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sion (if eGFR is $25 mL/min/1.73 m\n2).Potassium levels should be moni-\ntored. A\n11.6 In people with CKD who have\n$300 mg/g urinary albumin, a reduc-\ntion of 30% or greater in mg/g urinaryalbumin is recommended to slow CKDprogression. C\n11.7 For people with non –dialysis- | [
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11.7 For people with non –dialysis-\ndependent stage G3 or higher CKD,dietary protein intake should be aimedto a target level of 0.8 g/kg bodyweight per day. AFor individuals on\ndialysis, 1.0 –1.2 g/kg/day of dietary\nprotein intake should be consideredsince protein energy wasting is a ma-jor problem in some individua... | [
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11.8 Individuals should be referred\nfor evaluation by a nephrologist ifthey have continuously increasingurinary albumin levels and/or con-tinuously decreasing eGFR and/or ifthe eGFR is <30 mL/min/1.73 m\n2.A\n11.9 Promptly refer to a nephrologist\nfor uncertainty about the etiology ofAlbuminuria categories | [
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for uncertainty about the etiology ofAlbuminuria categories\nDescription and rangeGFR categories (mL/min/1.73 m2)\nDescription and rangeA1\nG1 ≥90\nG2 60–89\nG3a 45–59\nG3b 30–44\nG4 15–29\nG5 <15 Kidney failureSeverely decreasedModerately to\nseverely decreasedMildly to\nmoderately decreasedMildly decreasedNormal or h... | [
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Normal to mildly\nincreasedModerately\nincreasedSeverely\nincreased\n<30 mg/g\n<3 mg/mmol\nScreen\n1\nScreen\n1Treat\n1\nTreat\n1Treat and refer\n3\nTreat and refer\n3\nTreat\n1\nTreat\n2Treat\n2\nTreat and refer\n3Treat and refer\n3\nTreat and refer\n3\nTreat and refer*\n3\nTreat and refer\n4+Treat and refer*\n3\nTrea... | [
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3\nTreat and refer\n4+Treat and refer\n4+\nTreat and refer\n4+30–299 mg/g\n3–29 mg/mmol ≥300 mg/g\n ≥30 mg/mmolCKD is classified based on:\n\x81 Cause (C)\n\x81 GFR (G)\n\x81 Albuminuria (A)\nLow risk (if no other markers of kidney disease, no CKD)\nModerately increased riskHigh riskVery high risk | [
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Moderately increased riskHigh riskVery high risk\nFigure 11.1— Risk of CKD progression, frequency of visits, and referral to nephrology according to GFR and albuminuria. The numbers in the boxes\nare a guide to the frequency of screening or monitoring (number of times per year). Green re flects no evidence of CKD by est... | [
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minuria, with screening indicated once per year. For monitoring of prevalent CKD, suggested monitoring varies from once per year (yellow) to four\ntimes or more per year (i.e., every 1 –3 months, [deep red]) according to risks of CKD progression and CKD complications (e.g., cardiovascular dis- | [
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ease, anemia, hyperparathyroidism). These are general parameters based only on expert opinion and underlying comorbid conditions, and diseasestate must be taken into account, as well as the likelihood of impacting a change in management for any individual. CKD, chronic kidney disease;GFR, glomerular filtration rate. Rep... | [
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disease;GFR, glomerular filtration rate. Reprinted and adapted from de Boer et al. (1).S220 Chronic Kidney Disease and Risk Management Diabetes Care Volume 47, Supplement 1, January 2024 | [
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©AmericanDiabetesAssociation | [
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kidney disease, diffi cult management\nissues, and rapidly progressing kidney\ndisease. B\nEPIDEMIOLOGY OF DIABETES AND\nCHRONIC KIDNEY DISEASE\nChronic kidney disease (CKD) is diag-\nnosed by the persistent elevation of uri-nary albumin excretion (albuminuria),low estimated glomerular filtration rate\n(eGFR), or other m... | [
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(eGFR), or other manifestations of kid-\nney damage (1). In this section, the\nfocus is on CKD attributed to diabetes(diabetic kidney disease) in adults, whichoccurs in 20 –40% of people with diabe-\ntes (1 –4). Diabetic kidney disease typi-\ncally develops after a diabetes durationof 10 years in type 1 diabetes (the m... | [
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c o m m o np r e s e n t a t i o ni s5 –15 years af-\nter the diagnosis of type 1 diabetes) but\nmay be present at diagnosis of type 2diabetes. CKD can progress to end-stagekidney disease (ESKD) requiring dialysisor kidney transplantation and is theleading cause of ESKD in the U.S. (5). In\naddition, among people with ... | [
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addition, among people with type 1 or\ntype 2 diabetes, the presence of CKDmarkedly increases cardiovascular riskand health care costs (6). For details onthe management of diabetic kidney dis-ease in children, please see Section 14,“Children and Adolescents.”\nASSESSMENT OF ALBUMINURIA\nAND ESTIMATED GLOMERULARFILTRATI... | [
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ASSESSMENT OF ALBUMINURIA\nAND ESTIMATED GLOMERULARFILTRATION RATE\nScreening for albuminuria can be most\neasily performed by urinary albumin- | [
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easily performed by urinary albumin-\nto-creatinine ratio (UACR) in a randomspot urine collection (1). Timed or 24-hcollections are more burdensome andadd little to prediction or accuracy.Measurement of a spot urine samplefor albumin alone (whether by immu-\nnoassay or by using a sensitive dipstick\ntest speci fic for a... | [
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test speci fic for albuminuria) without\nsimultaneously measuring urine creati-nine is less expensive but susceptibleto false-negative and false-positive de-terminations as a result of variation inurine concentration due to hydration\n(7). Thus, semiquantitative or qualita-\ntive (dipstick) screening will need to beconfi... | [
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credited laboratory (8,9). Hence, it isbetter to simply collect a spot urinesample for albumin-to-creatinine ratiobecause it will ultimately need to be\ndone.\nNormal level of urine albumin excre-\ntion is de fined as <30 mg/g creatinine,\nmoderately elevated albuminuria is de-\nfined as$30–300 mg/g creatinine, and | [
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fined as$30–300 mg/g creatinine, and\nseverely elevated albuminuria is de fined\nas$300 mg/g creatinine. However, UACR\nis a continuous measurement, and differ-\nences within the normal and abnormal\nranges are associated with kidney and\ncardiovascular outcomes (6,10,11). Fur-thermore, because of high biological vari-ab... | [
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in urinary albumin excretion, two of threespecimens of UACR collected within a3- to 6-month period should be abnormalbefore considering an individual to have\nmoderately or severely elevated albumin- | [
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moderately or severely elevated albumin-\nuria (1,12,13). Exercise within 24 h, infec-tion, fever, congestive heart failure,marked hyperglycemia, menstruation,and marked hypertension may elevate\nUACR independently of kidney damage\n(14).\nTraditionally, eGFR is calculated from | [
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(14).\nTraditionally, eGFR is calculated from\nserum creatinine using a validated for-mula (15). eGFR is routinely reported by\nlaboratories along with serum creati-\nnine, and eGFR calculators are availableonline at nkdep.nih.gov. An eGFR persis-tently<60 mL/min/1.73 m\n2and/or an\nurinary albumin value of >30 mg/g cr... | [
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2and/or an\nurinary albumin value of >30 mg/g cre-\natinine is considered abnormal, thoughoptimal thresholds for clinical diagnosisare debated in older adults over age\n70 years (1,16). Historically, a correction\nfactor for muscle mass was included ina modi fied equation for African Ameri- | [
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can people; however, race is a socialand not a biologic construct, making\nit problematic to apply race to clinical\nalgorithms, and the need to advancehealth equity and social justice is clear.Thus, it was decided that the equation\nshould be altered such that it applies to | [
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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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0.023809954524040222,
0.051559045910835266,
-0.015499325469136238,
0.... |
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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0.08930745720863342,
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0.018257195129990578,
0.02983609028160572,
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-0... |
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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0.02785845845937729,
-0.04591704159975052,
0.007738064043223858,
-0.023580927401781082,
-0.024997858330607414,
0.14146557450294495,
-0.031142905354499817,
-0.03405798226594925,
0.014111938886344433,
-0.03793996572494507,
-0.027267128229141235,
0.0... |
(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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0.04882536083459854,
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-0.01318253856152296,
0.019499177113175392,
-0.05469575151801109,
-0.001... |
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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0.044692523777484894,
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0.002736858557909727,
-0.045729584991931915,
0.03432... |
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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0.04414665326476097,
-0.009783973917365074,
-0.010176995769143105,
-0.00... |
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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0.00484... |
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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0.0... |
(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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0.0... |
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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0.010767721571028233,
0.05564434453845024,
0.004241262096911669,
0.018... |
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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-0.0223642997443676,
0.0146... |
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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-0.031001189723610878,
... |
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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0.0034255050122737885,
-0.028070013970136642,
-0.... |
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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0.013988982886075974,
0.06125178560614586,
0.026082536205649376,
0.019890518859028816,
0.0014153033262118697,
0.020386043936014175,
0.008971603587269783,
-0.0... |
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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0.013086358085274696,
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0.012290235608816147,
0.14929625391960144,
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0.011803669854998589,
0.029133684933185577,
-0.0284480731934309,
-0.010671288706362247,
0.0... |
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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0.06243805214762688,
0.016178429126739502,
-0.028983503580093384,
0.04913626238703728,
-0.019116636365652084,
-0.05883331969380379,
0.063... |
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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0.045352667570114136,
0.06804292649030685,
0.014878000132739544,
-0.021735161542892456,
0.038624107837677,
0.02020573429763317,
-0.04070989787578583,
0.08274... |
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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-0.022904474288225174,
-0.03948945924639702,
-0.017593447118997574,
-0.015003534965217113,
0.15201473236083984,
-0.006674593314528465,
-0.044388797134160995,
0.0071506621316075325,
0.048939287662506104,
-0.02945161424577236... |
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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0.0007793710101395845,
-0.05104043334722519,
0.018884658813476562,
-0.05887220799922943,
0.04468284174799919,
-0.009723564609885216,
0.06484674662351608,
-0.021563351154327393,
-0.05109008029103279,
-0.004156405571848154,
-0.004628447350114584,
-0.008044525049626827,
... |
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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-0.08565875887870789,
-0.06382308900356293,
-0.04515175148844719,
0.15842385590076447,
0.0230611190199852,
-0.018511991947889328,
-0.03844250738620758,
0.06450878083705902,
-0.0019075804157182574,
0.0... |
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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-0.04454221948981285,
0.06862476468086243,
-0.021004995331168175,
-0.01348062139004469,
0.06643704324960709,
0.10046560317277908,
-0.03181979060173035,
-0.01507959607988596,
-0.013954713940620422,
0.06561192125082016,
-0.034067314118146896,
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 | [
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0.03854553773999214,
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-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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0.0030599485617130995,
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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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0.012548277154564857,
0.07151485979557037,
0.05122951790690422,
-0.008180901408195496,
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0.08451537787914276,
-0.024124963209033012,
-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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0.02456595003604889,
0.03606749325990677,
0.09304419904947281,
0.009351888671517372,
-0.0521814301609993,
0.016278522089123726,
0.05397108569741249,
-0.019113248214125633,
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,
-0.08517675846815109,
-0.06331079453229904,
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,
-0.00016718986444175243,
-0.03751251846551895,
-0.007487072609364986,
0.11573158949613571,
-0.022398358210921288,
-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,
-0.020108286291360855,
-0.007080913987010717,
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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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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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... | [
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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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0.14207035303115845,
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0.0017080368706956506,
0.1053214892745018,
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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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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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... |
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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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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-... |
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 | [
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0.05752488225698471,
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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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0.0003433784004300833,
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... |
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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0.008192316628992558,
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-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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0.10393990576267242,
0.024683665484189987,
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0.04389413446187973,
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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,
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0.030211446806788445,
-0.03182350471615791,
0.09677738696336746,
0.031750015914440155,
0.001528708846308291,
0.010240561328828335,
0.02590635046362877,
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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,
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0.014080054126679897,
0.041680727154016495,
0.07701343297958374,
0.036384034901857376,
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-0.02010006457567215,
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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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-0.057341769337654114,
-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,
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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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0.05225309729576111,
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0.07964687794446945,
0.0001270419015781954,
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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,
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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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0.046966586261987686,
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0.013785328716039658,
0.05510062351822853,
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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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0.04463119059801102,
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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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0.019214745610952377,
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0.04837992042303085,
0.11726774275302887,
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-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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-0.038917336612939835,
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,
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0.02162344567477703,
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0.010915534570813179,
0.04127779230475426,
0.1419786810874939,
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-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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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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0.0531567744910717,
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0.05456572026014328,
0.06606049090623856,
0.010517282411456108,
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0.0042152064852416515,
0.0036274853628128767,
-0.061692994087934494,
0.... |
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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0.015269971452653408,
0.035575807094573975,
0.00973392091691494,
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0.007285104598850012,
0.06327788531780243,
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-0.0... |
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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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- | [
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0.019269315525889397,
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0.061909839510917664,
0.04863838851451874,
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0.12352632731199265,
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-0.043658092617988586,
-0.07042750716209412,
0.06811083853244781,
-0.0006566197844222188,
... |
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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0.02274932526051998,
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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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0.0503557026386261,
-0.0004619575629476458,
-0.024648545309901237,
-0.02832503616809845,
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0.08843334019184113,
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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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0.09247252345085144,
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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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-0.013351074419915676,
-0.05268858000636101,
0.025596462190151215,
-0.07929152995347977,
0.... |
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