weir: I agree with both of you. The patient clearly needs more blood pressure reduction, and so increases in ramipril and amlodipine are indicated without increasing the pill count. I would submit to you, he might very well need a metformin dose reduction based on his GFR. I would agree with Christoph very much, he needs high dose super statin because of his cardiovascular risk. And quite honestly, if he had a good insurance plan, I would substitute a GLP-1 RA or his DPP-4 inhibitor. But I think it goes without saying an SGLT2 inhibitor and finerenone would be ideal to mitigate as best possible his risk for progression of kidney disease. This obviously would be the critical factors, it may increase his pill burden, but these therapies are well tolerated, he might lose some weight, you'll notice his BMI is 32 and he might be pleased with the opportunity with losing weight and be agreeable under those circumstances. But looking at his age, his gender and this medical comorbidity, I would be very surprised that he does not have some cardiovascular risk. And certainly, as Dr Tuttle discussed, much greater risk really for heart failure more than anything else, which is the most prominent cardiovascular problem we see in people with chronic kidney disease.

Dr Tuttle: I'll jump in and add at this point, he is experiencing dyspnea on exertion, which could be a manifestation of cardiac ischemia or an anginal equivalent. And to Dr Wanner’s point, if we want to reduce the pill burden, another advantage of the GLP-1 receptor agonist is that it's a once a week injection with no dose adjustment. It's really quite easy for patients to administer and these agents remain with their potency for glucose lowering in contrast to the SGLT2 inhibitors.

Dr Weir: Totally agree. I'd like to thank you both, your wonderful presentations, your great thought leaders in the area of kidney disease and its treatment. I hope all of you enjoyed MedscapeLIVE discussion and I hope you have a wonderful day and can employ some of these newer therapeutic opportunities for your patients. Take care and be well.

Dr Tuttle: Thank you very much.

This transcript has not been copyedited.

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