KDIGO CKD 2012

• Chapter 1: Definition and classification of CKD
• Chapter 2: Definition, identification, and
prediction of CKD progression
• Chapter 3: Management of progression and
complications of CKD
• Chapter 4: Other complications of CKD: CVD,
medication dosage, patient safety, infections,
hospitalizations, and caveats for investigating
• Chapter 5: Referral to specialists and models
of care

• CKD: What’s NEW?
•New CKD KDIGO Proposed Classification
•New CKD Definition
•New uACR
•New eGFR Formula
•Prevention & Treatment: Who & How?
•How to assess CKD Progression?

CKD is defined as abnormalities of
kidney structure or function, present
for > 3 months, with implications for
health
CKD DEFINITION

Summary of categorical meta-analysis
(adjusted RRs) for general population
cohorts with ACR.
Kidney Int 2011; 80: 17-28

Classification of CKD based on presence or absence of
systemic disease and location within the kidney of
pathologicanatomic findings

Relationship among categories for
albuminuria and proteinuria

CGA staging of CKD: examples of
nomenclature

Evaluation of GFR
• We recommend using serum creatinine and
a GFR estimating equation for initial assessment.(1A)
• We suggest using additional tests (such as cystatin C or
a clearance measurement) for confirmatory testing in
specific circumstances when eGFR based on serum
creatinine is less accurate. (2B)
• Report eGFRcreat in adults using the
2009 CKD-EPI creatinine equation.

Sources of error in GFR estimating
using creatinine

Performance of the CKD-EPI and MDRD Study
equations in estimating measured GFR in the external
validation data set
Ann Intern Med 2009; 150(9): 604-612.
CKD-EPI MDRD

Meta-analysis of NRI for all-cause
mortality, CVD mortality, and ESRD
JAMA 2012; 307(18): 1941-1951

Sources of error in GFR estimating
using cystatin C

DEFINITION AND IDENTIFICATION OF CKD
PROGRESSION

Management of progression and
• PREVENTION OF CKD
PROGRESSION
– BP and RAAS
interruption
– Glycemic control
– Hyperuricemia
– Protein intake
– Salt intake
• COMPLICATIONS
ASSOCIATED WITH
LOSS OF KIDNEY
FUNCTION
– Anemia
– CKD-MBD
– Acidosis

Clinical Practice Guideline of HT in CKD
• 2004 KDOQI (Kidney disease Outcomes
Quality Initiative) Clinical Practice Guidelines
on Hypertension and Antihypertensive Agents
in Chronic Kidney Disease
• KDIGO (The Kidney Disease Improving Global
Outcome) : Management of Blood Pressure in
Chronis Kidney Disease ; December 2012

KDIGO Clinical Practice Guideline for the Management
of Blood Pressure in Chronic Kidney Disease 2012
Non-diabetic Diabetic
BP goal
AER <30 ≤ 140/90 (1B) ≤ 140/90 (1B)
AER >30 ≤ 130/80 (2D,C) ≤ 130/80 (2D)
Medication
AER 30-300 ARB/ACEI (2B) ACEI/ARB (2D)
AER>300 ARB/ACEI (1B) ACEI/ARB (1B)

Lawrence J.Appel ; NEJM 2010 363:918-29.

AASK : Conclusion
• RCT in black with CKD
• N = 1094
• Randomly assigned : ramipril , metoprolol or amlodipine
• Target mABP intensive arm : 92 mmHg
• Target mABP standard arm : 102-107 mmHg
Result
• Primary endpoint: No difference in rate of GFR decline
• ACEI may be more effective than BB in slowing GFR decline
• Subgroup
– UPCR ≤ 0.22: No effect
– UPCR>0.22: Intensive BP retard CKD progression (a doubling
sCr,ESRD or death)

AASK

study/year outcome intervention control
HOPE
2001
MI, stroke in CKD Ramipril placebo
HOPE
2003
Dialysis, renal insufficiency Ramipril placebo
PREVEND
2004
CV events Fosinopril placebo
ALLHAT
2006
Renal failure &CAD with
CKD
In DM /non DM pt
lisinopril Chlorthalidone
PEACE
2006,2007
CV mortality in CKD trandolapril placebo
TRANSCEN
2009
Dialysis/sCr doubling telmisartan placebo
Val-HeFT
2009
Death valsartan Placebo

William C.Cushman;NEJM 2010;362:1575-85

Action to Control Cardiovascular Risk
in Diabetes : ACCORD study
• 10251 patients from 77 centers US. And Canada
• 4377 patients in ACCORD BP trial
• DM type II with HbA1C ≥7.5%
• ≥40 with CVD
• ≥55 with
– Evidence of atherosclerosis ,albuminuria or LVH
– 2 additional CV risk factors
• Assigned to either
– Intensive BP control (systolic BP<120mmHg)
– Conventional BP control (systolic BP<140 mmHg)

ACCORD study : conclusions
Intensive BP control
• Did not significantly reduce primary CV-event
• Some possible harm
– Hypotension
– Arrhythmia or bradycardia
– HyperK
– Elevate SCr

• Rationale
– DM II with microalbuminuria increased risk kidney
failure and CV events
– ACEI ,ARB reduce albuminuria in DM II with
microabluminia

• Ratinale
– Pt with DM and high levels of urine albumin high
risk of adverse CV and kidney outcomes
– Strong evidence from RCTs : ACEI &ARB protect
against kidney failure and reduce urine albumin
level

The Ongoing Telmisartan Alone and
in combinaion with Ramipril Global Endpoint Trial
ONTARGET
• Multicenter RCT
• 2001-2007
• Age >55 yrs with
– Atherosclerotic disease
– DM with end organ damage
• 25,630 were randomized to either
– Tarmisartan 80 mg/day
– Ramipril 10 mg/day
– Tarmisartan 80mg+ramipril 10mg/day

The ONTARGET study : conclusions
• Combination  no benefit in primary outcome
compare to Ramipril
• Combination  Worse kidney outcome
• Combination  Significantly increase
– Risk of hypotension
– Syncope
– Renal dysfuntion( requiring acute dialysis)
– Hyperkalemia
Johannes F E Mann;Lancet 2008;372:547-53

Add on aliskiren 300mg
More hyperK in combine aliskiren group

UKPDS( DM type II) extended follow up

DCCT/EDIC (DM type I)
• Additional 11 years
• A1C: 8% (equally)
• Result: Intensive therapy  Decrease
– Microalbuminuria
– Macroalbuminuria
– Doubling SCr  No
– SCr > 2  Yes
– HT
– 42% relative reduction in CV events
– Decrease mortality

KDOQI CLINICAL PRACTICE GUIDELINE FOR DIABETES
AND CKD: 2012 UPDATE

KDIGO CKD 2012
Kidney International Supplements (2013) 3, v

Serum Uric acid
• Elevated SUA (>7 in men, >6 in woman)
• Observational data: Elevate SUA
– Progression of CKD
– Increase All cause mortality
– Increase CV mortality
– CKD may be improved by specific uric acid lowering therapy.
• RCT design
• Small study show benefit in:
– Reduced LV mass1
– Improved endothelial function1
– Decrease CV events2
– Decrease hospitalization2
1 Kanbay M, Clin J Am Soc Nephrol 2011; 6: 1887–1894.
2 Goicoechea M, Clin J Am Soc Nephrol 5: 1388–1393, 2010

KDIGO 2012 Clinical Practice Guideline for the Evaluation
and Management of Chronic Kidney Disease

Protein intake
• We suggest lowering protein intake to
0.8 g/kg/day in adults with diabetes (2C) or
without diabetes (2B) and GFR <30 ml/min/
1.73 m2 (GFR categories G4-G5), with
appropriate education.
• We suggest avoiding high protein intake
>1.3 g/kg/day in adults with CKD at risk of
progression. (2C)

Salt intake
• We recommend lowering salt intake to < 90
mmol(<2 g) per day of sodium (corresponding
to 5 g ofsodium chloride) in adults. (1C)

Anemia in CKD patients
Semin Nephrol 26:261-268
RAS blockade

• 1.2.1: Diagnose anemia in adults and children
>15 years with CKD when the
Hb concentration is
<13.0 g/dl in males
<12.0 g/dl in females. (Not Graded)
Investigation of anemia
1.3: In patients with CKD and anemia (regardless of age
and CKD stage), include the following tests in initial
evaluation of the anemia (Not Graded):
•Complete blood count (CBC), which should
include Hb concentration, red cell indices, white
blood cell count and differential, and platelet count
• Absolute reticulocyte count
• Serum ferritin level
• Serum transferrin saturation (TSAT)
•Serum vitamin B12 and folate levels

USE OF IRON TO TREAT ANEMIA IN CKD
2.1.1: When prescribing iron therapy, balance
the potential benefits of avoiding or minimizing
blood transfusions, ESA therapy, and anemia
related symptoms against the risks of harm in
individual patients (e.g., anaphylactoid and
other acute reactions, unknown long-term
risks). (Not Graded)

2012
2.1.2: For adult CKD patients with anemia not on
iron or ESA therapy we suggest a trial of IV iron
(or in CKD ND patients alternatively a 1–3
month trial of oral iron therapy) if (2C):
• an increase in Hb concentration without
starting ESA treatment is desired* and
• TSAT is <30% and ferritin is <500 ng/ml (500
mg/l)

2012
2.1.3: For adult CKD patients on ESA therapy who are
not receiving iron supplementation, we suggest a
trial of IV iron (or in CKD ND patients alternatively a
1–3 month trial of oral iron therapy) if (2C):
• an increase in Hb concentration** or a decrease in
ESA dose is desired*** and
• TSAT is <30% and ferritin is <500 ng/ml (500 mg/l)

ESA INITIATION
• 3.1: Address all correctable causes of anemia
(including iron deficiency and inflammatory
states) prior to initiation of ESA therapy. (Not
Graded)
• 3.2: In initiating and maintaining ESA therapy,
we recommend balancing the potential
benefits of reducing blood transfusions and
anemia-related symptoms against the risks of
harm in individual patients (e.g., stroke,
vascular access loss, hypertension). (1B)

• 3.3: We recommend using ESA therapy with great
caution, if at all, in CKD patients with active
malignancy—in particular when cure is the
anticipated outcome—(1B), a history of stroke (1B),
or a history of malignancy (2C).

2.1.2 In the opinion of the Work Group, in
dialysis and nondialysis patients with CKD receiving
ESA therapy, the selected Hb target should generally
be in the range of 11.0 to 12.0 g/dL.
2.1.3 In dialysis and nondialysis patients
with CKD receiving ESA therapy, the Hb target should
not be greater than 13.0 g/dL
2006

• 3.4.1: For adult CKD ND patients with Hb
concentration >10.0 g/dl (>100 g/l), we suggest that
ESA therapy not be initiated. (2D)
• 3.4.2: For adult CKD ND patients with Hb
concentration <10.0 g/dl (<100 g/l) we suggest that
the decision whether to initiate ESA therapy be
individualized based on
– the rate of fall of Hb concentration
– prior response to iron therapy,
– the risk of needing a transfusion, the risks related to ESA
therapy and the presence of symptoms attributable to
anemia. (2C)
ESA INITIATION : CKD ND

ESA INITIATION : CKD 5D
• 3.4.3: For adult CKD 5D patients, we suggest that
ESA therapy be used to avoid having the Hb
concentration fall below 9.0 g/dl (90 g/l) by
starting ESA therapy when the hemoglobin is
between 9.0–10.0 g/dl (90–100 g/l). (2B)
• 3.4.4: Individualization of therapy is reasonable
as some patients may have improvements in
quality of life at higher Hb concentration and ESA
therapy may be started above 10.0 g/dl (100 g/l).
(Not Graded)

ESA MAINTENANCE THERAPY
• 3.5.1: In general, we suggest that ESAs not be used to
maintain Hb concentration above 11.5 g/dl (115 g/l) in
adult patients with CKD. (2C)
• 3.5.2: Individualization of therapy will be necessary as
some patients may have improvements in quality of life
at Hb concentration above 11.5 g/dl (115 g/l) and will
be prepared to accept the risks. (Not Graded)
• 3.6: In all adult patients, we recommend that ESAs not
be used to intentionally increase the Hb
concentration above 13 g/dl (130 g/l). (1A)

MEDICATION MANAGEMENT AND
PATIENT SAFETY IN CKD
• We recommend that prescribers should take GFR
into account when drug dosing. (1A)
• We recommend that adults with CKD seek
medical or pharmacist advice before using over-
the-counter medicines or nutritional protein
supplements. (1B)
• We recommend not using herbal remedies in
people with CKD. (1B)

MEDICATION MANAGEMENT AND
PATIENT SAFETY IN CKD
• We recommend that metformin be continued in
people with GFR >45 ml/min/1.73 m2 (GFR
categories G1-G3a);
• its use should be reviewed in those with GFR 30–
44 ml/min/1.73 m2 (GFR category G3b);
• it should be discontinued in people with GFR <30
ml/min/1.73 m2 (GFR categories G4-G5). (1C)

IMAGING STUDIES : Radiocontrast
• We recommend that all people with
GFR <60 ml/min/1.73 m2 undergoing elective
investigation involving the IV iodinated radiocontrast
media should be managed according to the KDIGO
Clinical Practice Guideline for AKI including:
– Avoidance of high osmolar agents (1B);
– Use of lowest possible radiocontrast dose (Not Graded);
– Withdrawal of potentially nephrotoxic agents before and
after the procedure (1C);
– Adequate hydration with saline before, during, and after the
procedure (1A);
– Measurement of GFR 48–96 hours after the procedure (1C).

IMAGING STUDIES : Gadolinium-based
contrast media
Nephrogenic systemic fibrosis

• We recommend not using gadolinium-
containing contrast media in people with GFR
<15 ml/min/1.73 m2 (GFR category G5) unless
there is no alternative appropriate test. (1B)
• We suggest that people with a GFR <30
ml/min/1.73 m2 (GFR categories G4-G5) who
require gadolinium containing contrast media
are preferentially offered a macrocyclic
chelate preparation.
IMAGING STUDIES : Gadolinium-based
contrast media

Bowel preparation
• We recommend not to use oral phosphate-
containing bowel preparations in people with
a GFR < 60 ml/min/1.73 m2 (GFR categories
G3a-G5) or in those known to be at risk of
phosphate nephropathy. (1A)

Regimen : 45 ml two dose taken 10-12
hrs apart ,the evening before and the
morning of colonoscopy
Each 45 ml contain 5.8 g of elemental
phosphorus
Ramathibodi SWIFF solution
Kidney International (2009) 76,1027-103

REFERRAL TO SPECIALIST SERVICES

TIMING THE INITIATION OF RRT
• We suggest that dialysis be initiated when one or more
of the following are present
– symptoms or signs attributable to kidney failure (serositis,
acid-base or electrolyte abnormalities, pruritus)
– inability to control volume status or blood pressure
– a progressive deterioration in nutritional status refractory
to dietary intervention
– cognitive impairment.
• This often but not invariably occurs in the GFR range
between 5 and 10 ml/min/1.73 m2. (2B)

TIMING THE INITIATION OF RRT
• Living donor preemptive renal transplantation
in adults should be considered when the GFR
is <20 ml/min/1.73 m2, and there is evidence
of progressive and irreversible CKD over the
preceding 6–12 months.(Not Graded)

KDIGO CKD 2012

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