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T2D, type 2 diabetes. Reprinted from de Boer et al. (1).diabetesjournals.org/care Chronic Kidney Disease and Risk Management S225\n©AmericanDiabetesAssociation | [
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renal death), time to the first occur-\nrence of either of the components of\nthe cardiovascular composite (cardio-vascular death or hospitalization forheart failure), and time to death from\nany cause. The trial had 4,304 partici-\npants with a mean eGFR at baselineof 43.1 ± 12.4 mL/min/1.73 m\n2(range\n25–75 mL/min/1.... | [
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2(range\n25–75 mL/min/1.73 m2)a n dam e d i a n\nUACR of 949 mg/g (range 200 –5,000\nmg/g). There was a signi ficant bene fit\nby dapagli flozin for the primary end\npoint (hazard ratio [HR] 0.61 [95% CI\n0.51–0.72]; P<0.001) (105). The HR for\nthe kidney composite of a sustained de-\ncline in eGFR of $50%, ESKD, or death... | [
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from renal causes was 0.56 (95% CI\n0.45–0.68; P<0.001). The HR for the\ncomposite of death from cardiovascular\ncauses or hospitalization for heart failurewas 0.71 (95% CI 0.55 –0.92; P=0 . 0 0 9 ) .\nFinally, all-cause mortality was decreased\nin the dapagli flozin group compared\nwith the placebo group ( P<0.004).\nT... | [
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The most recently published clinical\ntrial was EMPA-KIDNEY (Study of Heartand Kidney Protection with Empagli flo-\nzin) (106). This study enrolled partici-\npants with kidney disease with an eGFRof at least 20 but less than 45 mL/min/1.73 m\n2or who had an eGFR of at least\n45 but less than 90 mL/min/1.73 m2 | [
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2or who had an eGFR of at least\n45 but less than 90 mL/min/1.73 m2\nwith a UACR of at least 200 mg/g creati-nine. Approximately one-half of the6,609 participants had diabetes. The em-\npagliflozin-treated participants had lower\nrisk of progression of kidney disease and\nlower risk of death from cardiovascularcauses (H... | [
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0.001).\nWith respect to cardiovascular out-\ncomes, SGLT2 inhibitors have demon-strated reduced risk of heart failurehospitalizations and some also demon-\nstrated cardiovascular risk reduction.\nGLP-1 RAs have clearly demonstratedcardiovascular bene fits. (See Section 10,\n“Cardiovascular Disease and Risk\nManagement,... | [
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Management, ”for further detailed\ndiscussion.)\nOf note, while the glucose-lowering ef-\nfects of SGLT2 inhibitors are blunted witheGFR<45 mL/min/1.73 m\n2,t h er e n a l\nand cardiovascular benefi ts were still\nseen at eGFR levels as low as 20 mL/min/1.73 m\n2even with no signi ficant change\nin glucose (29,31,49,60,9... | [
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in glucose (29,31,49,60,90,102,105 –107).\nMost participants with CKD in these trials\nalso had diagnosed atherosclerotic cardio-\nvascular disease (ASCVD) at baseline,although /C2428% of CANVAS participants\nwith CKD did not have diagnosed ASCVD(32).\nBased on evidence from the CRE-\nDENCE, DAPA-CKD, and EMPA-KIDNEY | [
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Based on evidence from the CRE-\nDENCE, DAPA-CKD, and EMPA-KIDNEY\ntrials, as well as secondary analyses of\ncardiovascular outcomes trials with SGLT2inhibitors, cardiovascular and renal eventsare reduced with SGLT2 inhibitor use in\nindividuals with an eGFR of 20 mL/min/\n1.73 m\n2, independent of glucose-lowering\nef... | [
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1.73 m\n2, independent of glucose-lowering\neffects (101,104).\nWhile there is clear cardiovascular\nrisk reduction associated with GLP-1 RA\nuse in people with type 2 diabetes and\nCKD, the possibility for bene fit on renal\noutcomes will come with the results ofthe ongoing FLOW (A Research Study toSee How Semaglutide ... | [
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with Placebo in People With Type 2 Dia-\nbetes and Chronic Kidney Disease) trialwith injectable semaglutide (108). Asnoted above, published data address\na limited group of people with CKD,\nmostly with coexisting ASCVD. Renalevents, however, have been examined asboth primary and secondary outcomes\nin large published ... | [
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in large published trials. Adverse event\nprofiles of these agents also must be\nconsidered. Please refer to Table 9.2 for\nmedication-speci fic factors, including\nadverse event information, for theseagents. Additional clinical trials focus-ing on CKD and cardiovascular out-comes in people with CKD are ongoingand will b... | [
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years.\nFor people with type 2 diabetes and\nCKD, the selection of speci fica g e n t sm a y\ndepend on comorbidity and CKD stage.SGLT2 inhibitors are recommended for in-\ndividuals at high risk of CKD progression(i.e., with albuminuria or a history of docu-mented eGFR loss) ( Fig. 9.3). For people\nwith type 2 diabetes... | [
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with type 2 diabetes and CKD, use of\nan SGLT2 inhibitor in individuals with\neGFR$20 mL/min/1.73 m\n2and UACR\n$200 mg/g creatinine is recommendedto reduce CKD progression and cardio-\nvascular events. The reason for the\nlimit of eGFR is as follows. The majorclinical trials for SGLT2 inhibitors thatshowed benefi t for... | [
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kidney disease are CREDENCE, DAPA-CKD,and EMPA-KIDNEY. CREDENCE enrollmentcriteria included eGFR >30 mL/min/1.73\nm\n2and UACR >300 mg/g (29,101).\nDAPA-CKD enrolled individuals with eGFR\n>25 mL/min/1.73 m2and UACR >200 | [
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>25 mL/min/1.73 m2and UACR >200\nmg/g. Subgroup analyses from DAPA-CKD(109) and analyses from the EMPERORheart failure trials suggest that SGLT2 in-hibitors are safe and effective at eGFRlevels of >20 mL/min/1.73 m\n2.T h eE m -\npagliflozin Outcome Trial in Patients With | [
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2.T h eE m -\npagliflozin Outcome Trial in Patients With\nChronic Heart Failure With PreservedEjection Fraction (EMPEROR-Preserved)enrolled 5,998 participants (110), and theEmpagli flozin Outcome Trial in Patients | [
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With Chronic Heart Failure and a ReducedEjection Fraction (EMPEROR-Reduced) en-rolled 3,730 participants (111); enrollmentcriteria included eGFR >60 mL/min/1.73\nm\n2, but ef ficacy was seen at eGFR >20\nmL/min/1.73 m2in people with heart\nfailure. Most recently, the EMPA-KIDNEY trial showed ef ficacy in participants\nwi... | [
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with eGFR as low as 20 mL/min/1.73 m\n2\n(106). Hence, the new recommendationis to use SGLT2 inhibitors in individualswith eGFR as low as 20 mL/min/1.73 m\n2. | [
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2.\nIn addition, the DECLARE-TIMI 58 trialsuggested effectiveness in participantswith normal urinary albumin levels (112).In sum, for people with type 2 diabetesand diabetic kidney disease, use of anSGLT2 inhibitor is recommended to re-duce CKD progression and cardiovascular\nevents in people with an eGFR $20 mL/\nmin/... | [
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events in people with an eGFR $20 mL/\nmin/1.73 m\n2.\nOf note, GLP-1 RAs may also be used\nat low eGFR for cardiovascular protec-\ntion but may require dose adjustment(113).\nRenal and Cardiovascular Outcomes\nof Mineralocorticoid Receptor\nAntagonists in Chronic KidneyDisease\nMRAs historically have not been well stu... | [
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MRAs historically have not been well stud-\nied in diabetic kidney disease because ofthe risk of hyperkalemia (114,115). How-ever, data that do exist suggest sustainedbenefit on albuminuria reduction. There | [
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are two different classes of MRAs, steroi-dal and nonsteroidal, with one group notextrapolatable to the other (116). Late in2020, the results of the first of two trials,\nthe Finerenone in Reducing Kidney Failure\nand Disease Progression in Diabetic Kidney\nDisease (FIDELIO-DKD) trial, which exam-ined the renal effects ... | [
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demonstrated a signi ficant reduction in\ndiabetic kidney disease progression andcardiovascular events in people with ad-vanced diabetic kidney disease (33,117).This trial had a primary end point of timetofirst occurrence of the composite end | [
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point of onset of kidney failure, a sus-tained decrease of eGFR >40% fromS226 Chronic Kidney Disease and Risk Management Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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baseline over at least 4 weeks, or renal\ndeath. A prespeci fied secondary outcome\nwas time to first occurrence of the com-\nposite end point of cardiovascular deathor nonfatal cardiovascular events (myocar-\ndial infarction, stroke, or hospitalization | [
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dial infarction, stroke, or hospitalization\nfor heart failure). Other secondary out-comes included all-cause mortality, timeto all-cause hospitalizations, and change\nin UACR from baseline to month 4, and\ntime to first occurrence of the following\ncomposite end point: onset of kidneyfailure, a sustained decrease in eG... | [
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of$57% from baseline over at least\n4 weeks, or renal death.\nThe double-blind, placebo-controlled\ntrial randomized 5,734 people with CKD\nand type 2 diabetes to receive finere-\nnone, a nonsteroidal MRA, or placebo.Eligible participants had a UACR of 30to<300 mg/g, an eGFR of 25 to <60\nmL/min/1.73 m\n2, and diabetic ... | [
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mL/min/1.73 m\n2, and diabetic retinopa-\nthy, or a UACR of 300 –5,000 mg/g and\nan eGFR of 25 to <75 mL/min/1.73 m2.\nThe potassium level had to be #4.8\nmmol/L. The mean age of participantswas 65.6 years, and 30% were female.\nThe mean eGFR was 44.3 mL/min/\n1.73 m\n2, and the mean albuminuria was\n852 mg/g (interqua... | [
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852 mg/g (interquartile range 446 –1,634\nmg/g). The primary end point was re-\nduced with finerenone compared with\nplacebo (HR 0.82 [95% CI 0.73– 0.93]; P=\n0.001), as was the key secondary compos-\nite of cardiovascular outcomes (HR 0.86[95% CI 0.75 –0.99]; P= 0.03). Hyperkale- | [
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... |
mia resulted in 2.3% discontinuation inthe study group compared with 0.9% inthe placebo group. However, the studywas completed, and there were no deaths\nrelated to hyperkalemia. Of note, 4.5% of\nthe total group were being treated withSGLT2 inhibitors.\nThe Finerenone in Reducing Cardiovas-\ncular Mortality and Morbid... | [
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cular Mortality and Morbidity in Diabetic\nKidney Disease (FIGARO-DKD) trial assessed\nthe safety and ef ficacy of finerenone in re-\nducing cardiovascular events among peoplewith type 2 diabetes and CKD with ele-\nvated UACR (30 to <300 mg/g creatinine)\nand eGFR 25 –90 mL/min/1.73 m\n2(118).\nThe potassium level had to... | [
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2(118).\nThe potassium level had to be #4.8 mmol/L.\nThe study randomized eligible subjects to\neither finerenone ( n= 3,686) or placebo\n(n= 3,666). Participants with an eGFR of\n25–60 mL/min/1.73 m2at the screening\nvisit received an initial dose at baseline of10 mg once daily, and if eGFR at screening\nwas$60 mL/min/... | [
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-... |
was$60 mL/min/1.73 m\n2, the initial dose\nwas 20 mg once daily. An increase in thedose from 10 to 20 mg once daily was en-\ncouraged after 1 month, provided the se-rum potassium level was #4.8 mmol/L\nand eGFR was stable. The mean age ofparticipants was 64.1 years (31% were fe-\nmale), and the median follow-up duratio... | [
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male), and the median follow-up duration\nwas 3.4 years. The median A1C was7.7%, the mean systolic blood pressurewas 136 mmHg, and the mean GFR was\n67.8 mL/min/1.73 m\n2.P e o p l ew i t hh e a r t\nfailure with a reduced ejection fraction\nand uncontrolled hypertension wereexcluded.\nThe primary composite outcome was | [
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... |
The primary composite outcome was\ncardiovascular death, myocardial infarc-tion, stroke, and hospitalization for heartfailure. The finerenone group showed a\n13% reduction in the primary end point\ncompared with the placebo group (12.4%\nvs. 14.2%; HR 0.87 [95% CI 0.76 –0.98];\nP=0 . 0 3 ) .T h i sb e n e fit was primari... | [
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P=0 . 0 3 ) .T h i sb e n e fit was primarily\ndriven by a reduction in heart failure hos-\npitalizations: 3.2% vs. 4.4% in the placebo\ngroup (HR 0.71 [95% CI 0.56– 0.90]).\nOf the secondary outcomes, the most\nnoteworthy was a 36% reduction inESKD: 0.9% vs. 1.3% in the placebo group\n(HR 0.64 [95% CI 0.41– 0.995]). Th... | [
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(HR 0.64 [95% CI 0.41– 0.995]). There was\na higher incidence of hyperkalemia in\nthefinerenone group, 10.8% vs. 5.3%, al-\nthough only 1.2% of the 3,686 individuals\nonfinerenone stopped the study due to\nhyperkalemia.\nThe FIDELITY prespeci fied pooled effi -\ncacy and safety analysis incorporated in-\ndividuals from bot... | [
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dividuals from both the FIGARO-DKD\nand FIDELIO-DKD trials ( N= 13,171) to\nallow for evaluation across the spec-\ntrum of severity of CKD, since the popu-lations were different (with a slight\noverlap) and the study designs were\nsimilar (119). The analysis showed a14% reduction in composite cardiovas-cular death, non... | [
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... |
tion, nonfatal stroke, and hospitalization\nfor heart failure for finerenone vs. pla-\ncebo (12.7% vs. 14.4%; HR 0.86 [95% CI0.78–0.95]; P= 0.0018).\nIt also demonstrated a 23% reduction\nin the composite kidney outcome, con-sisting of sustained $57% decrease in\neGFR from baseline over $4w e e k s ,o r\nrenal death, fo... | [
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renal death, for finerenone vs. placebo\n(5.5% vs. 7.1%; HR 0.77 [95% CI 0.67 –\n0.88]; P=0 . 0 0 0 2 ) .\nThe pooled FIDELITY trial analysis\nconfirms and strengthens the positive\ncardiovascular and renal outcomes with\nfinerenone across the spectrum of CKD, | [
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finerenone across the spectrum of CKD,\nirrespective of baseline ASCVD history(with the exclusion of those with heartfailure with reduced ejection fraction).\nREFERRAL TO A NEPHROLOGIST\nHealth care professionals should con-\nsider referral to a nephrologist if the in- | [
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... |
sider referral to a nephrologist if the in-\ndividual with diabetes has continuouslyrising UACR levels and/or continuouslydeclining eGFR, if there is uncertaintyabout the etiology of kidney disease, fordifficult management issues (anemia,\nsecondary hyperparathyroidism, signi fi- | [
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0.... |
secondary hyperparathyroidism, signi fi-\ncant increases in albuminuria in spite ofgood blood pressure management, met-abolic bone disease, resistant hyperten-sion, or electrolyte disturbances), orwhen there is advanced kidney disease(eGFR<30 mL/min/1.73 m\n2) requiring | [
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0... |
2) requiring\ndiscussion of renal replacement therapyfor ESKD (1). The threshold for referralmay vary depending on the frequencywith which a health care professionalencounters people with diabetes andkidney disease. Consultation with a ne-phrologist when stage 4 CKD develops\n(eGFR<30 mL/min/1.73 m\n2)h a sb e e n | [
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-0.01... |
(eGFR<30 mL/min/1.73 m\n2)h a sb e e n\nfound to reduce cost, improve quality of\ncare, and delay dialysis (120).\nHowever, other specialists and health\ncare professionals should also educatepeople with diabetes about the progres-sive nature of CKD, the kidney preserva-tion bene fits of proactive treatment of | [
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0.012121259234845638,
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blood pressure and blood glucose, andthe potential need for renal replace-ment therapy.\nReferences\n1. de Boer IH, Khunti K, Sadusky T, et al. Dia-\nbetes management in chronic kidney disease: aconsensus report by the American DiabetesAssociation (ADA) and Kidney Disease: ImprovingGlobal Outcomes (KDIGO). Diabetes Car... | [
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0.07332068681716919,
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0.031387679278850555,
0.04943351820111275,
-0.0186591986566782,
-0.04752030968666077,
-0.05652107298374176,
0.05028272420167923,
-0.10209163278341293,
-0.03571... |
2. Afkarian M, Zelnick LR, Hall YN, et al. Clinicalmanifestations of kidney disease among USadults with diabetes, 1988-2014. JAMA 2016;316:602– 610\n3. de Boer IH, Rue TC, Hall YN, Heagerty PJ,Weiss NS, Himmelfarb J. Temporal trends in theprevalence of diabetic kidney disease in theUnited States. JAMA 2011;305:2532– 25... | [
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0.017424069344997406,
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-0.018572373315691948,
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0.011233827099204063,
-0.02944682538509369,
-0.08226975053548813,
0.07986337691545486,
-0.04231073334813118,
0.0... |
4. DCCT/EDIC Research Group. Kidney diseaseand related findings in the Diabetes Control and\nComplications Trial/Epidemiology of DiabetesInterventions and Complications study. DiabetesCare 2014;37:24– 30 | [
-0.02547912858426571,
0.027534034103155136,
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0.05326775461435318,
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-0.015122945420444012,
-0.03105676919221878,
0.03747346252202988,
-0.03625979647040367,
... |
5. Johansen KL, Chertow GM, Foley RN, et al. USRenal Data System 2020 annual data report:epidemiology of kidney disease in the UnitedStates. Am J Kidney Dis 2021;77(Suppl. 1):A7 –A8 | [
0.03283115103840828,
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0.0026773237623274326,
-0.04518553242087364,
0.021007712930440903,
0.0160976592451334,
-0.001... |
6. Fox CS, Matsushita K, Woodward M, et al.;Chronic Kidney Disease Prognosis Consortium.Associations of kidney disease measures withdiabetesjournals.org/care Chronic Kidney Disease and Risk Management S227\n©AmericanDiabetesAssociation | [
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0.04469377547502518,
0.008436821401119232,
-0... |
12. Retinopathy, Neuropathy, and\nFoot Care: Standards of Care in\nDiabetes —2024\nDiabetes Care 2024;47(Suppl. 1):S231 –S243 |https://doi.org/10.2337/dc24-S012American Diabetes Association\nProfessional Practice Committee *\nThe American Diabetes Association (ADA) “Standards of Care in Diabetes ”in- | [
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0.06272593885660172,
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0.04345559701323509,
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0.08375359326601028,
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0.02610... |
cludes the ADA ’s current clinical practice recommendations and is intended to\nprovide the components of diabetes care, general treatment goals and guide-\nlines, and tools to evaluate quality of care. Members of the ADA Professional\nPractice Committee, an interprofessional expert committee, are responsible for | [
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-0.06803533434867859,
0.05765634775161743,
-0.0445377491414547,
0.0022847396321594715,
0.07311242073774338,
0.07738664746284485,
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0.01100181881338358,
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0.036391... |
updating the Standards of Care annually, or more frequently as warranted. For adetailed description of ADA standards, statements, and reports, as well as theevidence-grading system for ADA ’s clinical practice recommendations and a full | [
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-0.0514310747385025,
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0.019980253651738167,
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0.013412732630968094,
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-0.07326127588748932,
0.0121... |
list of Professional Practice Committee members, please refer to Introductionand Methodology. Readers who wish to comment on the Standards of Care areinvited to do so at professional.diabetes.org/SOC.\nFor prevention and management of diabetes complications in children and adoles-\ncents, please refer to Section 14, “C... | [
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-0.10003404319286346,
0.00661... |
cents, please refer to Section 14, “Children and Adolescents. ”\nDIABETIC RETINOPATHY\nRecommendations\n12.1 Implement strategies to help people with diabetes reach glycemic goals\nto reduce the risk or slow the progression of diabetic retinopathy. A\n12.2 Implement strategies to help people with diabetes reach blood p... | [
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0.12768951058387756,
0.01203159336000681,
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0.07931753247976303,
0.016733365133404732,
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0.023275... |
lipid goals to reduce the risk or slow the progression of diabetic retinopathy. A\nDiabetic retinopathy is a highly speci fic neurovascular complication of both type 1 | [
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and type 2 diabetes, with prevalence strongly related to both the duration of diabe-tes and the level of glycemic control (1). Diabetic retinopathy is the most frequentcause of new cases of blindness among adults aged 20 –74 years in developed coun-\ntries. Glaucoma, cataracts, and other eye disorders occur earlier and... | [
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in people with diabetes.\nIn addition to diabetes duration, factors that increase the risk of, or are associated\nwith, retinopathy include chronic hyperglycemia (2,3), nephropathy (4), hypertension | [
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0.00... |
(5), and dyslipidemia (6). Intensive diabetes management with the goal of achievingnear-normoglycemia has been shown in large prospective randomized studies to pre-\nvent and/or delay the onset and progression of diabetic retinopathy, reduce the | [
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need for future ocular surgical procedures, and potentially improve self-reported vi-sual function (2,7 –10). A meta-analysis of data from cardiovascular outcomes studies | [
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showed no association between glucagon-like peptide 1 receptor agonist (GLP-1 RA)treatment and retinopathy per se, except through the association between retinopa-thy and average A1C reduction at the 3-month and 1-year follow-up. Long-term*A complete list of members of the American | [
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Diabetes Association Professional Practice Committeecan be found at https://doi.org/10.2337/dc24-SINT.\nDuality of interest information for each author is\navailable at https://doi.org/10.2337/dc24-SDIS.\nSuggested citation: American Diabetes Associ-\nation Professional Practice Committee. 12. Retino-pathy, neuropathy,... | [
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Care in Diabetes— 2024 . Diabetes Care 2024;47\n(Suppl. 1):S231– S243\n© 2023 by the American Diabetes Association.Readers may use this article as long as thework is properly cited, the use is educationaland not for pro fit, and the work is not altered. | [
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More information is available at https://www.diabetesjournals.org/journals/pages/license.12. RETINOPATHY, NEUROPATHY, AND FOOT CAREDiabetes Care Volume 47, Supplement 1, January 2024 S231\n©AmericanDiabetesAssociation | [
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impact of improved glycemic control on\nretinopathy was not studied in these tri-als. However, GLP-1 RAs including lira-\nglutide, semaglutide, and dulaglutide\nhave been shown to be associated\nwith an increased risk of rapidly wors-\nening diabetic retinopathy in random-ized trials. Further data from clinical\nstudie... | [
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studies with longer follow-up purposefully\ndesigned for diabetic retinopathy risk as-\nsessment, particularly including individu-\nals with established diabetic retinopathy,\nare warranted. Retinopathy status should\nbe assessed when intensifying glucose-lowering therapies such as those using\nGLP-1 RAs, since rapid r... | [
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GLP-1 RAs, since rapid reductions in A1C\ncan be associated with initial worsen-\ning of retinopathy (11).\nScreening\nRecommendations\n12.3 Adults with type 1 diabetes should\nhave an initial dilated and comprehen-\nsive eye examination by an ophthalmol-ogist or optometrist within 5 years afterthe onset of diabetes. B... | [
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12.4 People with type 2 diabetes\nshould have an initial dilated andcomprehensive eye examination byan ophthalmologist or optometrist atthe time of the diabetes diagnosis. B\n12.5 I ft h e r ei sn oe v i d e n c eo fr e t i n o p a -\nthy from one or more annual eye ex-ams and glycemic indicators are within\nthe goal r... | [
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the goal range, then screening every\n1–2y e a r sm a yb ec o n s i d e r e d .I fa n y\nlevel of diabetic retinopathy is present,subsequent dilated retinal examinationsshould be repeated at least annually byan ophthalmologist or optometrist. Ifretinopathy is progressing or sight-threatening, then examinations willbe r... | [
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12.6 Programs that use retinal pho-\ntography with remote reading orthe use of U.S. Food and Drug Ad-ministration –approved artifi cial intelli- | [
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gence algorithms to improve accessto diabetic retinopathy screening areappropriate screening strategies fordiabetic retinopathy. Such programsneed to provide pathways for timelyreferral for a comprehensive eye ex-amination when indicated. B\n12.7 Counsel individuals of child-\nbearing potential with preexistingtype 1 o... | [
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bearing potential with preexistingtype 1 or type 2 diabetes who are\nplanning pregnancy or who are preg-\nnant on the risk of developmentand/or progression of diabetic reti-\nnopathy. B\n12.8 Individuals with preexisting type 1\nor type 2 diabetes should receive aneye exam before pregnancy and in thefirst trimester and ... | [
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tored every trimester and for 1 yearpostpartum as indicated by the degree\nof retinopathy. B\nThe preventive effects of therapy and\nthe fact that individuals with any level of\ndiabetic retinopathy or macular edema\nmay be asymptomatic provide strong\nsupport for screening to detect diabetic\nretinopathy. Prompt diagn... | [
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retinopathy. Prompt diagnosis allows tri-\nage of people with diabetes and timely\nintervention that may prevent vision loss\nin individuals who are asymptomatic de-\nspite advanced diabetic eye disease.\nDiabetic retinopathy screening should\nbe performed using validated approaches\nand methodologies. Youth with type ... | [
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and methodologies. Youth with type 1 or\ntype 2 diabetes are also at risk for com-\nplications and need to be screened for\ndiabetic retinopathy (12) (see Section 14,\n“Children and Adolescents ”). If diabetic\nretinopathy is evident on screening,prompt referral to an ophthalmologist\nis recommended. Subsequent examina... | [
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is recommended. Subsequent examina-\ntions for individuals with type 1 or type 2\ndiabetes are generally repeated annually\nfor individuals with minimal to no reti-\nnopathy. Exams every 1 –2y e a r sm a yb e\ncost-effective after one or more normaleye exams. In a population with well-\ncontrolled type 2 diabetes, ther... | [
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controlled type 2 diabetes, there was lit-\ntle risk of development of signi ficant reti-\nnopathy within a 3-year interval after anormal examination (13), and less fre-\nquent intervals have been found in simu-\nlated modeling to be potentially effective\nin screening for diabetic retinopathy in | [
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in screening for diabetic retinopathy in\nindividuals without diabetic retinopathy(14). However, it is important to adjust\nscreening intervals based on the pres-\nence of speci fic risk factors for retinop-\nathy onset and worsening retinopathy.More frequent examinations by the\nophthalmologist will be required if reti... | [
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ophthalmologist will be required if reti-\nnopathy is progressing or risk factors\nsuch as uncontrolled hyperglycemia, ad-\nvanced baseline retinopathy, or diabetic\nmacular edema are present.\nRetinal photography with remote read-\ning by experts has great potential to pro-vide screening services in areas where | [
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qualified eye care professionals are notreadily available (15 –17). High-quality\nfundus photographs can detect most clin-\nically signi ficant diabetic retinopathy. In-\nterpretation of the images should be\nperformed by a trained eye care profes-\nsional. Retinal photography may also en-hance ef ficiency and reduce cost... | [
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the expertise of ophthalmologists can be\nused for more complex examinations\nand for therapy (15,18,19). In-person ex-ams are still necessary when the retinalphotos are of unacceptable quality and\nfor follow-up if abnormalities are detected. | [
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for follow-up if abnormalities are detected.\nRetinal photos are not a substitute for di-lated comprehensive eye exams, whichshould be performed at least initially and\nat yearly intervals thereafter or more fre-\nquently as recommended by an eye careprofessional. Arti ficial intelligence systems\nthat detect more than ... | [
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that detect more than mild diabetic reti-\nnopathy and diabetic macular edema, au-\nthorized for use by the U.S. Food andDrug Administration (FDA), represent analternative to traditional screening ap-\nproaches (20). There are now three FDA-\napproved arti ficial intelligence algorithms | [
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approved arti ficial intelligence algorithms\nfor diabetic retinopathy screening andexamination. These services are now cov-\nered by most insurances. There are pub-\nlished prospective multicenter clinical trialson the diagnostic accuracy for each (21 –23).\nHowever, the bene fits and optimal utiliza- | [
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However, the bene fits and optimal utiliza-\ntion of this type of screening have yet to befully determined. Results of all screeningeye examinations should be documenteda n dt r a n s m i t t e dt ot h er e f e r r i n gh e a l t hc a r e\nprofessional.\nType 1 Diabetes\nBecause retinopathy is estimated to take at | [
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Type 1 Diabetes\nBecause retinopathy is estimated to take at\nleast 5 years to develop after the onset ofhyperglycemia, people with type 1 diabetes\nshould have an initial dilated and compre-\nhensive eye examination within 5 years af-ter the diagnosis of diabetes (14).\nType 2 Diabetes\nPeople with type 2 diabetes who... | [
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Type 2 Diabetes\nPeople with type 2 diabetes who may\nhave had years of undiagnosed diabetes\nand have a signi ficant risk of prevalent\ndiabetic retinopathy at the time of diag-nosis should have an initial dilated and\ncomprehensive eye examination at the\ntime of diagnosis.\nPregnancy | [
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comprehensive eye examination at the\ntime of diagnosis.\nPregnancy\nIndividuals who develop gestational di-abetes mellitus do not require eye ex-\naminations during pregnancy since they\ndo not appear to be at increased risk ofS232 Retinopathy, Neuropathy, and Foot Care Diabetes Care Volume 47, Supplement 1, January 2... | [
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developing diabetic retinopathy during\npregnancy (24). However, individuals of\nchildbearing potential with preexistingtype 1 or type 2 diabetes who are plan-ning pregnancy or who have become\npregnant should be counseled on the | [
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pregnant should be counseled on the\nbaseline prevalence and risk of devel-opment and/or progression of diabeticretinopathy. In a systematic review andmeta-analysis of 18 observational stud-\nies of pregnant individuals with preex-\nisting type 1 or type 2 diabetes, theprevalence of any diabetic retinopathyand prolifer... | [
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(PDR) in early pregnancy was 52.3%\nand 6.1%, respectively. The pooled pro-gression rate per 100 pregnancies fornew diabetic retinopathy development\nwas 15.0 (95% CI 9.9 –20.8), worsened\nnonproliferative diabetic retinopathy was\n31.0 (95% CI 23.2 –39.2), pooled sight-\nthreatening progression rate from non-prolifera... | [
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was 6.3 (95% CI 3.3 –10.0), and worsened\nPDR was 37.0 (95% CI 21.2 –54.0), demon-\nstrating that close follow-up should be\nmaintained during pregnancy to prevent\nvision loss (25). In addition, rapid imple-\nmentation of intensive glycemic man-agement in the setting of retinopathy isassociated with early worsening of... | [
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A systematic review and meta-analysis\nand a controlled prospective study dem-onstrate that pregnancy in individualswith type 1 diabetes may aggravate reti-nopathy and threaten vision, especiallywhen glycemic management is poor or\nretinopathy severity is advanced at the | [
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retinopathy severity is advanced at the\ntime of conception (25,26). Laser photo-coagulation surgery can minimize therisk of vision loss during pregnancy for\nindividuals with high-risk PDR or center-\ninvolved diabetic macular edema (26).The use of anti –vascular endothelial | [
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growth factor (anti-VEGF) injections inpregnant individuals may be justi fied\nonly if the potential bene fit outweighs\nthe potential risk to the fetus and onlyif clearly indicated. Current anti-VEGFmedications have been assigned to\npregnancy category C by the FDA (ani-\nmal studies have revealed evidence ofembryo –fet... | [
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controlled data in human pregnancy),\nand caution should be used in pregnant\nindividuals with diabetes because oftheoretical risks to the vasculature ofthe developing fetus.Treatment\nRecommendations\n12.9 Promptly refer individuals with\nany level of diabetic macular edema,\nmoderate or worse nonproliferative di- | [
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moderate or worse nonproliferative di-\nabetic retinopathy (a precursor of pro-liferative diabetic retinopathy [PDR]),or any PDR to an ophthalmologist\nwho is knowledgeable and experi-\nenced in the management of dia-betic retinopathy. A\n12.10 Panretinal laser photocoagu- | [
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12.10 Panretinal laser photocoagu-\nlation therapy is indicated to reducethe risk of vision loss in individualswith high-risk PDR and, in some cases,severe nonproliferative diabetic reti-\nnopathy. A\n12.11 Intravitreous injections of anti –\nvascular endothelial growth factor | [
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0.03659217432141304,
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0.0232... |
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