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should be altered such that it applies to\nall. Hence, a committee was convened,resulting in the recommendation for im-mediate implementation of the Chronic\nKidney Disease Epidemiology Collabora-\ntion (CKD-EPI) creatinine equation re fit\nwithout the race variable in all laborato-ries in the U.S. (17). The CKD-EPI Re ... | [
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equation is the eGFR formula that is\nnow recommended for everyone (18).\nAdditionally, increased use of cystatin C(another marker of eGFR) is suggested incombination with serum creatinine be-\ncause combining filtration markers (cre-\natinine and cystatin C) is more accurateand would support better clinical deci-sions ... | [
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DIAGNOSIS OF DIABETIC KIDNEY\nDISEASE\nDiabetic kidney disease is a clinical diag-\nnosis made based on the presence ofalbuminuria and/or reduced eGFR inthe absence of signs or symptoms ofother primary causes of kidney damage.\nThe typical presentation of diabetic kid- | [
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The typical presentation of diabetic kid-\nney disease is considered to includelong-standing duration of diabetes, reti-nopathy, albuminuria without gross he-maturia, and gradually progressive lossof eGFR. However, signs of diabetic kid-\nney disease may be present at diagnosis | [
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ney disease may be present at diagnosis\nor without retinopathy in type 2 diabe-tes. Reduced eGFR without albuminuriahas been frequently reported in type 1and type 2 diabetes and is becomingmore common over time as the preva-\nlence of diabetes increases in the U.S.\n(2,3,16,19– 21). An active urinary sedi- | [
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(2,3,16,19– 21). An active urinary sedi-\nment (containing red or white bloodcells or cellular casts), rapidly increasingalbuminuria or total proteinuria, thepresence of nephrotic syndrome, rapidly\ndecreasing eGFR, or the absence of reti- | [
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decreasing eGFR, or the absence of reti-\nnopathy (in type 1 diabetes) suggests al-ternative or additional causes of kidneydisease. For individuals with these fea-tures, referral to a nephrologist for fur-ther diagnosis, including the possibility\nof kidney biopsy, should be considered. | [
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of kidney biopsy, should be considered.\nIt is rare for people with type 1 diabetesto develop kidney disease without reti-nopathy. In type 2 diabetes, retinopathy isonly moderately sensitive and speci ficf o r\nCKD caused by diabetes, as con firmed by\nkidney biopsy (22).\nSTAGING OF CHRONIC KIDNEY\nDISEASE\nStage G1 and... | [
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DISEASE\nStage G1 and stage G2 CKD are de fined\nby evidence of high albuminuria with\neGFR$60 mL/min/1.73 m2, and stages\nG3–G5 CKD are de fined by progressively\nlower ranges of eGFR (23) ( Fig. 11.1 ). At | [
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lower ranges of eGFR (23) ( Fig. 11.1 ). At\nany eGFR, the degree of albuminuria isassociated with risk of cardiovascular dis-ease (CVD), CKD progression, and mortal-ity (6). Therefore, there is an additionalsubclassifi cation by level of urine albumin\n(Fig. 11.1). Furthermore, Kidney Disease: | [
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(Fig. 11.1). Furthermore, Kidney Disease:\nImproving Global Outcomes (KDIGO)recommends a more comprehensiveCKD staging that incorporates albumin-uria at all stages of eGFR; this system isdiabetesjournals.org/care Chronic Kidney Disease and Risk Management S221\n©AmericanDiabetesAssociation | [
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more closely associated with risk but is\nalso more complex and does not trans-late directly to treatment decisions (1).\nThus, based on the current classi fication\nsystem, both eGFR and albuminuriamust be quanti fied to guide treatment\ndecisions. Quanti fication of eGFR levels\nis essential for modi fications of medica- | [
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is essential for modi fications of medica-\ntion dosages or restrictions of use ( Fig.\n11.1) (23,24), and the degree of albu-\nminuria should in fluence the choice of\nantihypertensive medications (see Sec-\ntion 10, “Cardiovascular Disease and\nRisk Management ”)o rg l u c o s e - l o w e r i n g | [
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Risk Management ”)o rg l u c o s e - l o w e r i n g\nmedications (see below). Observed his-tory of eGFR loss (which is also associ-\nated with risk of CKD progression and\nother adverse health outcomes) and\ncause of kidney damage (including pos-\nsible causes other than diabetes) may\nalso affect these decisions (25)... | [
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also affect these decisions (25).\nACUTE KIDNEY INJURY\nAcute kidney injury (AKI) is diagnosed by asustained increase in serum creatinine\nover a short period of time, which is also\nrefle c t e da sar a p i dd e c r e a s ei ne G F R\n(26,27). People with diabetes are at higherrisk of AKI than those without diabetes | [
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(28). Other risk factors for AKI include pre-\nexisting CKD, the use of medications that\ncause kidney injury (e.g., nonsteroidal\nanti-in flammatory drugs), certain intrave-\nnous dyes (e.g., iodinated radiocontrast\nagents) and the use of medications that\nalter renal blood flow and intrarenal he- | [
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alter renal blood flow and intrarenal he-\nmodynamics. In particular, many antihy-pertensive medications (e.g., diuretics,\nACE inhibitors, and angiotensin receptor\nblockers [ARBs]) can reduce intravascular\nvolume, renal blood flow, and/or glomer-\nular filtration. There was concern that\nsodium –glucose cotransporter 2... | [
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sodium –glucose cotransporter 2 (SGLT2)\ninhibitors may promote AKI through vol-ume depletion, particularly when com-bined with diuretics or other medications\nthat reduce glomerular filtration; how-\never, this has not been found to be truein randomized clinical outcome trials of\nadvanced kidney disease (29) or high C... | [
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advanced kidney disease (29) or high CVD\nrisk with normal kidney function (30 –32).\nIt is also noteworthy that the nonsteroi-dal mineralocorticoid receptor antago-\nnists (MRAs) do not increase the risk of\nAKI when used to slow kidney disease\nprogression (33). Timely identi fication\nand treatment of AKI is importan... | [
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and treatment of AKI is important be-\ncause AKI is associated with increasedrisks of progressive CKD and other poor\nhealth outcomes (34).\nElevations in serum creatinine (up to\n30% from baseline) with renin-angioten-\nsin system (RAS) blockers (such as ACEinhibitors and ARBs) must not be con-\nfused with AKI (35). A... | [
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fused with AKI (35). An analysis of the\nAction to Control Cardiovascular Risk inDiabetes Blood Pressure (ACCORD BP)trial demonstrated that participants ran-\ndomized to intensive blood pressure | [
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domized to intensive blood pressure\nlowering with up to a 30% increase in se-rum creatinine did not have any increasein mortality or progressive kidney disease(36,37). Moreover, a measure of markers\nfor AKI showed no signi ficant increase\nof any markers with increased creatinine | [
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of any markers with increased creatinine\n(37). Accordingly, ACE inhibitors and ARBsshould not be discontinued for increases\nin serum creatinine ( <30%) in the ab-\nsence of volume depletion.\nSURVEILLANCE\nBoth albuminuria and eGFR should be\nmonitored annually to enable timely di-\nagnosis of CKD, monitor progressio... | [
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agnosis of CKD, monitor progression of\nCKD, detect superimposed kidney dis-eases including AKI, assess risk of CKDcomplications, dose medications appro-\npriately, and determine whether ne-\nphrology referral is needed. Amongpeople with existing kidney disease, al-buminuria and eGFR may change due to\nprogression of C... | [
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progression of CKD, development of a\nseparate superimposed cause of kidneydisease, AKI, or other effects of medica-tions, as noted above. Serum potassiumshould also be monitored in individuals\ntreated with diuretics because these\nmedications can cause hypokalemia,which is associated with cardiovascularrisk and morta... | [
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with eGFR <60 mL/min/1.73 m\n2re-\nceiving ACE inhibitors, ARBs, or MRAs\nshould have serum potassium mea-sured periodically. Additionally, people\nwith this lower range of eGFR should\nhave their medication dosing veri fied,\ntheir exposure to nephrotoxins (e.g.,\nnonsteroidal anti-in flammatory drugs\nand iodinated con... | [
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and iodinated contrast) should be min-\nimized, and they should be evaluatedfor potential CKD complications ( Table\n11.1 ).\nThere is a clear need for annual quan-\ntitative assessment of urinary albumin\nexcretion. This is especially true after a | [
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excretion. This is especially true after a\ndiagnosis of albuminuria, institution of ACEinhibitors or ARB therapy to maximumtolerated doses, and achievement of blood\npressure targets. Early changes in kidney\nfunction may be detected by increases inalbuminuria before changes in eGFR (41),and this also signifi cantly af... | [
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cular risk. Moreover, an initial reduction of\n>30% from baseline, subsequently main-\ntained over at least 2 years, is considered\na valid surrogate for renal bene fitb y\nthe Division of Cardiology and Nephrol-ogy of the U.S. Food and Drug Adminis-tration (FDA) (9). Continued surve illance | [
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can assess both response to therapy anddisease progression and may aid in as-sessing participation in ACE inhibitor orARB therapy. In addition, in clinical trialsof ACE inhibitors or ARB therapy in peo-\nple with type 2 diabetes, reducing albu-\nminuria to levels <300 mg/g creatinine\nor by>30% from baseline has been a... | [
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or by>30% from baseline has been asso-\nciated with improved renal and cardiovas-cular outcomes, leading some to suggestthat medications should be titrated to\nmaximize reduction in UACR. Data from\npost hoc analyses demonstrate less bene-fit on cardiorenal outcomes at half doses | [
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of RAS blockade (42). In type 1 diabetes,remission of albuminuria may occur spon-\ntaneously, and cohort studies evaluating\nassociations of change in albuminuriawith clinical outcomes have reportedinconsistent results (43,44).\nThe prevalence of CKD complications\ncorrelates with eGFR (40). When eGFRis<60 mL/min/1.73 ... | [
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0.... |
2, screening for\ncomplications of CKD is indicated ( Table\n11.1). Early vaccination against hepatitis\nB virus is indicated in individuals likelyto progress to ESKD (see Section 4,“Comprehensive Medical Evaluation and\nAssessment of Comorbidities, ”for further\ninformation on immunization).\nPrevention | [
-0.01585458405315876,
0.03854553773999214,
-0.0250284094363451,
-0.0663311630487442,
0.023074481636285782,
0.09157334268093109,
0.0402645468711853,
0.07885969430208206,
-0.024341626092791557,
0.01181527879089117,
0.03283369168639183,
-0.025428401306271553,
0.04035123065114021,
-0.018600758... |
information on immunization).\nPrevention\nThe only proven primary prevention in-terventions for CKD in people with diabe-tes are blood glucose (A1C goal of 7%)and blood pressure control (blood pres-sure<130/80 mmHg). There is no evi-\ndence that renin-angiotensin-aldosterone\nsystem inhibitors or any other interven- | [
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0.1003083735704422,
0.0030599485617130995,
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0.01737377606332302,
0.031839098781347275,
0.08672327548265457,
0.011937716975808144,
0.010409196838736534,
0.010413927026093006,
0.01586814410984516,
-0.022067822515964508,
0.01755... |
system inhibitors or any other interven-\ntions prevent the development of dia-betic kidney disease in the absence ofhypertension or albuminuria. Thus, theAmerican Diabetes Association does notrecommend routine use of these medica-\ntions solely for the purpose of preven- | [
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0.039908070117235184,
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0.012548277154564857,
0.07151485979557037,
0.05122951790690422,
-0.008180901408195496,
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0.08451537787914276,
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-0... |
tions solely for the purpose of preven-\ntion of the development of diabetickidney disease.S222 Chronic Kidney Disease and Risk Management Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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0.03606749325990677,
0.09304419904947281,
0.009351888671517372,
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0.016278522089123726,
0.05397108569741249,
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0.02... |
INTERVENTIONS\nNutrition\nFor people with non –dialysis-dependent\nCKD, dietary protein intake should be\n/C240.8 g/kg body weight per day (the rec-\nommended daily allowance) (1). Com-\npared with higher levels of dietary\nprotein intake, this level slowed GFR de-\ncline with evidence of a greater effect\nover time. H... | [
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0.07857482135295868,
-0.00696245301514864,
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0.019010096788406372,
0.09743526577949524,
-0.056704066693782806,
-0.06250248104333878,
0.019802292808890343,
0.01484643667936325,
-0.07805822789669037,
-0.005... |
over time. Higher levels of dietary pro-\ntein intake ( >20% of daily calories from\nprotein or >1.3 g/kg/day) have been\nassociated with increased albuminuria,more rapid kidney function loss, and\nCVD mortality and therefore should be\navoided. Reducing the amount of dietary\nprotein below the recommended dailyallowan... | [
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0.036614760756492615,
0.02189158834517002,
0.0457947663962841,
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-0.007487072609364986,
0.11573158949613571,
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-0.056052066385746,
0.011612064205110073,
0.05319022759795189,
-0.04899974167346954,
0.030... |
mended because it does not alter blood\nglucose levels, cardiovascular risk meas-\nures, or the course of GFR decline (45).\nRestriction of dietary sodium (to\n<2,300 mg/day) may be useful to con-\ntrol blood pressure and reduce cardiovas-cular risk (46,47), and individualization of\ndietary potassium may be necessary ... | [
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0.06665660440921783,
0.019944142550230026,
0.0602685771882534,
-0.01794145070016384,
-0.017423445358872414,
0.009154175408184528,
0.012056685984134674,
-0.06282505393028259,
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0.035402778536081314,
-0.045359984040260315,
0.... |
dietary potassium may be necessary to\ncontrol serum potassium concentrations\n(28,38 –40). These interventions may be\nmost important for individuals with re-\nduced eGFR, for whom urinary excretion\nof sodium and potassium may be im-\npaired. For individuals on dialysis, higher\nlevels of dietary protein intake shoul... | [
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0.009724653325974941,
0.07422320544719696,
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0.07635516673326492,
0.055724505335092545,
-0.021689463406801224,
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0.019012194126844406,
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0.0... |
levels of dietary protein intake should be\nconsidered since malnutrition is a major\nproblem for some individuals on dialysis(48). Recommendations for dietary sodium\nand potassium intake should be individual-\nized based on comorbid conditions, medi-\ncation use, blood pressure, and laboratory\ndata.Glycemic Goals | [
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0.008857226930558681,
0.04382910951972008,
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-0.005569778848439455,
0.032269030809402466,
0.06941363215446472,
-0.08413582295179367,
-0.09147714823484421,
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0.024110224097967148,
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cation use, blood pressure, and laboratory\ndata.Glycemic Goals\nIntensive lowering of blood glucose with\nthe goal of achieving near-normoglycemia\nhas been shown in large, randomized\nstudies to delay the onset and progres-\nsion of albuminuria and reduce eGFR in\npeople with type 1 diabetes (49,50)\nand type 2 diabe... | [
0.05341619625687599,
0.06888386607170105,
-0.05122237652540207,
0.019816214218735695,
-0.04659246653318405,
0.033842962235212326,
0.09404890239238739,
0.09523064643144608,
-0.07131979614496231,
0.020181484520435333,
-0.043731771409511566,
-0.005393597763031721,
-0.09420888125896454,
0.0024... |
and type 2 diabetes (1,51 –56). Insulin\nalone was used to lower blood glucosein the Diabetes Control and Complica-\ntions Trial (DCCT)/Epidemiology of Dia-\nbetes Interventions and Complications\n(EDIC) study of type 1 diabetes, while a\nvariety of agents were used in clinical | [
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0.05914362147450447,
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0.016303321346640587,
0.05070178583264351,
0.14207035303115845,
-0.06852757930755615,
-0.002326053800061345,
0.0017080368706956506,
0.1053214892745018,
-0.05016569793224335,
0.04504... |
variety of agents were used in clinical\ntrials of type 2 diabetes, supporting theconclusion that lowering blood glucose\nitself helps prevent CKD and its progres-\nsion. The effects of glucose-lowering ther-\napies on CKD have helped de fine A1C\ngoals.\nThe presence of CKD affects the risks\nand bene fits of intensive ... | [
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0.05838008597493172,
-0.012529968284070492,
0.15267017483711243,
0.030235301703214645,
0.023204656317830086,
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0.0963190570473671,
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-0.05... |
and bene fits of intensive lowering of\nblood glucose and a number of speci fic\nglucose-lowering medications. Adverse\neffects of intensive management of\nblood glucose levels (hypoglycemia and\nmortality) were increased among peoplewith kidney disease at baseline (57).\nMoreover, there is a lag time of at least | [
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0.021842889487743378,
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0.1137058213353157,
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0.10291871428489685,
-0.01165110245347023,
... |
Moreover, there is a lag time of at least\n2y e a r si nt y p e2d i a b e t e st oo v e r1 0\nyears in type 1 diabetes for the effects\nof intensive glucose control to manifest\nas improved eGFR outcomes (54,58,59).\nTherefore, in some people with preva-\nlent CKD and substantial comorbidity,\ntreatment may be less int... | [
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0.019025087356567383,
0.06658140569925308,
0.03493482619524002,
0.0031536747701466084,
-0.03726009279489517,
0.08470980077981949,
0.027699990198016167,
-0.019211506471037865,
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0.11181483417749405,
-0.07312344014644623,
-0.03... |
treatment may be less intensive (i.e.,\nA1C goals may be higher) to decrease\nthe risk of hypoglycemia (1,60). A1C lev-\nels are also less reliable at advanced\nCKD stages.Blood Pressure and Use of ACE\nInhibitors and Angiotensin ReceptorBlockers\nACE inhibitors and ARBs remain a main-\nstay of management for people wi... | [
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-0.05153890326619148,
0.017921974882483482,
0.0012193795992061496,
0.02301490306854248,
-0.027148066088557243,
0.12525969743728638,
0.0003486606292426586,
0.003526141634210944,
-0.046754442155361176,
0.04973218962550163,
-0.02982894517481327,
-... |
stay of management for people with\nCKD with albuminuria and for the treat-ment of hypertension in people with di-\nabetes (with or without diabetic kidney\ndisease). Indeed, all the trials that eval-uated the bene fits of SGLT2 inhibition | [
-0.04237323999404907,
0.03234749659895897,
-0.050110578536987305,
-0.011979128234088421,
-0.00342648196965456,
0.003911095205694437,
0.03797565773129463,
0.08147735148668289,
-0.02516886219382286,
-0.06103852391242981,
0.05316755548119545,
0.05752488225698471,
-0.04563510790467262,
0.01161... |
or nonsteroidal mineralocorticoid recep-tor antagonist effects were done in indi-viduals who were being treated with an\nACE inhibitor or ARB, in some trials up\nto maximum tolerated doses.\nHypertension is a strong risk factor\nfor the development and progression of\nCKD (61). Antihypertensive therapy re-\nduces the r... | [
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-0.004696852061897516,
-0.04315560311079025,
0.002444495214149356,
-0.030874982476234436,
0.14347726106643677,
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0.0003433784004300833,
-0.0061147804372012615,
0.011627644300460815,
-0.0032220459543168545,
... |
duces the risk of albuminuria (62 –65),\nand among people with type 1 or 2\ndiabetes with established CKD (eGFR\n<60 mL/min/1.73 m\n2and UACR\n$300 mg/g creatinine), ACE inhibitor or\nARB therapy reduces the risk of progres-\nsion to ESKD (66 –75). Moreover, antihy-\npertensive therapy reduces the risk of\ncardiovascul... | [
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0.043960217386484146,
-0.0301374364644289,
0.0229064729064703,
0.020136278122663498,
0.008585920557379723,
0.015288854949176311,
0.14664094150066376,
0.005708880722522736,
0.008192316628992558,
-0.003735490143299103,
0.007851135917007923,
-0.05018137767910957,
-0.048... |
pertensive therapy reduces the risk of\ncardiovascular events (62).\nA blood pressure level <130/80 mmHg\nis recommended to reduce CVD mortality\nand slow CKD progression among all peo-\nple with diabetes. Lower blood pressure\ngoals (e.g., <130/80 mmHg) should be\nconsidered based on individual anticipated\nbenefits an... | [
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0.08415872603654861,
-0.007863325998187065,
-0.05191300809383392,
-0.10255278646945953,
0.016312196850776672,
-0.016152191907167435,
0.10393990576267242,
0.024683665484189987,
-0.02858479879796505,
-0.005105261690914631,
0.04389413446187973,
-0.021735314279794693,
-0.... |
benefits and risks. People with CKD are at\nincreased risk of CKD progression (particu-\nlarly those with albuminuria) and CVD;\ntherefore, lower blood pressure goals may\nbe suitable in some cases, especially in in-dividuals with severely elevated albumin-uria ($300 mg/g creatinine).\nACE inhibitors or ARBs are the pre... | [
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0.030952731147408485,
-0.007291377987712622,
-0.02030562050640583,
-0.04933729022741318,
0.030211446806788445,
-0.03182350471615791,
0.09677738696336746,
0.031750015914440155,
0.001528708846308291,
0.010240561328828335,
0.02590635046362877,
-0.02556740678846836,
-0.0... |
ACE inhibitors or ARBs are the pre-\nferred first-line agents for blood pressure\ntreatment among people with diabetes,\nhypertension, eGFR <60 mL/min/1.73 m\n2,\nand UACR $300 mg/g creatinine because\nof their proven bene fits for prevention of\nCKD progression (66,67,69). ACE inhibitors | [
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0.00338362087495625,
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0.020903924480080605,
-0.01674523949623108,
0.014080054126679897,
0.041680727154016495,
0.07701343297958374,
0.036384034901857376,
-0.004956039600074291,
-0.02010006457567215,
-0.007792153395712376,
-0.07651606947183609,
-0.0... |
CKD progression (66,67,69). ACE inhibitors\nand ARBs are considered to have similarbenefits (70,71) and risks. In the setting of\nlower levels of albuminuria (30 –299 mg/g\ncreatinine), ACE inhibitor or ARB therapyat maximum tolerated doses in trials hasreduced progression to more advanced al-\nbuminuria ($300 mg/g crea... | [
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-0.04813246428966522,
-0.057341769337654114,
-0.017912566661834717,
-0.043591614812612534,
0.021598927676677704,
-0.0038446998223662376,
0.0885976105928421,
0.004924017935991287,
-0.04712655395269394,
-0.0032176775857806206,
0.033857230097055435,
-0.017022371292114258,
... |
buminuria ($300 mg/g creatinine), slowed\nCKD progression, and reduced cardiovas-cular events but has not reduced progres-\nsion to ESKD (69,72). While ACE inhibitors\nor ARBs are often prescribed for moder-ately increased albuminuria (30 –299 mg/g | [
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0.031514015048742294,
-0.006030859891325235,
-0.07561195641756058,
0.01929984800517559,
0.17174194753170013,
0.021365340799093246,
-0.035933610051870346,
-0.015510329976677895,
0.04447849467396736,
-0.04568296670913696,
0... |
creatinine) without hypertension, outcomeTable 11.1 —Screening for selected complications of chronic kidney disease\nComplication Physical and laboratory evaluation\nBlood pressure >130/80 mmHg Blood pressure, weight, BMI\nVolume overload History, physical examination, weight\nElectrolyte abnormalities Serum electrolyt... | [
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0.023180440068244934,
-0.02711583487689495,
-0.010291552171111107,
-0.026714252308011055,
-0.022359099239110947,
0.006896821781992912,
0.09572096914052963,
-0.08658499270677567,
-0.04503265768289566,
-0.039108213037252426,
-0.05786735936999321,
-0.03034532442688942,
0... |
Electrolyte abnormalities Serum electrolytes\nMetabolic acidosis Serum electrolytes\nAnemia Hemoglobin; iron, iron saturation, ferritin testing if indicated\nMetabolic bone disease Serum calcium, phosphate, PTH, vitamin 25(OH)D\nComplications of chronic kidney disease (CKD) generally become prevalent when estimated | [
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0.019729942083358765,
0.022961100563406944,
-0.020119138062000275,
-0.022671405225992203,
0.016433505341410637,
0.06614621728658676,
-0.029761727899312973,
0.003754879580810666,
-0.00468060839921236,
0.0024140363093465567,
-0.009916611015796661,
... |
glomerular filtration rate falls below 60 mL/min/1.73 m2(stage G3 CKD or greater) and be- | [
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-0.010953331366181374,
0.05225309729576111,
-0.06470193713903427,
-0.054322659969329834,
-0.10694487392902374,
-0.06708212941884995,
0.07964687794446945,
0.0001270419015781954,
-0.027653025463223457,
0.01197150070220232,
-0.03951803222298622,
-0.0038320915773510933,
0... |
come more common and severe as CKD progresses. Evaluation of elevated blood pressureand volume overload should occur at every clinical contact possible; laboratory evaluationsare generally indicated every 6 –12 months for stage G3 CKD, every 3 –5 months for stage G4 | [
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0.007405634503811598,
0.03619673475623131,
-0.05182985961437225,
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-0.100753054022789,
0.032986655831336975,
0.010737668722867966,
-0.03693413734436035,
0.01174104306846857,
0.01788565330207348,
-0.02721891738474369,
-0.012917... |
CKD, and every 1 –3 months for stage G5 CKD, or as indicated to evaluate symptoms or\nchanges in therapy. PTH, parathyroid hormone; 25(OH)D, 25-hydroxyvitamin D.diabetesjournals.org/care Chronic Kidney Disease and Risk Management S223\n©AmericanDiabetesAssociation | [
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0.0438515730202198,
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-0.05908976495265961,
-0.0419861264526844,
-0.015383743681013584,
0.046966586261987686,
-0.0010290734935551882,
-0.025497157126665115,
0.013785328716039658,
0.05510062351822853,
-0.03893179073929787,
-0.... |
trials have not been performed in this set-\nting to determine whether they improve\nrenal outcomes. Moreover, two long-term,double-blind studies demonstrated no re-\nnoprotective effect of either ACE inhibi-\ntors or ARBs among people with type 1and type 2 diabetes who were normoten-sive with or without high albuminur... | [
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-0.0007256959215737879,
-0.08658093959093094,
0.04463119059801102,
-0.019426923245191574,
0.029391443356871605,
0.009491248056292534,
0.13058030605316162,
0.0016256747767329216,
-0.054757047444581985,
0.013958279974758625,
0.057523708790540695,
-0.03342268988490105,
... |
(formerly microalbuminuria, 30 –299 mg/g\ncreatinine) (73,74).\nIt should be noted that ACE inhibitors\nand ARBs are commonly not dosed at\nmaximum tolerated doses because of\nconcerns that serum creatinine will rise.\nAs previously noted, not maximizingthese therapies for this reason wouldbe considered suboptimal care... | [
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-0.05788859352469444,
-0.08158902823925018,
0.019214745610952377,
-0.043755192309617996,
-0.05048537254333496,
0.04837992042303085,
0.11726774275302887,
-0.03511824086308479,
-0.019941769540309906,
-0.03646917641162872,
0.06265176832675934,
-0.03021896444261074,
0.0... |
that in all clinical trials demonstrating\nefficacy of ACE inhibitors and ARBs in\nslowing kidney disease progression, the\nmaximum tolerated doses were used —\nnot very low doses that do not provide\nbene fit. Moreover, there are now stud-\nies demonstrating outcome bene fits on | [
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-0.023761915042996407,
-0.043154552578926086,
-0.044362105429172516,
-0.04158351942896843,
-0.038917336612939835,
0.012996324338018894,
0.12528710067272186,
0.04496932029724121,
-0.02975522167980671,
0.0049856374971568584,
0.09075788408517838,
0.013609163463115692,
-0... |
ies demonstrating outcome bene fits on\nboth mortality and slowed CKD progres-sion in people with diabetes who havean eGFR <30 mL/min/1.73 m\n2(75). Ad-\nditionally, when increases in serum cre-atinine reach 30% without associatedhyperkalemia, RAS blockade should becontinued (36,76).\nIn the absence of kidney disease, A... | [
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0.007012887857854366,
-0.056829195469617844,
0.02162344567477703,
-0.008982662111520767,
0.010915534570813179,
0.04127779230475426,
0.1419786810874939,
-0.017351742833852768,
-0.0026159731205552816,
-0.013396527618169785,
0.008861111477017403,
-0.013734301552176476,
0... |
In the absence of kidney disease, ACE\ninhibitors or ARBs are useful to manageblood pressure but have not proven su-perior to alternative classes of antihyper-tensive therapy, including thiazide-like\ndiuretics and dihydropyridine calcium | [
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-0.... |
diuretics and dihydropyridine calcium\nchannel blockers (77). In a trial of peoplewith type 2 diabetes and normal urinaryalbumin excretion, an ARB reduced or\nsuppressed the development of albumin-\nuria but increased the rate of cardiovas-cular events (78). In a trial of people with\ntype 1 diabetes exhibiting neither... | [
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type 1 diabetes exhibiting neither albu-\nminuria nor hypertension, ACE inhibitorsor ARBs did not prevent the develop-ment of diabetic glomerulopathy as-\nsessed by kidney biopsy (73). This was\nfurther supported by a similar trial inpeople with type 2 diabetes (74).\nTwo clinical trials studied the combi-\nnations of ... | [
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nations of ACE inhibitors and ARBs and\nfound no bene fits on CVD or CKD, and\nthe medication combination had higher\nadverse event rates (hyperkalemia and/or AKI) (79,80). Therefore, the combined\nuse of ACE inhibitors and ARBs should\nbe avoided.Direct Renal Effects of Glucose-\nLowering Medications\nSome glucose-lowe... | [
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-... |
Lowering Medications\nSome glucose-lowering medications also\nhave effects on the kidney that are di-\nrect, i.e., not mediated through glycemia.\nFor example, SGLT2 inhibitors reduce re-\nnal tubular glucose reabsorption, weight,\nsystemic blood pressure, intraglomerular\npressure, and albuminuria and slow GFR\nloss t... | [
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0.020245930179953575,
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0.09160713851451874,
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-0... |
loss through mechanisms that appear in-\ndependent of glycemia (31,81 –84). More-\nover, recent data support the notion thatSGLT2 inhibitors reduce oxidative stress\nin the kidney by >50% and blunt increases\nin angiotensinogen as well as reduceNLRP3 in flammasome activity (84 –86). Glu- | [
0.00005187542410567403,
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0.061909839510917664,
0.04863838851451874,
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0.12352632731199265,
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0.06811083853244781,
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... |
cagon-like peptide 1 receptor agonists(GLP-1 RAs) also have direct effects on the\nkidney and have been reported to improve\nrenal outcomes compared with placebo,\nalthough a defi nitive resolution as to the\nrenoprotective effects of GLP-1 RAs is yetto be determined (87 –91). Renal effects\nshould be considered when se... | [
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0.03339054808020592,
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0.09830641001462936,
0.08359827101230621,
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0.019... |
should be considered when selecting\nagents for glucose lowering (see Section 9,\n“Pharmacologic Approaches to Glycemic\nTreatment ”).\nSelection of Glucose-Lowering\nMedications for People With ChronicKidney Disease\nFor people with type 2 diabetes and es-\ntablished CKD, special considerations for\nthe selection of g... | [
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the selection of glucose-lowering medi-\ncations include limitations to available\nmedications when eGFR is diminished\nand a desire to mitigate risks of CKD\nprogression, CVD, and hypoglycemia\n(92,93). Medication dosing may require\nmodi fication with eGFR <60 mL/min/\n1.73 m2(1). Figure 11.2 shows the\nAmerican Diabe... | [
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0.14327429234981537,
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0.005127375014126301,
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0.0... |
American Diabetes Association and KDIGO\nconsensus recommendation algorithm\nfor medications in people with diabetes\nand CKD.\nThe FDA revised its guidance for the\nuse of metformin in CKD in 2016 (94),recommending use of eGFR instead of\nserum creatinine to guide treatment\nand expanding the pool of people with\nkidn... | [
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kidney disease for whom metformin\ntreatment should be considered. The re-\nvised FDA guidance states that 1)m e t -\nformin is contraindicated in individualswith an eGFR <30 mL/min/1.73 m\n2,2)\neGFR should be monitored while takingmetformin, 3) the bene fits and risks of\ncontinuing treatment should be reas-sessed whe... | [
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1.73 m\n2(95,96), 4) metformin shouldnot be initiated for individuals with an\neGFR<45 mL/min/1.73 m2,a n d5 )m e t -\nformin should be temporarily discontin-ued at the time of or before iodinatedcontrast imaging procedures in individu-\nals with eGFR 30 –60 mL/min/1.73 m\n2.\nA number of recent studies have\nshown car... | [
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A number of recent studies have\nshown cardiovascular protection from\nSGLT2 inhibitors and GLP-1 RAs as well as\nrenal protection from SGLT2 inhibitors\nand possibly from GLP-1 RAs. Selection ofwhich glucose-lowering medications touse should be based on the usual criteriaof an individual ’s risks (cardiovascular and | [
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0.011653... |
renal in addition to glucose control) aswell as convenience and cost.\nSGLT2 inhibitors are recommended\nfor people with eGFR $20 mL/min/\n1.73 m\n2and type 2 diabetes, as they\nslow CKD progression and reduce heartfailure risk independent of glucose man-agement (97). GLP-1 RAs are suggestedfor cardiovascular risk redu... | [
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risk is a predominant problem, as they\nreduce risks of CVD events and hypogly-cemia and appear to possibly slow CKDprogression (98 –101).\nA number of large cardiovascular out-\ncomes trials in people with type 2diabetes at high risk for CVD or with ex-isting CVD examined kidney effects assecondary outcomes. These tri... | [
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clude EMPA-REG OUTCOME [BI 10773\n(Empagli flozin) Cardiovascular Outcome\nEvent Trial in Type 2 Diabetes MellitusPatients], CANVAS (Canagli flozin Cardio-\nvascular Assessment Study), LEADER(Liraglutide Effect and Action in Diabe-tes: Evaluation of Cardiovascular Out-come Results), and SUSTAIN-6 (Trial to\nEvaluate Card... | [
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... |
Evaluate Cardiovascular and Other\nLong-term Outcomes With Semaglutidein Subjects With Type 2 Diabetes)(83,87,90,102). Speci fically, compared\nwith placebo, empagli flozin reduced the\nrisk of incident or worsening nephropa-thy (a composite of progression toUACR>300 mg/g creatinine, doubling\nof serum creatinine, ESKD, ... | [
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0.02633880078792572,
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0.014129642397165298,
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0.16134542226791382,
0.002459146548062563,
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-0.0... |
of serum creatinine, ESKD, or death\nfrom ESKD) by 39% and the risk of dou-\nbling of serum creatinine accompaniedby eGFR #45 mL/min/1.73 m\n2by 44%;\ncanagli flozin reduced the risk of progres- | [
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0.03681137412786484,
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0.07373415678739548,
-0.017208244651556015,
0.05059127137064934,
0.2292453497648239,
-0.031664684414863586,
0.033499088138341904,
0.015673795714974403,
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0.... |
2by 44%;\ncanagli flozin reduced the risk of progres-\nsion of albuminuria by 27% and the riskof reduction in eGFR, ESKD, or deathfrom ESKD by 40%; liraglutide reducedthe risk of new or worsening nephropa-thy (a composite of persistent macroal-\nbuminuria, doubling of serum creatinine, | [
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0.05309000238776207,
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0.016680076718330383,
0.20129169523715973,
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0.0391886830329895,
-0.02277105301618576,
0.004126009996980429,
-0.0237... |
buminuria, doubling of serum creatinine,\nESKD, or death from ESKD) by 22%; andS224 Chronic Kidney Disease and Risk Management Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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-0.0469508171081543,
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-0.010754457674920559,
0... |
semaglutide reduced the risk of new or\nworsening nephropathy (a composite ofpersistent UACR >300 mg/g creatinine,\ndoubling of serum creatinine, or ESKD) by\n36% (each P<0.01). These analyses were\nlimited by evaluation of study populations\nnot selected primarily for CKD and examina-tion of renal effects as secondary... | [
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0.016349516808986664,
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0.16136056184768677,
0.02809574268758297,
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0.016792699694633484,
-0.... |
Three large clinical trials of SGLT2 in-\nhibitors have focused on people withCKD and assessment of primary renaloutcomes. Canagli flozin and Renal Events\nin Diabetes with Established NephropathyClinical Evaluation (CREDENCE), a placebo-controlled trial of canagli flozin among | [
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0.0019041677005589008,
0.11564633250236511,
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-0.07859233021736145,
0.009011403657495975,
0.006707604043185711,
-0.03557301312685013,
... |
4,401 adults with type 2 diabetes, UACR$300 –5,000 mg/g creatinine, and eGFR\nrange 30 –90 mL/min/1.73 m\n2(mean\neGFR 56 mL/min/1.73 m2with a mean al-\nbuminuria level of >900 mg/day), had a\nprimary composite end point of ESKD,doubling of serum creatinine, or renalor cardiovascular death (29,103). It wasstopped early... | [
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0.026104584336280823,
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0.03658810630440712,
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0.009965081699192524,
0.16416673362255096,
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-0.005289631895720959,
0.... |
showed a 32% risk reduction for develop-ment of ESKD over control (29). Addition-ally, the development of the primary end\npoint, which included dialysis for $30\ndays, kidney transplantation or eGFR <15\nmL/min/1.73 m\n2sustained for $30 days\nby central laboratory assessment, dou-\nbling from the baseline serum creat... | [
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0.05236568674445152,
0.006502902135252953,
-0.02067798376083374,
0.007026443257927895,
-0.02701306715607643,
-0.015316015109419823,
0.17946794629096985,
0.01033011544495821,
0.02402232401072979,
0.0006397818797267973,
-0.04687833786010742,
-0.01513658743351698,
-0.00... |
bling from the baseline serum creatinine\naverage sustained for $30 days by central\nlaboratory assessment, or renal death orcardiovascular death, was reduced by\n30%. This bene fit was on background\nACE inhibitor or ARB therapy in >99%\nof the participants (29). Moreover, inthis advanced CKD group, there wereclear ben... | [
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0.01668219454586506,
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0.03259062394499779,
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0.006638372782617807,
0.15261021256446838,
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0.0013603470288217068,
-0.07812664657831192,
-0.06434560567140579,
0.01142188161611557,
0.0139... |
comes demonstrating a 31% reductionin cardiovascular death or heart failure\nhospitalization and a 20% reduction in\ncardiovascular death, nonfatal myocardialinfarction, or nonfatal stroke (29,101,104).\nA second trial in advanced diabetic\nkidney disease was the Dapagli flozin\nand Prevention of Adverse Outcomes inChro... | [
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0.06452718377113342,
-0.02463001199066639,
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0.08361469954252243,
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0.061471469700336456,
-0.05480661988258362,
-0... |
study (105). This trial examined a cohort\nsimilar to that in CREDENCE except67.5% of the participants had type 2diabetes and CKD (the other one-thirdhad CKD without type 2 diabetes), andthe end points were slightly different.\nThe primary outcome was time to the\nfirst occurrence of any of the compo-\nnents of the comp... | [
0.0382787249982357,
0.03119092434644699,
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0.060011666268110275,
-0.03100397437810898,
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-0.0021264133974909782,
0.11816104501485825,
0.001456432044506073,
0.012729172594845295,
0.004428049083799124,
0.057018179446458817,
-0.07772628217935562,
-0.0... |
nents of the composite, including $50%\nsustained decline in eGFR or reachingESKD or cardiovascular death, or renaldeath. Secondary outcome measures in-\ncluded time to the first occurrence of\nany of the components of the compos-\nite kidney outcome ( $50% sustained\ndecline in eGFR or reaching ESKD or | [
0.018382882699370384,
0.05702657252550125,
0.04710874706506729,
-0.01810947246849537,
0.015257608145475388,
-0.006715684197843075,
-0.006411839742213488,
0.17373934388160706,
0.018578847870230675,
0.021377263590693474,
0.03405986726284027,
-0.042902786284685135,
0.010636943392455578,
0.022... |
decline in eGFR or reaching ESKD or\nHealthy diet Weight management Smoking cessation Physical activity\nMetformin\n(if eGFR ≥30)SGLT2i\n(Initiate if eGFR ≥20;\ncontinue until dialysis\nor transplant)RAS inhibitor at maximum\ntolerated dose (if HTN*)Moderate- or\nhigh-intensity statin\nGLP-1 RA if needed to\nachieve in... | [
-0.034620605409145355,
0.04838771000504494,
-0.01623460277915001,
0.04545130580663681,
0.026010464876890182,
-0.021196916699409485,
0.0005303160287439823,
0.14184105396270752,
-0.06643246114253998,
0.014306857250630856,
0.04551921784877777,
-0.0031347356270998716,
0.00811601523309946,
0.02... |
high-intensity statin\nGLP-1 RA if needed to\nachieve individualized\nglycemic targetNonsteroidal MRA† if \nACR ≥30 mg/g and\nnormal potassiumDihydropyridine CCB\nand/or diuretic* if\nneeded to achieve\nindividualized\nBP targetAntiplatelet\nagent for\nclinical ASCVDLifestyle\nFirst-line\ndrug therapy\nAdditionalrisk-b... | [
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-0.08593326807022095,
0.02832808718085289,
-0.008945103734731674,
0.004209894221276045,
-0.023124106228351593,
0.14403560757637024,
-0.046558137983083725,
0.034839875996112823,
-0.010069124400615692,
0.03339563310146332,
-0.03452363610267639,
0.... |
drug therapy\nAdditionalrisk-basedtherapy\nOther glucose-lowering\ndrugs if needed to\nachieve individualized\nglycemic targetSteroidal MRA if\nneeded for resistant\nhypertension\nif eGFR ≥45Ezetimibe, PCSK9i,\nor icosapent ethyl if\nindicated based on\nASCVD risk and lipids\nRegular\nrisk factor\nreassessment\n(every ... | [
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0.034884825348854065,
-0.019213851541280746,
-0.025991689413785934,
-0.06428947299718857,
-0.021588921546936035,
-0.022532064467668533,
0.16567738354206085,
-0.030725941061973572,
0.03616045042872429,
-0.030410829931497574,
0.023381788283586502,
-0.06002764403820038,
... |
risk factor\nreassessment\n(every 3–6\nmonths)\nT2D only\nAll patients\n(T1D and T2D)Regular reassessment\nof glycemia, albuminuria,\nBP , CVD risk, and lipids\nFigure 11.2— Holistic approach for improving outcomes in people with diabetes and CKD. Icons presented indicate the following bene fits: BP cuff, | [
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-0.0005555346142500639,
-0.040794894099235535,
-0.... |
BP lowering; glucometer, glucose lowering; heart, cardioprotection; kidney, kidney protection; scale, weight management. eGFR is presented in\nunits of mL/min/1.73 m2. *ACEi or ARB (at maximal tolerated doses) should be first-line therapy for hypertension when albuminuria is present. | [
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-0.022037822753190994,
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Otherwise, dihydropyridine calcium channel blocker or diuretic can also be considered; all three classes are often needed to attain BP targets.\n†Finerenone is currently the only ns-MRA with proven clinical kidney and cardiovascular bene fits. ACEi, angiotensin-converting enzyme inhibitor; | [
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-0.010725598782300949,
-0.0930512398481369,
0... |
ACR, albumin-to creatinine ratio; ARB, angiotensin receptor blocker; ASCVD, atherosclerotic cardiovascular disease; BP, blood pressure; CCB, cal-\ncium channel blocker; CVD, cardiovascular disease; eGFR, estimated glomerular filtration rate; GLP-1 RA, glucagon-like peptide 1 receptor agonist; | [
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0.04693938046693802,
-0.08545393496751785,
-0.0690997764468193,
0.029725... |
HTN, hypertension; MRA, mineralocorticoid receptor antagonist; ns-MRA, nonsteroidal mineralocorticoid receptor antagonist; PCSK9i, proproteinconvertase subtilisin/kexin type 9 inhibitor; RAS, renin-angiotensin system; SGLT2i, sodium –glucose cotransporter 2 inhibitor; T1D, type 1 diabetes; | [
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-0.0015459781279787421,
-0.009025674313306808,
-0.03887981176376343,
-0.053541891276836395,
... |
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