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yo female/male with HTN, HLD, DM, CAD, CKD, CHF present today for diabetes management.
Diabetes: Type 1/2
1. Diagnosed in
2. Meds: Current:
Patient is adherent to current medications.
Prior: Metformin, Sulfonylurea, Pioglitazone, GLP-1 agonist, DPP-4 inhibitors, SGLT-2 inhibitor, Basal Insulin, Prandial Insulin.
SE:
Hyperglycemia symptoms: Polyuria, polydipsia, polyphagia. Recent ER visit/ Hospitalizations in last few years:
Contraindications to DM meds:
H/o pancreatitis:
Family history of personal h/o thyroid cancer: H/o yeast infection/ UTI:
H/o osteoporosis:
Complications:
No ASCVD, stroke, PVD, CHF.
No DM nephropathy - Normal creatinine, neg microalbuminuria in
No DM retinopathy - Last eye exam
No neuropathy, foot ulcers or amputations.
Health Care maintenance:
HLD: on aspirin, statin.
HTN: on ACEI/ARB
I
Patient was advised on the need for annual DM eye exams, regular foot exam.
o Lifestyle:
Diet: B: L: D:
Beverages and Snack:
Carb counting:
Physical Activity:
Weight change:
Blood glucose monitoring at home:
Glucometer:
Check times/ day/week.
Hypoglycemia: frequency, timing, cause: Last episode was: Reading: Has awareness- symptoms of palpitations, tremors, sweating, hunger.
-O-
Metformin
1. First-line therapy generally includes metformin.
2. Mechanism of Action: Decreases hepatic glucose production, decreases intestinal absorption of glucose and increases peripheral glucose uptake
3. A1C lowering effects: 1-2%
4. Usual Dose: 500, 850, 1000mg, Max dose 2550g/day
5. Kidney Impairment: GFR< 30: No, GFR 30-45: 500mg bid 6. Side effects: Gl side effects, Lactic Acidosis, Vit B 12 deficiency
GLP-1 agonist
1. GLP 1 agonists, SGLT2 inhibitors, with or without metformin based on glycemic needs, are appropriate initial therapy for T2DM with or at high risk for CVD disease, HF, and/or CKD.
2. A1C lowering effects: 0.5-2%
3. Dose:
Rybelsus/ Semaglutide 3mg/7mg/14mg titrate every month daily Ozempic/ Semaglutide 0.25-> 0.5->1->2mg weekly**
Trulicity/ Dulaglutide 0.75mg->1.5mg->3mg->4.5mg weekly** Victoza / Liraglutide 0.6mg -> 1.2mg -> 1.8mg -> 2.4mg -> 3mg daily** 4. Side effects: GI side effects, Gallbladder disease,
5. Contraindications: Medullary thyroid cancer
SGLT-2 inhibitors
1. GLP 1 agonists, SGLT2 inhibitors, with or without metformin based on glycemic needs, are appropriate initial therapy for T2DM with or at high risk for CVD disease, HF, and/or CKD.
2. A1C lowering effects : 0.5-0.7%
3. Dose:
Invokana/ canagliflozin 100mg-> 300mg **HF CKD MACE (GFR <30, do not initiate, can continue 100mg)
Jardiance/ empagliflozin 10mg (GFR>20) -> 25mg **HF CKD MACE Farxiga/ dapagliflozin 5mg -> 10mg **HF CKD
(GFR< 25, do not initiate, can continue 10mg)
Steglatro/ ertugliflozin 5mg-> 15mg (GFR> 45)* HF
4. Side effects: UTI, yeast infection, Ketoacidosis,
DPP-4 inhibitor
1. A1C lowering effects : 0.5-0.8% 2. Dose:
3. Trajenta Linagliptin 5mg daily
Januvia Sitagliptin 100mg (GFR<30 25mg, GFR 30-45:50mg)
Onglyza Saxagliptin 2.5-5mg daily (GFR<45 2.5mg ) *
Nesina Alogliptin 25mg (GFR<30 6.25, GFR 30-60 12.5mg) 4. Side effects: Minimmal
Dual GLP-1 & GIP receptor agonist
1. A1C lowering effects: 2-2.5%
2. Dose:
Mounjaro/ tirzepatide 2.5->5->7.5->10->12.5->
15 mg
once weekly
mounjaro
(tirzepatide) injection 0.5 mL
2.5 mg 5 mg | 75 mg | 10mg | 12.5 mg | 15 mg
Go to mounjaro.lily.com
mounjaro
mounjaro
10
mounjaro 15
Sulfonylurea/ Glinide
1. A1C lowering effects: 1-2%
2. Dose:
Glipizide 2.5mg-> 5mg->10mg->20mg, max 40mg (GFR>10) Glimepiride 1mg-> 2mg->4mg, max 8mg (GFR>15)
Glyburide 0.75, 3mg max12mg. 1.25/ 2.5/ 5mg max20mg (GFR>60)
Repaglinide 0.5mg, 1mg 2mg before each meal max 16mg (CKD, HD, PD)
Nateglinide Starlix 60mg/120mg before each meal, max 360mg daily use with precaution (GFR<15 use with caution)
4. Side effects: Hypoglycemia, weight gain.
TZD Thiazolidinedion
1. A1C lowering effects: 0.5-1.4%
2. Dose: Pioglitazone Actos 15mg 30mg 45mg
3. Side effects: Fluid retention, CHF, bladder cancer,
Insulin
1. The early introduction of insulin should be considered if there is evidence of ongoing catabolism (weight loss), if symptoms of hyperglycemia are present, or when A1C levels (>10%) or blood glucose levels (2300 mg/dL) are very high.
2. Clinicians should be aware of the potential for overbasalization with insulin therapy. Clinical signals that may prompt evaluation of overbasalization include basal dose more than ~0.5 IU/kg/day, high bedtime-morning or post-preprandial glucose differential, hypoglycemia, and high glycemic variability.
Antihyperglycemic agents
UKPDS and follow up trial
25% risk reduction for microvascular complications with intensive versus regular treatment
Despite a rapid convergence of A1c levels in both arms after the close of UKPDS the intensive cohort maintained the microvascular risk reduction at 24% after the additional 10 years.
This demonstrates the critical need for intensive glycemic control to help minimize the risk of long term microvascular complications
1/4 to 1/2 of insured patients a1c > 9%, diagnosed age 50 dies 6 years earlier than someone without diabetes
atorvastatin 40-80mg, rosuvastatin 20-40mg
Moderate intensity:
LDL < 100mg/dL
< 70 with high risk (established vascular disease, hypertension)
erectile dysfunction with sildenafil, tadalafil
treat gastroparesis with metoclopramide or erythromycin
microvascular with gabapentin, pregabalin or duloxetine
[Music]
thank you
hello again everybody we're going to
talk here about the outpatient
management of diabetes so we have uh
diagnosed a patient with diabetes and
we're going to be focusing here on Type
them uh how do we monitor their health
you know we're not going to talk here
about what medications we're going to
put them on for the diabetes
particularly I talk about that in
another talk we're going to be focusing
here on how we maintain these People's
Health how we prevent comorbidities
because remember that diabetes as a
consequence of obesity but diabetes
itself is a major major cause of both
complications morbidities mortality as
well as just general stress on our
health care System
if you haven't had the chance yet please
consider subscribing to my patreon you
can get there by clicking the link in
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more and more videos up
okay so just kind of a uh review of uh
Diabetes Type 2 diabetes specifically we
always screen overweight and obese
patients who are aged 35 to 70 every
three years okay always
um so that's going to be important
particularly for step three that you
understand that we need to screen
patients who are overweight or obese
especially when they're in that age
range where type 2 diabetes tends to
develop and you can do this either by
getting a fasting blood glucose an oral
glucose tolerance test or you can just
jump to an A1C it doesn't really matter
now with a new diagnosis of type 2
diabetes you then have to determine how
the patient will be treated and we do
that with an A1C level I talk about this
in a previous talk you can go back and
watch my other talks on diabetes
so what are the complications there are
a number so there are macrovascular
complications which involve the large
vessels we're talking here about
increased risk for stroke heart attack
they can get angina of course it's on
that Continuum with heart attack and
peripheral vascular disease now
microvascular we think of things like
retinopathy nephropathy all of that is
due to due to problems with the very
small vessels they can also get erectile
dysfunction and they have a higher risk
of osteomyelitis
as well as infection
uh then some of these neuropathic
manifestations uh the one we often think
of is diabetic neuropathy that is very
common but there are some of these other
things like autonomic neuropathy which
can cause gastroparesis
now our initial outpatient management is
going to be focused on complications so
we want to screen these patients for
high blood pressure because that is
going to that's going to compound the
problem particularly for some of those
macrovascular complications we want to
get a urinalysis we're looking for
proteinuria here looking for the
beginning of renal damage we're going to
get a lipid panel and the reason again
here is because diabetes itself raises
your risk of things like stroke and
heart attack so if these patients have
high cholesterol we have to get on top
of that and as a matter of fact we have
stricter LDL cutoffs as far as when we
commence therapy we're going to do an
eye exam this is recommended every year
to look for retinopathy and then
infection prophylaxis obesity and
smoking cessation we'll go through each
of these so hypertension we screen their
blood pressure
as normal so ideally twice a year if
they are hypertensive meaning they have
two readings of more than 140 over 90
either systolic or diastolic then we are
going to put them on an Ace inhibitor or
an Angiotensin receptor blocker they are
uh they're they're nephroprotective so
they will not only treat the
hypertension but they also protect the
kidneys so either an Ace inhibitor or an
ARB it doesn't really matter uh usually
we go with ACE inhibitors they are known
they're they're more well known than the
arbs but it doesn't matter a lot of
people will have to go on to arbs just
because of the side effects of the ACE
inhibitors
our goal is going to be to get them
below 130 over 80. if the control is not
satisfactory with ACE inhibitor or ARB
alone then we will add a diuretic
particularly a thiazide diuretic and as
a matter of fact there are a lot of
medications that combine both the ace
inhibitor and the Hydrochlorothiazide or
an ARB and a hydrochlorothiazide
nephropathy is screened via your
analysis we're looking just here at the
urine protein if we do see proteinuria
then that pretends some degree of renal
damage and so if that is present then we
will give an Ace inhibitor or an ARP so
just like we would for hypertension
these medications are known to slow
progression to end-stage renal disease
now as far as lipids um now there are a
variety of recommendations the American
Association of clinical endocrinologists
recommends that lipid panels be done
every year however there are other
organizations that recommend less
frequently so we're just going to go
with every year here our LDL Target and
otherwise healthy patients is to keep
under 100 however most diabetics are not
healthy many of them have an established
vascular disease history maybe they've
had a heart attack in the past they've
got angina or they have hypertension
obviously very common in those cases we
want stricter control
target then we go with a Statin we go
with high intensity sentence so
atorvastatin resuvastatin one of those
if the LDL remains above Target with
that Statin then we'll add another
medication onto it so you can do a bio
acid sequesterant you can do niacin or
you can do cholesterol absorption
Inhibitors that's acetamide and there
are some statins that come with
acetamide in it so you can easily
provide these to patients because it's
just one pill
um it's important to bear in mind that
exercise has a nice effect on the body
it both lowers the blood glucose
improving glycemic control and it also
raises the HDO so it's very very very
recommended in anybody but particularly
uh diabetics with hyperlipidemia
retinopathy is screened with an
ophthalmologic exam every year what
we're looking for here is damage to the
microvasculature of the retina if
patients do develop retinopathy
generally it it starts out as a
worsening Acuity they can get floaters
and and blurred vision this is one of
the most feared complications of
diabetes because obviously it's really
going to affect your quality of life
um so that's pretty much all you need to
know for retinopathy know that these
patients need to be surveilled every
year by an ophthalmologist or possibly
an optometrist and then if this develops
they need to be referred to
ophthalmology
infection prophylaxis remember that
diabetes does leave patients in a
semi-immunicompromised state there are
complex effects of diabetes both on the
innate and on the Adaptive immune
response so it's very important that
these patients get their vaccinations
the so obviously influenza every year
that's recommended for everybody the
pneumococcal vaccine generally
recommended in older people however it
will be recommended in younger people
with diabetes and there's a whole Litany
of extra recommendations for the
Pneumovax covid-19 as recommended
diabetics are at risk of more severe
covid and then other routine
vaccinations so remember Tdap and
shingles and Hep B
all right uh now with obesity obviously
we screen that just by getting their
weight every time they come into the
clinic remember that obesity is causally
linked with type 2 diabetes so what that
means is that some patients if they have
type 2 diabetes and they're able to lose
weight their type 2 diabetes may
actually go away in other words they'll
become more insulin sensitive and so
they won't
um they won't be spiking their fasting
blood sugar for instance so this is one
of those things that's part of Lifestyle
modification it's always part of
management for diabetes but if you do
have an established diagnosis of type 2
diabetes it's all the more important to
continue trying to lose weight now there
are a number of things that we can do do
we give them medications to help weight
loss you know that can be difficult
because a lot of those medications are
stimulants and we don't want to make
them hypertensive because that creates
problems so a lot of this is just diet
and exercise
now in some cases if they're severely
obese or morbidly obese they can be
referred to bariatric surgery
particularly when you're dealing with
younger patients who are more likely to
recover well from the bariatric surgery
and who have a long life ahead of them
ideally
smoking cessation is obviously going to
be recommended to everybody but smoking
stopping smoking does reduce your risk
of many of these complications and has
other obvious health benefits you can
consider pharmacotherapy in these
patients uh you know quitting cold
turkey is ideal but it's difficult so
there are medications that can help
there's the over-the-counter nicotine
replacement therapy they can go buy at
the pharmacy there's Wellbutrin
bupropion and then and that's also used
as an antidepressant by the way and then
there's verenicline or Chantix now both
of these are contraindicated in patients
with epilepsy or seizure disorder so
that's important to recognize those that
does come up on exams
some others erectile dysfunction this is
a microvascular complication you can
treat it with the pd5 Inhibitors like
sildenafil tadalafel but it's important
before you do that to make sure that the
patient is healthy enough for sex so
that's kind of a judgment call so you
you need to make sure that that you are
fully evaluating the patient you don't
just give these medications willy-nilly
also you don't give these medications if
the patient is on nitrates usually for
Angina so if a patient is on
nitroglycerin or something like that
then isosorbide dinitrate you will not
be giving these medications okay
gastroparesis is more of a severe
manifestation of diabetes it causes
dyspepsia nausea vomiting diarrhea this
is something that you're going to see in
patients with very poorly controlled
diabetes What's Happening Here is the
stomach is just not emptying properly
the patients go to eat their stomach
fills up and they throw up they can also
get other problems besides that but
that's kind of the gist of it you can
use prokinetic agents like
metaclopramide that would help with the
nausea as well or erythromycin which is
an antibiotic that just happens to have
prokinetic properties peripheral
neuropathy is a big problem in diabetes
and so what we're looking at here is a
patient who has diabetes they come in
and they said my feet hurt my hands hurt
they're numb they're tingling they're
they're prickly
that's peripheral neuropathy now you can
get peripheral neuropathy from diabetes
in a variety of ways number one you get
direct damage to the small nerve herbs
you also kind of complicating this is
that you can have peripheral artery
disease so this is why Foot Care is so
important with diabetes because they're
not only going to have the neuropathy
but they may have some peripheral artery
disease so it's very important that
they're looking at their feet that they
are
moisturizing that they're wearing good
shoes because that's going to prevent
the injury it's not the peripheral
neuropathy that's that's harmful
necessarily it's the injuries that can
come from that if you're not feeling
your feet properly and you step on a
nail you're not going to know that's why
it's really important to check your feet
you know at least every year A lot of
times these patients will see a
podiatrist
for the neuropathy itself for the pain
Gabapentin pregabalin or diloxetine
this is just a summary here so this is
everything we went over you should know
how to screen for each of these you
should know each of the complications
how to screen how often especially if
you're taking step three and then when
we treat and how we treat so this is
just a general overview of the
outpatient management of diabetes thank
you
foreign
[Music]
Type 2 diabetes: Treat with additional kidney-protective therapy — In addition to the general measures discussed above plus the use of an ACE inhibitor (or ARB) in albuminuric patients, patients with type 2 diabetes and DKD should be treated with sodium-glucose cotransporter 2 (SGLT2) inhibitors.
Among patients with type 2 diabetes who have measured or estimated albuminuria ≥30 mg/day despite an ACE inhibitor (or ARB) and an SGLT2 inhibitor (or if an SGLT2 inhibitor is not tolerated), we suggest treatment with a nonsteroidal selective mineralocorticoid receptor antagonist (MRA; specifically finerenone), where available, provided the patient has a serum potassium ≤5 mEq/L and eGFR ≥25 mL/min/1.73 m2 (see 'General measures applicable to all patients with DKD' above and 'Severely increased albuminuria: Treat with angiotensin inhibition' above):
●SGLT2 inhibitors – We recommend treatment of most patients with type 2 diabetes and DKD with an SGLT2 inhibitor, regardless of the degree of glycemic control (algorithm 1) [30,31]. Initiating SGLT2 inhibitors should generally be avoided among patients with an eGFR <20 mL/min/1.73 m2 although they can likely be continued safely among patients whose eGFR ultimately falls below 20 mL/min/1.73 m2 [32]. If canagliflozin is used, the dose is 100 mg once daily. If dapagliflozin is used, the dose is 10 mg once daily.
SGLT2 inhibitors can prevent important kidney endpoints, including ESKD [31,33]. Although the relative risk reduction of kidney failure is similar among patients with and without severely increased albuminuria (measured or estimated urine albumin excretion ≥300 mg/day), the absolute risk reduction is greater among those with severely increased albuminuria, since such patients have a higher absolute risk of developing a major kidney event. Thus, our recommendation is stronger for those with severely increased albuminuria than for those with normoalbuminuria or moderately increased albuminuria. The rationale for our approach is presented in detail below.
●Nonsteroidal selective MRAs – Among patients with type 2 diabetes who have measured or estimated albuminuria ≥30 mg/day despite an ACE inhibitor (or ARB) and an SGLT2 inhibitor (or if an SGLT2 inhibitor is not tolerated), we suggest treatment with a nonsteroidal selective MRA, specifically finerenone, where available, provided the patient has a serum potassium ≤5 mEq/L and eGFR ≥25 mL/min/1.73 m2. The starting dose of finerenone is 20 mg once daily if eGFR is ≥60 mL/min/1.73 m2 and 10 mg once daily if eGFR is ≥25 to 60 mL/min/1.73 m2. The serum potassium and creatinine should be measured four weeks after starting finerenone. If the starting dose was 10 mg once daily, the dose can be increased to 20 mg once daily four weeks later if serum potassium is ≤4.8 mEq/L and eGFR has not declined by more than 30 percent.
Finerenone reduces the progression of kidney function impairment and cardiovascular events in patients with type 2 diabetes and DKD, while not substantially impacting blood pressure and only slightly increasing serum potassium levels. Finerenone has been studied in patients taking maximally tolerated doses of ACE inhibitors or ARBs but has not been studied extensively in patients taking SGLT2 inhibitors plus maximally tolerated doses of ACE inhibitors or ARBs.
●Glucagon-like peptide 1 (GLP-1) receptor agonists – SGLT2 inhibitors have a weak glucose-lowering effect, particularly in patients with reduced eGFR, and therefore patients whose glycated hemoglobin is far from their goal are likely to require additional glucose-lowering therapy. Aside from SGLT2 inhibitors, the glucose-lowering drugs with the strongest evidence of benefit on cardiovascular and kidney outcomes in patients with preexisting cardiovascular or kidney disease are the GLP-1 receptor agonists [31]. Thus, in patients with type 2 diabetes and DKD who have not achieved glycemic control despite initial glucose-lowering therapy (which is typically metformin) and an SGLT2 inhibitor, a GLP-1 receptor agonist can improve glycemic control and may provide additional benefit [34-36]. GLP-1 receptor agonists are discussed below and in other topics. (See "Initial management of hyperglycemia in adults with type 2 diabetes mellitus" and "Management of persistent hyperglycemia in type 2 diabetes mellitus" and "Glucagon-like peptide 1-based therapies for the treatment of type 2 diabetes mellitus".)
Our recommendations outlined above are consistent with guidelines from the American Diabetes Association (ADA) and the Kidney Disease Improving Global Outcomes (KDIGO) on the treatment of patients with DKD [37,38].
Among those with an eGFR >45 mL/min/1.73 m2, SGLT2 inhibitors act by blocking reabsorption of glucose in the proximal tubule through SGLT2, which lowers the renal glucose threshold and leads to substantial glycosuria. The glycosuria is dependent upon kidney function, and therefore the magnitude of glycosuria and lowering of blood glucose is smaller among individuals with reduced kidney function.
SGLT2 inhibitors have additional effects on the kidney, and, given their weak glucose-lowering effect, these effects are likely independent of glycemic control. By blocking the cotransporter, they reduce sodium reabsorption, which is usually increased in patients with diabetes due to the excess tubular glucose load. The resulting natriuresis reduces intravascular volume and blood pressure, but it also increases the delivery of sodium to the macula densa. Increased sodium delivery to the macula densa normalizes tubuloglomerular feedback and thereby reduces intraglomerular pressure (ie, reduces glomerular hyperfiltration) through constriction of the abnormally dilated afferent arteriole [39]. This decrease in glomerular hyperfiltration can, hypothetically, slow the rate of progression of kidney disease (see "Diabetic kidney disease: Pathogenesis and epidemiology", section on 'Glomerular hyperfiltration'). A range of additional mechanisms may explain the benefits of SGLT2 inhibitors on kidney disease progression [40].
SGLT2 inhibitors reduce the risk of kidney disease progression among patients with DKD who are already taking ACE inhibitors (or ARBs) [33,41-47], as well as the incidence of cardiovascular disease [33]. Among patients with DKD and severely increased albuminuria, the best data come from three large trials:
●The Canagliflozin and Renal Events in Diabetes with Established Nephropathy Clinical Evaluation (CREDENCE) trial compared canagliflozin (100 mg once daily) with placebo in 4401 diabetic patients with an eGFR between 30 and 89 mL/min/1.73 m2 and urine ACR >300 mg/g (median, 927 mg/g) despite taking an ACE inhibitor or ARB [42]. At 2.6 years, canagliflozin reduced the incidence of ESKD (5.3 versus 7.5 percent), doubling of serum creatinine (5.4 versus 8.5 percent), hospitalization for heart failure (4.0 versus 6.4 percent), cardiovascular death (5.0 versus 6.4 percent), and all-cause mortality (7.6 versus 9.1 percent), although the effects on cardiovascular death and all-cause mortality were not separately statistically significant. The beneficial effects of canagliflozin on slowing kidney function decline appeared to be similar among those with baseline eGFR <30 mL/min/1.73 m2 (ie, among trial participants whose eGFR fell to below 30 mL/min/1.73 m2 between enrollment and initiation of study medication) [48].
●In the similarly designed Dapagliflozin and Prevention of Adverse Outcomes in Chronic Kidney Disease (DAPA-CKD) trial, 4304 individuals with eGFR 25 to 75 mL/min/1.73 m2 and urine ACR 200 to 5000 mg/g (median 950 mg/g) were randomly assigned to dapagliflozin (10 mg once daily) or placebo [49]. Approximately two-thirds of enrolled patients had type 2 diabetes; 98 percent were taking an ACE inhibitor or ARB. At 2.4 years, dapagliflozin reduced all-cause mortality (4.7 versus 6.8 percent), as well as the incidence of ESKD (5.1 versus 7.5 percent), and also reduced the risk of a 50 percent or greater decline in eGFR (5.2 versus 9.3 percent). The beneficial effect of dapagliflozin was similar in patients with DKD and in patients with other forms of kidney disease, reinforcing the concept that beneficial effects are independent of glycemic control. There were no differences between the treatment groups with respect to major adverse effects.
●In the Study of Heart and Kidney Protection with Empagliflozin (EMPA-KIDNEY) trial, 6609 patients with eGFR 20 to 44 mL/min/1.73 m2 (regardless of albuminuria) or 45 to 89 mL/min/1.73 m2 (if albumin-to-creatinine ratio was at least 200 mg/g) were randomly assigned to empagliflozin 10 mg daily or placebo [50]. Less than half (46 percent) of participants had diabetes. At two years, empagliflozin reduced the incidence of ESKD (3.3 versus 4.8 percent), the incidence of a sustained decline in eGFR to <10 mL/min/1.73 m2 (3.5 versus 5.1 percent), and the incidence of a sustained decrease in eGFR of 40 percent or more (10.9 versus 14.3 percent). The risks of all-cause mortality (4.5 versus 5.1 percent) and nonfatal cardiovascular events (4.3 versus 4.6 percent) were similar between the groups. Effects were similar in patients with and without diabetes and regardless of the eGFR at the start of the study. The benefit from empagliflozin was larger in patients with albumin-to-creatinine ratio ≥300 mg/g and substantially less in patients with lower albumin excretion.
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