Good evening from Houston. I am Bhargavi Patham, and I will be co-hosting the ASAP Live Seminar on Diabetes along with Dr. Mazhari today. We'll start with introductions. I'm an Associate Professor of Clinical Medicine at Houston Methodist Hospital and an Associate Program Director of Endocrinology Fellowship. I'll now welcome Dr. Mazhari to introduce herself. Hi. It's nice to be with you all this evening. I am a Professor of Medicine at Loyola University Medical Center in Maywood, Illinois. I am part of the Department of Endocrinology, and I'm excited to be here. Please note that the content today is from ASAP 2023, and it has been curated under the guidance of Dr. Siraj, Editor-in-Chief of ASAP, and Dr. Gopalakrishnan, Chair of Fellows Education Committee for ACE. I do not have any disclosures. I do not either. So just to give session overview, type your questions in Q&A box. Anytime during the case presentation, you can see or upvote questions posted by other participants. When the Zoom poll opens, select your answers. Questions from the audience will be addressed at the end of the case discussions. We'll start with our first case. A 55-year-old man with type 2 diabetes since age 40 comes to the clinic to establish care. His diabetes is complicated by nonproliferative diabetic retinopathy. He checks his blood sugar levels every morning, reporting values from 120 to 140 milligram per deciliter with occasional mild hypoglycemic events overnight or early morning. His A1c value is 8.7%. His treatment regimen consists of metformin 1,000 milligram twice a day, semaglutide one milligram weekly, insulin glargine 60 units daily, and atorvastatin 40 milligrams daily. The patient's blood pressure is 128 over 74. His pulse rate is 74. His height is 178 centimeters. His weight is 108 kgs. And BMI is 34.4. What would be the next best step in the management of this patient? Add mealtime insulin as part, continue current management, increase the dose of insulin glargine, obtain ambulatory glucose profile using continuous glucose monitor. All right, 100% of you picked choice D, which is the most appropriate. ACGM can provide valuable information about glycemic patterns, which in turn can be used to modify behaviors and implement appropriate pharmacotherapeutic adjustments in patients with both type 1 and type 2 diabetes. Several randomized controlled trials have shown benefits of using CGM to reduce A1C and or hypoglycemia in study participants with both type 1 and type 2 diabetes. Study findings in participants with type 2 receiving either multiple daily injections or basal have consistently shown a reduction in A1C. The reduction in A1C in patients with type 2 diabetes occurred largely without changes in diabetes medications, suggesting a relationship of glycemic improvement with medication, diet, and exercise adherence. CGM in these patients can help with meal modification, reduction in caloric intake, and increase in physical activity. In this patient, postprandial glycemic excursions were missed and he could have checked the morning continue. His improved glycemic control mostly by implementing lifestyle changes, reducing carbohydrate intake, and increasing exercise after observing his blood sugar levels. Adding insulin as part may be an appropriate option. However, more glucose monitoring is important to better access the pattern of hypoglycemia. Increasing Lantus would increase the risk of overnight hypoglycemia and validity of glucose. A1C is not appropriate as A1C is above goal. Not making any changes is not appropriate as A1C is above goal. I have a quick question. So we're seeing CGM being used more and more often. And one of the tricky parts is who can get coverage for it. Sometimes people ask for it and they can't. Would you mind letting us know what the new Medicare CGM coverage guidelines are? Since this year, which is around April. Yeah, a great question. Previously, before April, CMS required the beneficiary to be insulin treated with multiple daily administrations of insulin or have an insulin pump. That has changed. The CMS has expanded the coverage for CGMs for services provided on April 16th or later. They cover all patients, type 1, type 2, and gestational diabetes who are treated with insulin or have hypoglycemia. Either two or more documented hypoglycemia of less than 54 or a level three hypoglycemia, which is less than 54 with altered mental status. So that's a very big change. It offers a broader scope of coverage. So I think we all should be aware of this and take advantage of this for our patients. Thank you. I'm gonna be presenting case two. So this is a 57 year old man with type 2 diabetes diagnosed approximately 12 years ago who was seen in the endocrinology outpatient clinic for possible low hemoglobin A1C of 4.9%. He doesn't have any sweating or palpitations and his fasting glucose readings are anywhere between 120 and 140 milligram per deciliter with pre-meal concentration ranging from 140 to 200 milligrams per deciliter. He is taking metformin, 1000 milligrams twice a day, insulin glargine, 58 units at bedtime and aspart insulin, 10 to 12 units before meals. His medical history includes hypothyroidism, celiac disease and hypertension. Other medications include amlodipine, dapsone, 100 milligrams twice a day and levothyroxine, 50 microgram daily. He has no symptoms suggestive of hypoglycemia. He has no recent weight changes and his physical exam findings are normal with the exception of a BMI or body mass index of 31. His laboratory findings include a hematocrit of 45%, thyroid stimulating hormone level of 2.1 and lactate dehydrogenase of 344, which is in the normal range. His serum creatinine and GFR are normal as are his liver function tests, including bilirubin as well as his hemoglobin. His A1C in the past has ranged between 4.9 and 6.1% over the past two years. A fructoseamine level is also ordered by the endocrinologist and it comes back at 375 milligrams per deciliter. Which of the following mechanisms is likely to cause, be the cause of this patient's falsely low A1C level? A, dapsone related, B, carbamylation of hemoglobin derivatives, C, acute blood loss or D, inhibition of hemoglobin glycation. So, 100% picked A, dapsone-related. So, we're gonna go now to the rationale. So, this patient's falsely low A1C levels are caused by drug-induced hemolysis. Glycated hemoglobin is formed by non-enzymatic permanent linkage of glucose in the bloodstream. With an average red blood cell lifespan of 128 days, it provides a measure of blood glucose levels over the preceding 90 to 120 days. Dapsone is used to treat dermatitis herpetiformis, which is a skin condition associated with celiac disease. Dapsone can cause oxidative stress leading to methemoglobinemia, which is responsible for hemolysis. There is usually no associated anemia clinically or on laboratory findings. Fructosamine can be used to measure average blood glucose values in the preceding 14 to 21 days, which is the half-life of albumin. A value of 375 milligram per deciliter is equivalent to an A1C of approximately 8%. Therefore, this patient's falsely low A1C finding is the result of drug-induced hemolysis. You guys did a good job of picking the right answer. The normal albumin reference range is 200 to 285. Chemically modified derivatives of hemoglobin, such as carbamylated hemoglobin, are seen in conditions such as chronic renal failure, which can also cause a falsely low A1C. This patient has normal renal function, so option B was incorrect. Acute blood loss can also reduce A1C by shortening the lifespan of red blood cells, but there is no indication of blood loss in this patient's history or laboratory findings. Therefore, option C was incorrect. Vitamin C and E have been reported to reduce A1C by inhibiting glycation of hemoglobin, which would be the option D answer. However, this patient is not taking either of these vitamins. Other drugs causing falsely low A1C are sulfasalazine, ribavirin, and antiretroviral drugs. You are muted currently. Oh, sorry. It's okay, it's part of the routine of being on Zoom calls, isn't it? I'm so sorry. Based on your clinical experience, what are some other situations that you can think of where you have ordered fructosamine levels for further evaluation? It's a very good question. When I find that there is a discrepancy between what I'm seeing in the A1C patient-reported glucose data, which is my least favorite, I like to have the meter that we can download. So if I see the meter data is really high and we can verify if the meter is giving accurate readings and there's a discrepancy, that can be very helpful. And these days, I also look at the Dexcom data or Libre data, any sort of CGM data that we have, and I've found sometimes there's a big discrepancy between the A1C and that, and that prompts me to go ahead and do a fructosamine level to figure out which marker we need to follow because I don't want to falsely give patients the information that their diabetes is controlled just based on an A1C if it's inaccurate. Yeah, thank you. And you just illustrated an example of real-world use of CGMs beyond just titrating the drug and diabetes medication. So thank you for that. No problem. Let's go to case three. A 50-year-old woman with no significant medical history is being evaluated after a recent diagnosis of diabetes. She has gone to a walk-in clinic six weeks ago for a 20-pound unintentional weight loss, increased urinary frequency, and increased thirst of two weeks duration. She was found to have glycosuria and an office-based finger stick glucose value of 350 milligrams per deciliter. Lab testing showed a blood glucose of more than 400 milligrams per deciliter and an A1C of 9.5%. She was not experiencing diabetic ketoacidosis and remaining lab values, including the complete blood count, renal function tests, hepatic function tests, were normal. Her C-peptide also measured when her glucose was 350 milligrams per deciliter was low at 2.7 nanograms per ml. She was started on insulin treatments five weeks ago and is going well with improvement in her glucose levels. She has a strong family history of diabetes and autoimmune disease, and now wants to know if she has type 1 or type 2 diabetes. Which of the following is the most useful test to identify type 1 diabetes in this patient? A, measurement of C-peptide. B, measurement of anti-GAD antibody. C, measurement of anti-insulin antibody. D, genetic testing. All right, all of you picked B, which is the right answer, and let's see why. Type 1 diabetes is characterized by destruction of islet cells of pancreas leading to insulin deficiency. This is usually autoimmune with autoantibodies such as islet cell antibodies, insulin antibodies, anti-GAD65, and autoantibodies to tyrosine phosphatases, 2 and 2 beta. In this patient with established newly diagnosed diabetes, the anti-GAD antibody is likely the most sensitive and would be the most helpful to determine the presence of autoimmune diabetes. It is also more commonly elevated in adult onset type diabetes and latent autoimmune diabetes of the adult. Although a positive insulin antibody result would be helpful in confirming the type 1 diabetes, testing for insulin antibody should not be completed more than after two weeks of insulin therapy. Other antibodies may also be tested including zinc transporter 8, which helps to assess the risk of type 1 diabetes. C-peptide testing can be useful in evaluating for endogenous insulin production in patients with diabetes. It can be used to differentiate type 1 from type 2, but its usefulness is greatest in the longstanding diabetes, unlike this patient who's been newly diagnosed. At the time of the diagnosis, there may be a substantial overlap of C-peptide levels between type 1 and type 2 diabetes, and the level is useful only if it's persistently low. Higher levels may not be indicative of type 2, but can be seen in honeymoon phase of type 1 also when there's residual insulin secretion that persists for weeks to years. In this patient, a single C-peptide measurement in the setting of severe hyperglycemia may not be as useful as antibody testing. The major susceptibility genes identified for type 1 are HLA-DR3, DQ2, and DR4-DQ8, and these are seen with high frequency in type 1 diabetes, but not sufficient alone to induce type 1 diabetes. Genetic testing for monogenic diabetes of the young, or MAUDI, should be considered in patients with strong family history. An autosomal dominant pattern, which is greater than two generations, was diagnosed before the age of 25, is not obese, and has negative antibodies, but would not be necessary in this patient given her history and when the onset was. In the future, if the result of antibody testing is negative, genetic testing could be considered. Thank you. I had a quick question. So for, if you're gonna check the insulin antibodies after a newly diagnosed type 1 diabetes was found, when is the optimal timeline for checking it? Yeah, usually within the first two weeks. Now, early appearance of anti-insulin antibodies is, it already suggests that insulin is an important autoantigen. Insulin autoantibodies are usually first to appear in children, followed from birth, and progressing to diabetes, and are highest in young children developing diabetes. However, those people who have received insulin subcutaneously, mostly all of those individuals develop insulin antibodies, and thus insulin antibodies measurements after two weeks of insulin injections cannot be used as marker for immune-mediated diabetes. So something to keep in mind when there is a new diagnosis of diabetes on board. Yeah, it's always good to know the circumstances to make sure you're interpreting the labs correctly. Yes, endocrine has a lot about that. Yeah, normal doesn't mean normal, or abnormal doesn't mean abnormal. So yeah, you have to know what the context is and the variables contributing. That is so true. All right, moving on to case four. A 67-year-old woman recently moved to your city and comes to your clinic for the first time. She has had type 2 diabetes for about 14 years and has been taking metformin 1,000 milligram twice a day and somaglutide one milligram weekly. She states that she has known retinopathy, nephropathy, and neuropathy. She also has coronary artery disease and has had stents placed over the past year. She is taking losartan 100 milligram a day for blood pressure control and to protect her kidneys, as well as atorvastatin 40 milligrams and clopidogrel 75 milligram daily. She has a history of frequent urinary tract infections. Her examination is significant for a BMI of 34, blood pressure of 138 over 84, microaneurysms on eye exam, decreased vibratory sensation in her feet, and absent achilles reflexes. Her laboratory findings are A1C of 7.2%, an EGFR of 50, a urine albumin to creatinine ratio of 356, which is elevated, and an LDL of 81. In addition to healthy lifestyle, intensification of glycemic control, and hypertension management, which medication would be considered to reduce the risk of chronic kidney disease progression? A, alicacarin, B, dipacloflozin, C, finarinone, or D, lisinopril. So 100% picked finarinone. All right, we need harder questions. That's very good. All right, let's see what the rationale is. All right, so diabetes is a common cause of chronic kidney disease. Patients with diabetic nephropathy have higher rates of morbidity and mortality due to cardiovascular disease. The presence of microalbuminuria, albuminuria, and declining GFR are all known predictors of cardiovascular disease. Finarinone is a non-steroidal selective mineralocorticoid receptor antagonist that is shown to reduce progression of kidney disease and cardiovascular events in patients with type 2 diabetes and diabetic nephropathy compared to placebo. So option C was the correct answer. In the Fidelio DKD trial, over 5,000 patients with CKD and type 2 diabetes were randomized to receive finarinone or placebo. Eligible patients had a UACR of 30 to less than 300, GFR between 25 to less than 60, and diabetic retinopathy, or they had a UACR of 300 to 5,000 milligrams per gram and an EGFR of 25 to less than 75. The primary outcome was time to first occurrence of the composite endpoint of onset of kidney failure, a sustained decrease in EGFR of over 40% from baseline of at least four weeks, or renal death. The secondary outcome was time to first occurrence of the composite endpoint cardiovascular death or non-fatal cardiovascular events such as myocardial infarction, stroke, hospitalization for heart failure. During a median followup of 2.6 years, a primary outcome event occurred in 17.8% of patients in the finarinone group and 21.1% in the placebo group. And there was a significant reduction in the secondary composite of cardiovascular outcome. A higher incidence of hyperkalemia related discontinuation occurred in the study group than in the placebo group. And this was 2.3 versus 0.9%. Use of sodium glucose co-transporter 2 or SGLT2 inhibitors is recommended in patients with diabetes type 2 and kidney disease with a GFR over 25 and a urinary albumin to creatinine ratio of over 300 equal to or over 300 to reduce progression of CKD and cardiovascular events. However, SGLT2 inhibitors can increase the frequency of urinary tract infections. Hence, dopagliflozin is not a good option for this patient in this clinical vignette because of the history of frequent urinary tract infection. Combination therapy using an ACE inhibitor or an ARB should not be used because it does not prevent progression of kidney disease but increases the incidence of adverse effects. Similarly, a direct renin inhibitor, alaskirin, would not be used along with an ACE inhibitor or ARB. Dr. Mazzari, I have a question for you. Should the providers be concerned regarding hyperkalemia when prescribing finarinone? Yeah, that's a very good question because especially when you are using multiple drugs that can affect a certain electrolyte, in this case potassium, it is important to know what are the guidelines for starting it and how often you need to monitor it. So you want to make sure that you look at the GFR and the potassium should not be above five and the dosing is based on GFR and it could be 10 or 20 milligrams. And then it is important to make sure you know what your baseline potassium is and then to monitor the potassium level is recommended at a month, four months, and then every four months after that and just make sure that is being monitored for safety reasons. Thank you. All right, case five. A 76 year old man comes to the clinic with a history of moderate diabetes control and coronary artery disease. He's taking two grams of metformin daily, two milligrams of glumeptide and 24 units of insulin glargine in the evening. His glycated hemoglobin is 7.4% and he states he is generally feels well but has gained some weight. He usually eats three meals a day and sometimes notices he gets quite hungry at breakfast or in the afternoon. His lab tests are noteworthy for a fasting glucose of 81 and his morning clinic visit. He denies hypoglycemia, but his wife is worried by his increased eating and weight gain. He only checks his blood sugars in the morning. He has an estimated glomerular filtration rate of 49 ml per minute per 1.73 meters square. His blood pressure is 144 over 58 millimeters of mercury and he has decreased fetal pulses. The patient was advised to stop glumeptide treatment. However, by mistake, he restarted his glumeptide treatment and wound up in the ED eight months later with severe hypoglycemia. In the afternoon, the neurological manifestation when he forgot to eat lunch. His GFR is now 38. The hypoglycemia has been corrected and 5% dextrose containing fluids are being administered by the emergency department staff. What would be the best recommendation for patients and his family? A, he should be admitted to the hospital for observation and monitoring. B, he should go home, advise again not to resume his glumeptide and increase his insulin dose given his A1C concentration of 7.4%. C, he should go home and discontinue his insulin and D, he should go home on his usual regimen but always eat lunch to avoid hypoglycemia. Oh, all right, you're all are rocking. The patient should be admitted to the hospital for observation and monitoring. He is elderly and presented with acute renal failure in the setting of chronic renal dysfunction which increases the risk of severe and recurrent hypoglycemia while receiving sulfonylurea treatment. Recurrent hypoglycemia is characteristic of long acting sulfonylureas, particularly with glyburide in which the parent compound and its first metabolite both contribute towards recurrent hypoglycemia sometimes despite infusions of dextrose. Because the patient is still experiencing recurrent hypoglycemia, going home and discontinuing glumeptide or going home on his usual regimen but always eating lunch to avoid hypoglycemia are incorrect choices. Recurrent hypoglycemia is associated with significant morbidity, impairs physiological defenses against hypoglycemia and can lead to hypoglycemia unawareness. In addition, option D is incorrect as sending the patient home on glumeptide treatment even after this episode has resolved still puts them at risk of experiencing another episode like this one. If the hypoglycemia due to sulfonylurea treatment does not resolve with dextrose infusion and the patient continues to have recurrent hypoglycemia, he may benefit from treatment with ocreotide but it would not be his first treatment plan. Other factors such as insulin errors in elderly can be seen, sometimes due to patient mistakes such as failing to eat but taking their medication, sometimes due to caregiver's error. The combination of intensive glucose control and complex regimens is particularly dangerous in elderly patients. Going home and discontinuing insulin is not appropriate either. The patient is still at high risk of experiencing recurrent hypoglycemia and therefore needs to be admitted for observation until he's outside of that window. Given that his patient's GFR has dropped to 38, his metformin dose needs to be adjusted. The dose can now be reduced to 500 milligrams twice daily with close monitoring of his renal function. If GFR drops below 30, metformin treatment needs to be stopped. Use of other class of medications, including GLP-1 agonists and SGLT2 inhibitors instead of sulfonylurea should be kept in mind when there is no contraindications given low risks of severe hypoglycemia and cardiovascular and or renal benefits in addition to glycemic improvement. For SGLT2 inhibitors, there are differences in manufacturer-recommended thresholds for GFR based on the agent being prescribed. Thank you. That is something that we do come across. And last I checked, it is 2023. So my question for you is, currently, why are we still having issues with sulfonylurea-induced hypo or hyperglycemia in this time when we have so many other agents with better hypoglycemia safety profiles? Gosh, that is the bane of our existence right now, isn't it? It is hurting all of us to see that there are newer agents, safer agents, better profile from the glycemic control perspective. And yet we are seeing patients on sulfonylureas just because they are inexpensive. And unfortunately, that's the reality we are facing. GLP-1 and SGLT2 inhibitor coverage is still not as great as we would like it to be. And so this is where we are facing the dilemma of whether the patient can afford these medications or not. And the physicians are lining up in this situation of prescribing sulfonylureas even if they don't want to. Yeah, I get messages from patients and unfortunately you have to be realistic about what you can get, but at the same time educate patients about what are some of the pitfalls or side effects or risks of these patients and to make sure they take them appropriately, agreed. Yeah. All right, so case six. A 76-year-old man comes to the clinic with a history of moderately controlled type 2 diabetes, pancreatitis and coronary artery disease. He is taking one gram of metformin twice a day and yes, two milligram of glimaferide once a day and 24 units of insulin glargine in the evening. His A1c is 7.4% and he states that he generally feels well, but has gained some weight. He usually eats three meals a day and sometimes notices that he gets quite hungry at breakfast or in the afternoon. His laboratory test results are noteworthy for a fasting glucose of 81 milligram per deciliter at his morning clinic visit. He denies hypoglycemia, but his wife is worried by his increased eating and weight gain. He only checks his sugar once in the morning. He has an estimated GFR of 49. His blood pressure is 144 over 58 and he has decreased fetal pulses. Which of the following is the best treatment strategy for this patient? A, stop his insulin and change to glucagon-like peptide one or GLP-1 agonist. B, stop his sulfonylurea. C, stop his metformin. Or D, ask him to check his glucose at times more than just once a day. Okay, so I am very glad that we did not get 100% response on this one. So majority are voting for B, which is stop his sulfonylurea, and the runner-up is asking to check his blood sugars at other times of the day. So let's go to the rationale. This patient has two medications that are most likely to be associated with hypoglycemia, insulin glargine and glimepiride, which is a long-acting sulfonylurea. Older adults with diabetes can be particularly vulnerable to hypoglycemia given the potential for impaired hypoglycemic awareness. Therefore, minimizing the risk of hypoglycemia should be a priority. Having less aggressive glycemic controls, including a higher A1C target for older adults is reasonable when the risk of harm from treatment can be greater than the benefits of glycemic reduction. Treatment of cardiovascular risk factors and cardiovascular disease should also be individuals in this patient population, keeping in mind the time frame of benefit from more aggressive treatments. Although the patient is taking a low dose of glimepiride, it's two milligram, it can cause both overnight hypoglycemia and low blood glucose in the middle of the day from a peak glucose lowering effect when taken in the morning. This can be particularly problematic in older patients with renal dysfunction. In this case, it would be reasonable to stop the glimepiride, making option B the correct choice, which most of you picked. Changing insulin to a GLP-1 agonist can be considered in certain patients, especially given lower risk of hypoglycemia and cardiovascular benefits associated with this medication class. However, because of this patient's history of pancreatitis, the use of GLP-1 is not the best option due to the association of this class of drugs with pancreatitis. Although the option of lowering his insulin dose by itself is not offered, the patient may also need to reduce his basal insulin depending on his individualized glycemic targets and if he continues to have hypoglycemia. In addition, the patient may benefit from more frequent monitoring of his blood sugar at different times of the day. However, that does not directly address hypoglycemia and therefore option D is not the best next step. Metformin rarely causes hypoglycemia and is usually not the culprit when patients are taking other agents associated with hypoglycemia. At his GFR, a dose adjustment is not necessary. For metformin use, if the GFR is greater than 45, no dose adjustment is necessary. If the GFR is between 30 and 45, some guidelines do not recommend starting metformin while others recommend initial therapy with 500 mg once a day and that can be increased to two times a day as long as kidney function is monitored closely. If the GFR is less than 30, the metformin use is contraindicated. Also, it is important to note that the option of sodium glucose co-transporter to your SGLT2 inhibitor was not offered as a treatment option for this patient. This class of medication has been shown to provide cardiovascular benefit. It is noteworthy that the glycemic efficacy of SGLT2 inhibitors is reduced when GFR is less than 30 to 45. There are differences in the manufacturer recommended threshold for GFR based on which SGLT2 inhibitor is being prescribed. Based on this patient's GFR, treatment with an SGLT2 inhibitor would also be an option, but they can be considered. Wow. So many things to consider and it's a constant process. Every time you see the patient in the next few months, our rationale could constantly be changing. I have a question for you. What would be something else that you would consider in this patient's management to help with better glucose controlled and minimizing hypoglycemia? It's funny because we're circling back to something we discussed earlier. This patient is 76, so it's highly likely that he is on Medicare. And we said that the guidelines are changed recently and he's on one shot of insulin. So I think I would definitely discuss with him that he qualifies for a continuous glucose monitoring system. And if he's open to proceeding with it, I think that would be a really good option, especially because this patient is giving you some signs of hypoglycemia, but maybe it's not being recognized. And for safety reasons, that would be helpful and potentially also minimizing some of the other medications he's on if we have more data regarding what his glucose patterns are. I think that in the current timeline that we are, it's really important to think of diabetes management more globally, minimizing hypoglycemia and weight gain, having agents that give us more than just glycemic control, if we can offer cardiovascular benefits or renal protection, and then any technology that we can help our patients with to optimize their therapy while minimizing medications and minimizing risk of hypoglycemia. So that's why I think that would be very helpful in this patient. Yeah, I feel like we are in a golden age for diabetes management. It's exciting field, it's exploding for sure with newer agents being considered with additional profiles much beyond glycemic control. So I'm excited to see that journey. I think that concludes our cases. Let me see the chat. Okay, I don't see any messages on chat. All right. Well, we made it through six cases. We definitely have to make some questions harder, I think maybe for next session, but everybody did a great job. We wanted to thank you all for joining us today. We hope that this was an informative session for you. We wanted to thank ACE, Dr. Siraj, and Dr. Gul Pakkarishnan for making this possible, and for Beth Welch for coordinating and making sure everything went smoothly. And of course, to you for co-hosting this with me. It's been very nice going through the cases with you and discussing where we are with diabetes management at this point. Yeah, excited to be here. See you all next time. Sounds good. Stay safe and have a nice evening. Bye.

diabetes management

continuous glucose monitor

glycemic patterns

anti-GAD antibodies

chronic kidney disease progression

finarunone

sulfonylurea medication

hypoglycemia