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Evaluation and Management of Chronic Kidney Disease: Synopsis ofthe Kidney Disease: Improving Global Outcomes 2012 ClinicalPractice GuidelinePaul E. Stevens, MBBS, BSc, and Adeera Levin, MD, BSc, for the Kidney Disease: Improving Global Outcomes Chronic Kidney Disease

Guideline Development Work Group Members*

Description: The Kidney Disease: Improving Global Outcomes(KDIGO) organization developed clinical practice guidelines in 2012to provide guidance on the evaluation, management, and treat-ment of chronic kidney disease (CKD) in adults and children whoare not receiving renal replacement therapy.

Methods: The KDIGO CKD Guideline Development Work Groupdefined the scope of the guideline, gathered evidence, determinedtopics for systematic review, and graded the quality of evidencethat had been summarized by an evidence review team. Searchesof the English-language literature were conducted through Novem-ber 2012. Final modification of the guidelines was informed by the

KDIGO Board of Directors and a public review process involvingregistered stakeholders.

Recommendations: The full guideline included 110 recommenda-tions. This synopsis focuses on 10 key recommendations pertinentto definition, classification, monitoring, and management of CKD inadults.

Ann Intern Med. 2013;158:825-830. www.annals.org

For author affiliations, see end of text.

* For a list of the members of the KDIGO CKD Guideline Development Work

Group, see the Appendix (available at www.annals.org).

A decade of research after the publication of the firstinternationally accepted definition and classification

of CKD (1) led the Kidney Disease: Improving GlobalOutcomes (KDIGO) organization to develop an updatedClinical Practice Guideline for the Evaluation and Man-agement of Chronic Kidney Disease (2). The updatedguideline applied to all persons with chronic kidney disease(CKD) who were not receiving renal replacement therapy and included aspects related to both adults and children.

Within the guideline, implications for clinical practice,

public policy, and international considerations were high-lighted, along with areas of controversy, confusion, or non-consensus. The detailed work-up for specific causes of CKD was beyond the scope of the guideline, as were spe-cific approaches to acute kidney injury (AKI) and otheracute kidney diseases, diagnostic work-up or treatment of specific causes of CKD, management of CKD in preg-nancy, detailed management of endocrine and metaboliccomplications, and detailed drug dosing.

The guideline sought to provide comprehensive guid-ance encompassing the whole CKD pathway, from early identification and diagnosis through initiation of renal re-

placement therapy for end-stage renal disease or end-of-lifecare. The recognition of the importance of patient safety and inclusion of caveats in the use and interpretation of commonly used tests was unique and highly practical.These details can be found in the full guideline (2), andrecommendations are listed in the Supplement (availableat www.annals.org). This synopsis focuses on the evalua-tion and classification of CKD, areas that have generatedsubstantial controversy. We also discuss some key recom-mendations, including the management of CKD progres-sion and complications, and the relationship between AKIand CKD.

GUIDELINE DEVELOPMENT PROCESS, EVIDENCE

GRADING, AND STAKEHOLDER AND PUBLIC

CONSULTATION

The work group consisted of an international groupof clinicians and researchers, including kidney specialists,primary care physicians, a diabetologist, an epidemiologist,a clinical chemist, administrators, and a professional evi-dence review team. The work group formulated the scopeof the guideline, graded evidence on the basis of theGRADE (Grading of Recommendations Assessment, De-

velopment and Evaluation) system (3–5) ( Appendix Ta-bles 1 and 2, available at www.annals.org), and made con-sensus recommendations even when the quality of evidence

was low to highlight key concepts and areas of confusion inclinical practice. In addition, the evidence review team didsystematic reviews for 8 topics of interest ( Appendix Table3, available at www.annals.org), and searches were last con-ducted in June 2011 and supplemented with additionalevidence through November 2012. Further guideline de-velopment, evidence synthesis, and writing of the guidelineitself was done by the work group. Full details of the guide-line development process, topic discussion, and consensus

development can be found in the published guideline (2).The draft guideline was reviewed by the KDIGO

Board of Directors, and revisions were incorporated beforea structured, Internet-based public review process. Feed-

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back from this was reviewed by the work group, and finalrevisions were incorporated before publication of theguideline.

RECOMMENDATIONS RELATING TO THE DEFINITION AND

CLASSIFICATION OF CKD

1.1.1. CKD is defined as abnormalities of kidney struc-ture or function, present for 3 months, with implica-tions for health. (Not Graded)

Criteria for CKD are shown in Table 1. Diagnosticthresholds for glomerular filtration rate (GFR) of less than60 mL/min per 1.73 m2 and an albumin–creatinine ratio(ACR) of 30 mg/g or greater were retained. This wasdriven by studies examining risk for all-cause and cardio-vascular mortality, AKI, CKD progression, and kidney fail-ure in the general population and populations with in-creased risk for cardiovascular disease (6–9). However, theaddition of “with implications for health” reflects the no-tion that although various abnormalities of kidney struc-ture or function exist, not all have implications for a per-son’s health. For example, although age-associated GFR decline is seen in longitudinal as well as cross-sectionalstudies, it varies substantially. A GFR less than 60 mL/minper 1.73 m2 is less than half of the normal value in young adult men and women (which is approximately 125 mL/min per 1.73 m2) and is associated with a higher risk forcomplications of CKD than in persons with CKD andconserved GFR. The mechanisms underlying these associ-ations are not fully understood, but there is a clinically significant effect of reduced GFR on drug toxicity, endo-

crine and metabolic complications, and risk for cardiovas-cular disease and death. These are relevant to all patients

with reduced GFR, regardless of country, age, or cause. An ACR of 30 mg/g is greater than 3 times the normal valuein young adult men and women (which is approximately 10 mg/g) and is associated with an increased risk for com-plications of CKD.

1.2.1. We recommend that CKD is classified based oncause, GFR category, and albuminuria category (CGA).(1B)

The classification system has been revised to encom-pass cause and severity. Identifying cause is emphasizedbecause of its fundamental importance in predicting out-come and guiding choice of cause-specific treatments. Se-verity is expressed by level of GFR and albuminuria (Table2). Severity is linked to risks for adverse outcomes, includ-

ing death and kidney outcomes.The GFR categories mapping to the previous 5-stageclassification have been retained but with subdivision of the G3 category of 30 to 59 mL/min per 1.73 m2 intocategories G3a (45 to 59 mL/min per 1.73 m2) and G3b(30 to 44 mL/min per 1.73 m2). This was driven by data supporting different outcomes and risk profiles in thesecategories (6–10). Many other concurrent complicationsare associated with decreased categories of GFR, including infection, impaired cognitive and physical function, andthreats to patient safety.

Three albuminuria categories were proposed both forsimplification and initial assessment and prognostication.

Further classification into higher and nephrotic ranges(ACR 2220 mg/g) may be appropriate for specific cir-cumstances in specialist centers.

RECOMMENDATIONS FOR EVALUATION OF GFR AND

URINARY ALBUMIN EXCRETION

The Chronic Kidney Disease Epidemiology Collabo-ration (CKD-EPI) equation was recommended for report-ing estimated GFR (eGFR) in adults from serum creatininelevels measured by an assay calibrated to the isotope-dilution mass spectrometry reference method. Systematic

review supported the strength of this recommendation(evidence level 1B). The CKD-EPI equation had less biasthan the MDRD (Modification of Diet in Renal Disease)Study equation, especially at a GFR of 60 mL/min per1.73 m2 or greater; a small improvement in precision; andgreater accuracy (11). Most but not all studies from North

America, Europe, and Australia show that the CKD-EPIequation is more accurate than the MDRD Study equa-tion, especially at greater GFR, enabling reporting of nu-merical values across the range of GFRs. Selection of a single equation for use should facilitate communicationamong providers, patients, researchers, and public health

officials. However, where CKD-EPI has been modified foruse in other racial and ethnic groups, and where validatedcountry- or region-specific equations have been developed,these should be used in preference to unmodified equations.

1.4.3.5. We suggest measuring cystatin C in adults with eGFRcreat [creatinine-based eGFR] 45-59 ml/min/1.73 m2 who do not have other markers of kidney damage if confirmation of CKD is required. (2C)

The guideline acknowledged that this is a contentiousarea with potential health economics consequences andthat not all laboratories internationally will be able to assay

Table 1. Criteria for Chronic Kidney Disease*

Markers of kidney damage (>1 for >3 mo)

Albuminuria (AER 30 mg/d; ACR 30 mg/g)

Urinary sediment abnormalities

Electrolyte and other abnormalities due to tubular disorders

Abnormalities detected by histology

Structural abnormalities detected by imaging

History of kidney transplantation

Decreased GFR (for >3 mo)

GFR 60 mL/min per 1.73 m2 (GFR categories G3a–G5)

ACR albumin–creatinine ratio; AER albumin excretion rate; GFR glo-merular filtration rate.* Reproduced from reference 2.

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cystatin C. Evidence supports the use of cystatin C–basedeGFR (eGFRcys) in persons without albuminuria (cate-gory A1) or other markers of kidney damage, especially those with an eGFRcreat of 45 to 59 mL/min per 1.73 m2

(category G3a) (12, 13). This group represents 3.6% of theU.S. population and 41% of persons in the United Statesestimated to have CKD on the basis of eGFRcreat andurinary ACR alone. Because the diagnosis of CKD in thesepersons is an area of substantial controversy with potentialimplications from disease labeling, the potential utility of a confirmatory marker is important. Use of eGFRcys to con-firm CKD in populations has shown that two thirds of

persons with eGFRcreat less than 60 mL/min per 1.73 m2

have a diagnosis of CKD confirmed by eGFRcys less than60 mL/min per 1.73 m2 and had markedly elevated risksfor death, cardiovascular disease, and end-stage renal dis-ease compared with those with eGFRcys greater than 60mL/min per 1.73 m2.

1.4.4.2. We recommend that clinical laboratories re-port albumin:creatinine ratios (ACR) and protein:crea-tinine ratios (PCR) in untimed urine samples inaddition to albumin concentration or proteinuria con-centrations rather than the concentrations alone. (1B)

Measurement of urinary ACR was recommended forevaluation of proteinuria in preference to urinary total pro-tein for many reasons. Albumin is the most important pro-tein lost in the urine in most cases of CKD. In populationstudies, urinary ACR accurately predicts kidney and car-diovascular risks (6–9, 14–19). Reduction in ACR in in-tervention trials targeted at blood pressure (BP) reductionor renin–angiotensin blockade has shown benefit for pro-gression of CKD. Urinary ACR has greater sensitivity fordetecting low-grade but clinically important albuminuria and is more precise at low but diagnostically importantconcentrations (20).

1.4.4.2.1. The term microalbuminuria should no lon-ger be used by laboratories. (Not Graded)

Although the significance of the A2 category of ACR (30 to 300 mg/g) has been understood in persons withdiabetes for decades, use of this category to denote CKD,especially in those with higher GFRs, remains controver-sial. However, data demonstrate that, at any level of GFR,an ACR increase above normal is associated with increasedrisk for adverse outcomes and that this increased risk is a continuum (6–9). It was, therefore, suggested that theterm “microalbuminuria” no longer be used.

RECOMMENDATIONS FOR MONITORING CKDPersons with CKD should be assessed at least annu-

ally. The exact frequency of GFR and ACR monitoring will depend on the severity of CKD (Figure) and the risk for and rate of progression. Factors associated with pro-gression include cause of CKD, level of GFR, level of al-buminuria, AKI, age, sex, race or ethnicity, elevated BP,hyperglycemia, dyslipidemia, smoking, obesity, history of cardiovascular disease, ongoing exposure to nephrotoxicagents, and others.

Small fluctuations in GFR are common and do notnecessarily indicate progression. An approach involving anassessment of change in eGFR category confirmed by a minimal percentage of change in eGFR (25% or greater)

was recommended to define progression. The reasoning forthis was that although longitudinal cohort studies examin-ing progression have assumed that progression is linear,this is often not the case. The greater the fluctuation inkidney function, the higher the probability of nonlinearprogression (21, 22). A criterion requiring both a change inGFR category (that is, from category G2 to G3a) and per-centage of change would ensure that small changes in GFR (from 61 to 59 mL/min per 1.73 m2, for example, which

Table 2. GFR and Albuminuria Categories in the New Classification

Category GFR, mL/min per 1.73 m2 AER, mg/d ACR Equivalent, mg/g Descriptor

GFR – –

G1 90 – – Normal or high

G2 60–89 – – Mildly decreased*†

G3a 45–59 – – Mildly to moderately decreased

G3b 30–44 – – Moderately to severely decreased

G4 15–29 – – Severely decreased

G5 15 – – Kidney failure

Albuminuria

A1 – 30 30 Normal to mildly increased

A2 – 30–300 30–300 Moderately increased*

A3 – 300 300 Severely increased‡

ACR albumin–creatinine ratio; AER albumin excretion rate; GFR glomerular filtration rate.* Relative to young adult level.† In the absence of evidence of kidney damage, neither GFR category G1 nor G2 fulfill the criteria for chronic kidney disease.‡ Including the nephrotic syndrome (AER usually 2200 mg/d [ACR 2220 mg/g]).

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represents a change in category but a minimal change inGFR) would not be misinterpreted to represent progres-sion. Preliminary studies have indicated that this approachidentifies those at increased risk (23–25).

Data were insufficient to inform recommendations de-fining albuminuria progression, although increasing levelsof albuminuria suggest progression and has been shown tobe associated with increased risk for adverse outcomes.

MANAGEMENT OF CKDDetailed within the guideline were many management

recommendations for prevention of CKD progression andmanagement of specific complications of CKD (see Sup-plement ). Key recommendations relating to BP control,proteinuria reduction, AKI, and cardiovascular disease aresummarized.

3.1.4 We recommend that both diabetic and non-diabetic adults with CKD and urine albumin excretion30 mg/24 hours (or equivalent) whose office BP isconsistently 140 mm Hg systolic or 90 mm Hg

diastolic be treated with BP-lowering drugs to maintain

a BP that is consistently 140 mm Hg systolic and

90 mm Hg diastolic. (1B)

3.1.5 We suggest that both diabetic and non-diabetic

adults with CKD and with urine albumin excretion of

30 mg/24 hours (or equivalent) whose office BP is

consistently 130 mm Hg systolic or 80 mm Hg

diastolic be treated with BP-lowering drugs to maintain

a BP that is consistently 130 mm Hg systolic and

80 mm Hg diastolic. (2D)

3.1.7 We recommend that an ARB [angiotensin-

receptor blocker] or ACE-I [angiotensin-converting en-

zyme inhibitor] be used in both diabetic and non-

diabetic adults with CKD and urine albumin excretion

300 mg/24 hours (or equivalent). (1B)

Control of blood pressure and reduction of proteinuria are critical in preventing CKD progression. Studies haveconsistently shown that reduction of proteinuria using

Figure. Guide to frequency of monitoring by GFR and albuminuria categories.

Persistent Albuminuria Categories

Description and Range

G F R C a t e g o r i e s ( m L / m i n p e r 1 . 7 3 m 2 )

D e s c r i p t i o n a n d R a n g e

A1

Normal to

mildly

increased

ACR <30 mg/g

A2

Moderately

increased

ACR of 30–300 mg/g

A3

1 2

1 2

1 2 3

2 3 3

3 3 4+

4+

G1

G2

G3a

G3b

G4

G5

≥90

60–89

45–59

30–44

15–29

<15

Normal or high

Mildly decreased

Mildly to moderately

decreased

Moderately to

severely decreased

Severely decreased

Kidney failure 4+ 4+

Severely

increased

ACR >300 mg/g

1 if CKD

1 if CKD

This GFR and albuminuria grid reflects the risk for progression by intensity of coloring. The numbers in the boxes are a guide to the frequency of monitoring (number of times per year). Reproduced from reference 2. ACR albumin–creatinine ratio; CKD chronic kidney disease; GFR glomerular filtration rate.






renin–angiotensin–aldosterone system (RAAS) interrup-tion slows progression of both diabetic and nondiabeticnephropathy. Lowering blood pressure also slows CKDprogression, breaking a potentially vicious cycle associating hypertension and CKD. Evidence is insufficient to recom-mend combining an angiotensin-converting enzyme inhib-

itor with angiotensin-receptor blockers to prevent CKDprogression. In formulating statements about blood pres-sure control and RAAS interruption, the recommendationsin the KDIGO guidance on blood pressure control inCKD were followed to maintain consistency (26).

Lifestyle interventions (reduced sodium intake to 2 g per day, achieving a healthy body mass index of 20 to 25kg/m2, smoking cessation, and exercising for 30 minutes 5times per week) and good diabetes control (target hemo-globin A

1c level of 7%) are also linked to reduction of

proteinuria and alleviation of CKD progression (27–30).

3.1.12. We recommend that all people with CKD are

considered to be at increased risk of AKI. (1A)

The goal of this recommendation was to promoteawareness of the complex relationship between CKD and

AKI. Evidence demonstrates that CKD remains an inde-pendent risk factor for AKI, even after multivariate adjust-ment for comorbid conditions (31). Mounting evidencesuggests that AKI is a risk factor for both incident CKDand progression of CKD. Both CKD and AKI increase inprevalence with age, and we are an aging population.

4.1.2 We recommend that the level of care for ischemic

heart disease offered to people with CKD should not beprejudiced by their CKD. (1A)

Persons with CKD are more likely to have a cardio-vascular event than to progress to end-stage renal disease;have worse prognosis with higher mortality rates after acutemyocardial infarction; and higher risk for recurrent myo-cardial infarction, heart failure, and sudden cardiac death(32). Despite this, the level of care offered to persons withCKD is still frequently suboptimal.

DISCUSSION

The CKD classification system now encompassescause of CKD, GFR category, and albuminuria category.This 3-dimensional approach builds on the simpler earlierversion, and the timing of these changes is appropriate,given the current familiarity of general physicians with thesimpler version and the need to address common misun-derstandings in a systematic manner. It has been arguedthat additional factors, such as blood pressure, should beincluded within the classification (33); however, while re-fining the existing staging system, we also wanted to retainthe simplicity and easy applicability of a classification sys-tem in clinical, research, and public health practice. There-

fore, we chose to include only kidney-related measures, andby including cause of CKD, we acknowledge the true dif-ferences in the natural history of kidney disease of differentcauses. The revised classification provides a framework forthe next decade of reporting and research in CKD.

Whether decreased GFR or increased ACR in older

persons represents a disease or “normal aging” will alwaysbe debatable, and disease labeling will continue to provokecontroversy in an aging society. Persons older than 75 yearshave a spectrum of GFRs exceeding 60 mL/min per1.73 m2 with and without albuminuria, as well as valuesless than 60 mL/min per 1.73 m2. Aging is associated withaccruing comorbid conditions and the use of medicationsthat may result in reductions in GFR and albuminuria, andthat is an underappreciated aspect of the argument aboutaging and eGFR.

It is no accident that 37% of the recommendations inthe guideline were ungraded and only 10% were graded“A” for quality of the evidence. Much of the research gen-

erated in the past decade has been aimed at definition andevaluation of CKD, together with identification of persons

with CKD and description of the associated adverse out-comes of CKD. We have some good trial data about inter-ventions, such as RAAS blockade in proteinuric CKD anduse of statin therapy for CKD (34, 35), and limited trialdata in other areas, such as bicarbonate therapy for acido-sis. We need much more data if we want to affect out-comes. We need to know exactly which interventions arebeneficial in prevention or alleviation of both CKD pro-gression and the associated adverse outcomes and how and

when these interventions should be applied. We also need

to know when interventions that are believed to be bene-ficial may actually cause harm. For example, indiscriminateuse of RAAS blockade in those with lower GFR and nospecific indication other than hypertension may exposepersons to additional risk for AKI with no benefit. Allied tothese areas, we need a much better understanding of defi-nitions of CKD progression and how they affect clinicalpractice and trials, how the relationship between AKI andCKD relates to progression, and whether we can positively influence this relationship.

From Kent Kidney Care Centre, East Kent Hospitals University NHS

Foundation Trust, Canterbury, United Kingdom, and University of

British Columbia, Vancouver, British Columbia, Canada.

Acknowledgment: The authors thank the KDIGO co-chairs Bertram L.

Kasiske, Kai-Uwe Eckardt, David C. Wheeler; the evidence review team

(Katrin Uhlig, Dana C. Miskulin, Amy Earley, Shana Haynes, MichaelCheung); and all those who provided feedback during the public review

of the draft guideline.

Potential Conflicts of Interest: Dr. Levin: Consultancy (money to insti-

tution): Abbott Laboratories, Merck & Co; Grants/grants pending (money

to institution): Canadian Institutes of Health Research (CIHR), Kidney Foundation, Merck & Co, Ortho. Dr. Stevens: None disclosed. Disclo-

sures can also be viewed at www.acponline.org/authors/icmje/ConflictOf

InterestForms.do?msNumM13-0034.

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Requests for Single Reprints: Paul E. Stevens, MBBS, BSc, Kent Kid-

ney Care Centre, Kent and Canterbury Hospital, Ethelbert Road, Can-

terbury, Kent CT1 3NG, United Kingdom; e-mail, [email protected].

Current author addresses and author contributions are available at www

.annals.org.

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Beddhu S. Weight loss interventions in chronic kidney disease: a systematicreview and meta-analysis. Clin J Am Soc Nephrol. 2009;4:1565-74. [PMID:19808241]29. Wakasugi M, Kazama JJ, Yamamoto S, Kawamura K, Narita I. A combi-nation of healthy lifestyle factors is associated with a decreased incidence of chronic kidney disease: a population-based cohort study. Hypertens Res. 2012.[PMID: 23171953]30. National Kidney Foundation. KDOQI Clinical Practice Guideline for Dia-betes and CKD: 2012 Update. Am J Kidney Dis. 2012;60:850-86. [PMID:23067652]31. Bedford M, Farmer C, Levin A, Ali T, Stevens P. Acute kidney injury andCKD: chicken or egg? [Editorial]. Am J Kidney Dis. 2012;59:485-91. [PMID:22444492]32. Herzog CA, Asinger RW, Berger AK, Charytan DM, Dı́ ez J, Hart RG,et al. Cardiovascular disease in chronic kidney disease. A clinical update fromKidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 2011;80:

572-86. [PMID: 21750584]33. Burgos-Calderon R, Depine S. Systematic approach for the management of chronic kidney disease: moving beyond chronic kidney disease classification. CurrOpin Nephrol Hypertens. 2010;19:208-13. [PMID: 19779338]34. Remuzzi G, Benigni A, Remuzzi A. Mechanisms of progression and regres-sion of renal lesions of chronic nephropathies and diabetes. J Clin Invest. 2006;116:288-96. [PMID: 16453013]35. Baigent C, Landray MJ, Reith C, Emberson J, Wheeler DC, Tomson C,et al; SHARP Investigators. The effects of lowering LDL cholesterol with sim-vastatin plus ezetimibe in patients with chronic kidney disease (Study of Heartand Renal Protection): a randomised placebo-controlled trial. Lancet. 2011;377:2181-92. [PMID: 21663949]






Current Author Addresses: Dr. Stevens: Kent Kidney Care Centre,Kent and Canterbury Hospital, Ethelbert Road, Canterbury, Kent CT1

3NG, United Kingdom.

Dr. Levin: St. Paul’s Hospital, Providence Wing, Room 6010A, 1160Burrard Street, Vancouver, British Columbia V6Z 1Y8, Canada.

Author Contributions: Conception and design: A. Levin.

Analysis and interpretation of the data: A. Levin.Drafting of the article: P.E. Stevens, A. Levin.

Critical revision for important intellectual content: P.E. Stevens,

A. Levin.Final approval of the article: P.E. Stevens, A. Levin.

Administrative, technical, or logistic support: A. Levin.Collection and assembly of data: A. Levin.

APPENDIX: KDIGO CKD GUIDELINE DEVELOPMENT

WORK GROUP MEMBERS

Rudy W. Bilous, Josef Coresh, Angel L.M. de Francisco,

Paul de Jong, Kathryn E. Griffith, Brenda R. Hemmelgarn,Kunitoshi Iseki, Edmund J. Lamb, Andrew S. Levey, Miguel C.

Riella, Michael G. Shlipak, Haiyan Wang, Colin T. White, and

Christopher G. Winearls.

Appendix Table 1. GRADE Criteria Used for Grade Levels in the KDIGO CKD Guideline

Grade Level* Implications

Patients Clinicians Policy

1 (“Werecommend”)

Most persons in this situation would—and onlya small proportion would not—want therecommended course of action.

Most patients should receive the recommendedcourse of action.

The recommendation can be evaluated asa candidate for developing a policy or performance measure.

2 (“We suggest”) Most persons in this situation would—butmany would not—want the recommendedcourse of action.

Different choices will be appropriate for differentpatients. Each patient needs help to arrive at amanagement decision consistent with his or her values and preferences.

The recommendation is likely to requiresubstantial debate and involvement ofstakeholders before policy can bedetermined.

CKD chronic kidney disease; GRADE Grading of Recommendations Assessment, Development, and Evaluation; KDIGO Kidney Disease: Improving Global Outcomes.* The additional category “Not Graded” was typically used to provide guidance on the basis of common sense or where the topic does not allow adequate application of evidence.

Appendix Table 2. GRADE Criteria Used for Letter Grades in the KDIGO CKD Guideline

Letter Grade Quality of Evidence Meaning

A High We are confident that the true effect lies close to that of the estimate of the effect.B Moderate The true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially different.

C Low The true effect may be substantially different from the estimate of the effect.D Very low The estimate of the effect is very uncertain and often wi ll be far from the truth.

CKD chronic kidney disease; GRADE Grading of Recommendations Assessment, Development, and Evaluation; KDIGO Kidney Disease: Improving Global Outcomes.

Appendix Table 3. Topics Chosen for Systematic Review

Topic Question Population

Nontreatment

Prediction equations for GFR How do serum creatinine– or cystatin C–based prediction equationsperform compared with gold standard measurement of GFR?

Patients in steady state with or without CKD and other special populations (DM, hypertension, KTRs or donors, various age groups, races, or ethnic groups)

Prediction equations for riskfor kidney failure

What prediction equations predict kidney failure? Patients with a GFR 60 mL/min per 1.73 m2 or KTRs

Gadolinium exposure and NFD What is the incidence of NFD after exposure to gadolinium? Patients with a GFR

60 mL/min per 1.73 m2

or KTRsAKI and phosphate-containing

bowel preparationsWhat is the incidence of AKI after taking a phosphate-containing

bowel preparation?Patients within any GFR category; individuals without

CKD

Treatment

Treatment with bicarbonate Does treatment with bicarbonate in CKD improve clinical outcomes? Patients with a GFR 60 mL/min per 1.73 m2 or KTRs

Treatment with allopurinol Does treatment with allopurinol in CKD improve clinical outcomes? Patients with a GFR 60 mL/min per 1.73 m2 or KTRswith or without hyperuricemia

Timing of initiation of RRT inCKD

When should dia lys is be started (early or late)? Patients with a GFR 30 mL/min per 1.73 m2

Protein restriction Should patients with CKD be on a protein-restricted diet? Patients with a GFR 60 mL/min per 1.73 m2 or KTRs

AKI acute kidney injury; CKD chronic kidney disease; DM diabetes mellitus; GFR glomerular filtration rate; KTR kidney transplant recipient; NFD

nephrogenic fibrosing dermopathy; RRT renal replacement therapy.

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