Chronic Kidney Disease to Lung Oedema to

Haemodialysis
From Nephrologist point of View

Pranawa
Division of Nephrology and Hypertension – Department of Internal Medicine
Faculty of Medicine, Airlangga University – Dr. Sutomo Hospital
Surabaya
 Definition of Chronic Kidney Disease

Criteria
1.  Kidney damage for > 3 months, as defined by
structural or functional abnormalities of the kidney,
with or without decreased GFR, manifest by either :
•  Pathological abnormalities; or
•  Markers of kidney damage, including
abnormalities in the composition of the blood or
urine, or abnormalities in imaging tests
2.  GFR < 60 mL/min/1.73m2 for > 3 months, with or
without kidney damage

GFR = glomerular filtration rate

 Stages of Chronic Kidney Disease
GFR
Stage Description
(mL/min/1.73 m2)
1 Kidney damage with normal or " GFR > 90

2 Kidney damage with mild ! GFR 60 – 89

3 Moderate ! GFR 30 – 59

4 Severe ! GFR 15 – 29

5 Kidney failure < 15 or dialysis

Chronic kidney disease is defined as either kidney damage or GFR < 60 mL/min/
1.73 m2 for > 3 months. Kidney damage is defined as pathologic abnormalities or
markers of damage, including abnormalities in blood or urine tests or imaging
studies
1.2.3%Assign%GFR%categories%as%follows%(Not%Graded):%
%
%
•  Green:&low&risk&(if&no&other&markers&of&kidney&disease,&no&CKD);&Yellow:&
moderately&increased&risk;&Orange:&high&risk;&Red,&very&high&risk.&
AKI is defined as any of the following (Not Graded):

•  Increase in SCr by > 0.3 mg/dl (> 26.5 lmol/l) within 48

hours; or
•  Increase in SCr to >1.5 times baseline, which is known or
presumed to have occurred within the prior 7 days; or
•  Urine volume <0.5 ml/kg/h for 6 hourKDIGO Clinical
Practice Guideline for Acute Kidney Injurys.%
KDIGO&Clinical&Prac/ce&Guideline&for&Acute&Kidney&Injury&
Kidney&Interna/onal&Supplements&(2012)&2,&
Conceptual Model for Integration of
AKI, CKD and AKD

AKI&in&CKD&
KDIGO Clinical Practice Guideline for Acute Kidney Injury,
Online Appendices A-F, March 2012
 Pulmonary&Edema:&Pathophysiology&

•  A&pathophysiologic&condiHon,&not&a&disease&
– Fluid%in%and%around%alveoli%
– Interferes%with%gas%exchange%
– Increases%work%of%breathing%
•  Two&Types&
– Cardiogenic%(high%pressure)%
– NonECardiogenic%(high%permeability)%
 Pulmonary&Edema&
•  High&Pressure&(cardiogenic)%
• AMI%
• Chronic%HTN%
• MyocardiKs%
•  High&Permeability&(nonLcardiogenic)&
• Poor%perfusion,%Shock,%Hypoxemia%
• High%AlKtude,%Drowning%
• InhalaKon%of%pulmonary%irritants%
Cardiogenic&Pulmonary&Edema:&EHology%
•  LeN&ventricular&failure&
•  Valvular&heart&disease&
–  Stenosis&
–  Insufficiency&
•  Hypertensive&crisis&(high&aNerload)&
•  Volume&overload&
Increased Pressure in Pulmonary Vascular Bed
 Subtypes of Cardiorenal Syndrome
CRS&Type&I&(Acute&CardioLRenal&Syndrome)&
Abrupt%worsening%of%cardiac%funcKon%(e.g.%decompensated%congesKve%heart%failure%or%acute%%
cardiogenic%shock)%leading%to%acute%kidney%injury%

CRS&Type&II&(Chronic&CardioLRenal&Syndrome)&
Chronic%abnormaliKes%in%cardiac%funcKon%(e.g.%chronic%congesKve%heart%failure)%causing%
progressive%and%permanent%chronic%kidney%disease%
!

CRS&Type&III&(Acute&RenoLCardiac&Syndrome)&
Abrupt%worsening%of%renal%funcKon%(e.g.%Contrast%or%bypass%surgery%induced%AKI)%causing%
acute%cardiac%disorder%(e.g.%heart%failure,%arrhythmia,%ischemia)%%
!

CRS&Type&IV&(Chronic&RenoLCardiac&Syndrome)&
Chronic%kidney%disease%contribuKng%to%decreased%cardiac%funcKon,%cardiac%hypertrophy%
and/or%increased%risk%of%adverse%cardiovascular%events%

CRS&Type&V&(Secondary&CardioLRenal&Syndrome)&
Systemic%condiKon%(e.g.%diabetes%mellitus,%sepsis)%causing%both%cardiac%and%renal%dysfuncKon%

McCullough et al. Nephrol Dial Transplant (2010) 25:1777-1784

 Acute reno-cardiac syndrome (type 3)

Volume expansion
Acute Acute heart
kidney injury dysfunction
Drop in GFR

Sympathetic activation

RAA activation,
vasoconstriction

Electrolyte, acid-base &

coagulation imbalance

Humoral signaling

Ronco et al. Contrib Nephrol. Basel, Karger, 2010, vol 165, pp. 54-67
 Chronic reno-cardiac syndrome (type 4)
Chronic
kidney
disease

Acquired risk factors

Glomerular / Primary nephropathy
interstitial damage

Anemia
Uremic toxins Chronic
Ca/P abnormalities
Nutritional status, BMI heart
Na-H2O overload disease
Chronic inflammation

Anemia and malnutrition

Sclerosis-fibrosis Ca/P abnormalities
Na-H2O overload
Metabolic acidosis
inflammation
Dialysis
Ronco et al. Contrib Nephrol. Basel, Karger, 2010, vol 165, pp. 54-67
Cardiorenal Syndrome Type 4

Anemia, uremic toxins

Ca & Phos abnormalities
Nutritional status, BMI
Na + H2O overload
Chronic inflamation&

Anenia & malnutrition

Ca & Phos abnormalities
Soft tissue calcification
Na + H2O overload
EPO resistance
Uremmic toxins

Cytokine
production

(Ronco, C. et al. J Am Coll Cardiol 2008;52:1527-1539)

 Management&&

•  Follow%KDOQI%guidelines%for%CKD%management,%%
•  Exclude%precipitaKng%causes%(cardiac%
tamponade).%%
•  Treat%heart%failure%according%to%ESC%guidelines%
•  Consider%early%renal%replacement%support%
%
& Management&CRS&4&
# &Avoid&Hypervolaemia&&&PosiHve&sodium&balance&
# CorrecHng&anaemia&
# &Minimizing&vascular&calcificaHon&
# CardioprotecHve&strategies&$&ACEi&
$ &Started&at&a&lower&dose&
$ &Monitoring&the&paHent’s&hydraHon&status&

(Geisberg, 2006; Ronco, 2010)

5.3 &TIMING&THE&INITIATION&OF&RRT&
5.3.1 %We%suggest%that%dialysis%be%iniKated%when%one%or%
%more%of%the%following%are%present:%symptoms%or%
%signs%aXributable%to%kidney%failure%(serosiKs,%acidE
%base%or%electrolyte%abnormaliKes,%pruritus);%
%inability%to%control%volume%status%or%blood%
%pressure;%a%progressive%deterioraKon%in%nutriKonal%
%status%refractory%to%dietary%intervenKon;%or%
%cogniKve%impairment.%This%oZen%but%not%invariably%
%occurs%in%the%GFR%range%between%5%and%10% %ml/
min/1.73%m2.%(2B)%
5.3.2 %Living%donor%preempKve%renal%transplantaKon%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)%
Riviello&ED,&Christopher&KB,&Nephrology&Rounds&&(2006)4,issue&10&&
 Potential Extended Clinical Indicaions for
Supporting Initiation of RRT in Critically ill Patients
Category Characteristic
Severe AKI RIFLE-F/AKIN III
Mild-moderate AKI RIFLE-R or I/AKIN I or II plus consideration of
the following :
•  rapidly worsening AKI
•  multiple documented kidney insults
•  rapidly worsening illness severity
•  refactory fluid accumulation /overload
•  pre-existing chronic kidney disease
•  hypercatabolic state
•  permissive hypercapnea-induced acidosis
Bagshaw SM, Wald R, Contibution Nephrology, 2011, Vol. 174, pp 232-241
 Potential Extended Clinical Indicaions for
Supporting Initiation of RRT in Critically ill Patients

Category Characteristic
Other indications •  Refactory fluid overload
•  Refactory septic shock
•  Acute liver failure/ decompensated
chronic liver disease
•  Tumor lysis syndrome
•  Electrolyte disturbance
•  Selected endogenous/exogenous
toxins
•  Dysthermia
Bagshaw SM, Wald R, Contibution Nephrology, 2011, Vol. 174, pp 232-241
ESC&Guidelines&for&the&diagnosis&and&treatment&of&acute&and&chronic&heart&failure&2012.&
European&Journal&of&Heart&Failure&(2012)&14,&803–869&&&&&
 (Haemo)dialysis&in&pulmonary&oedema&&
•  CKD%st%5%HD%v/s%AKI%&%CKD%st%1E4%
•  Treatment%modaliKes%(%intermiXent%v/s%conKnues)%
•  UltrafiltraKon%rate%and%number%of%fluid%removal%
•  Timing%and%use%of%venKlator%
 (Haemo)dialysis&in&pulmonary&oedema&&
CKD&st&5&HD&v/s&AKI&&&CKD&st&1L4&
CKD%st%5%HD%
•  End%stage%renal%disease%

AKI%&CKD%st%1E4%
•  Preserved%residual%renal%funcKon%
 (Haemo)dialysis&in&pulmonary&oedema&&
•  CKD%st%5%HD%v/s%AKI%&%CKD%st%1E4%
•  Treatment&modaliHes&(&intermi^ent&v/s&conHnues)&
•  UltrafiltraKon%rate%and%number%of%fluid%removal%
•  Timing%and%use%of%venKlator%
Major%Renal%Replacement%Techniques%
IntermiXent% ConKnuous%

IHD% CVVH%
IntermiXent% ConKnuous%venoEvenous%
haemodialysis% haemofiltraKon%

IUF% CVVHD%
Isolated% ConKnuous%venoEvenous%
UltrafiltraKon% haemodialysis%

CVVHDF%
ConKnuous%venoEvenous%
haemodiafiltraKon%

SCUF%
Slow%conKnuous%
ultrafiltraKon%
Major%Renal%Replacement%Techniques%
IntermiXent% Hybrid% ConKnuous%

IHD% SLEDD% CVVH%

IntermiXent% Sustained%(or%slow)% ConKnuous%venoEvenous%
haemodialysis% low%efficiency%daily% haemofiltraKon%
dialysis%

IUF% SLEDDEF% CVVHD%

Isolated% ConKnuous%venoEvenous%
UltrafiltraKon% Sustained%(or%slow)% haemodialysis%
low%efficiency%daily%

CVVHDF%
dialysis%with%
filtraKon%
ConKnuous%venoEvenous%
haemodiafiltraKon%

SCUF%
Slow%conKnuous%
ultrafiltraKon%
 AKI Guideline 5.6

1.  Use continuous and intermittent RRT as

complementary therapies in AKI patients. (Not Graded)

2.  We suggest using CRRT, rather than standard intermittent

RRT, for hemodynamically unstable patients. (2B)

3.  We suggest using CRRT, rather than intermittent RRT, for

AKI patients with acute brain injury or other causes of
increased intracranial pressure or generalized brain
edema. (2B)
Individualized Approach

SLED

IHD CRRT
Renal%Replacement%Therapy—UltrafiltraKon:%%
Recommenda/ons&Class&IIb&&
&
1.  UltrafiltraKon%may%be%considered%for%paKents%with%obvious%
volume%overload%to%alleviate%congesKve%symptoms%and%fluid%
weight.(Level%of%Evidence:%B)%%
2.  UltrafiltraKon%may%be%considered%for%paKents%with%refractory%
congesKon%not%responding%to%medical%therapy.%(Level%of%
Evidence:%C)%
•  Cost,%the%need%for%venoEvenous%access,%provider%experience,%
and%nursing%support%remain%concerns%about%the%rouKne%use%of%
ultrafiltraKon.%%
•  ConsultaKon%with%a%nephrologist%is%appropriate%before%
iniKaKng%ultrafiltraKon,%especially%in%circumstances%where%the%
non%nephrology%provider%does%not%have%sufficient%experience%
with%ultrafiltraKon.%

2013&ACCF/AHA&Guideline&for&the&Management&of&Heart&Failure&
Circula/on.&2013;128:e240Ye327.&
 (Haemo)dialysis&in&pulmonary&oedema&&
•  CKD%st%5%HD%v/s%AKI%&%CKD%st%1E4%
•  Treatment%modaliKes%(%intermiXent%v/s%conKnues)%
•  UltrafiltraHon&rate&and&number&of&fluid&removal&
•  Timing%and%uses%of%venKlator%
•  No%spesific%guidelines%
•  Cardiorenal%benefits%:%Fluid%removal%improve%cardiac%funcKon,%
improving%renal%perfusion%and%GFR,%restoraKon%sensiKvity%to%
diureKcs.%
•  Improved%neurohormonal%markers%and%significant%reducKon%in%
circulaKng%level%of%inflamatory%cytokines%%
•  Matching%of%ultrfiltraKon%rate%(UFR)%and%plasma%refill%rate%
(PRR)%
 Treatment%parameters%HD%
CharacterisHc& Alternate&day& Daily&
DuraHon&of&session&(hours)& 3.4&+&0.5& 3.4&+&0.5&
&
Blood&flow&rate&(ml/min)& 243&+&25& 285&+&45&
& &
Dose&KT/V&
&&&&&Prescribed& 1.21&+&0.09& 1.19&+&0.11&
&&&&&Delivered& 0.94&+&0.11& 0.92&+&0.16&
&&&&&&Weekly&delivered& 3.0&+&0.6& 5.8&+&0.4&
Time&average&BUN& 104&+&18& 60&+&20&
Ultrafiltrate&volume(&L/session)& 3.5&+&0.3& 1.2&+&0.5&
 (Haemo)dialysis&in&pulmonary&oedema&&
•  CKD%st%5%HD%v/s%AKI%&%CKD%st%1E4%
•  Treatment%modaliKes%(%intermiXent%v/s%conKnues)%
•  UltrafiltraKon%rate%and%number%of%fluid%removal%
•  Timing&and&use&of&venHlator&
•  Failure%to%medical%treatment%
•  Benefit%in%paKents%who%had%urine%output%<%1%L/day%
•  Start%BUN%<%100%mg/dl%
 Timing of RRT in AKI

Patients with Early AKI

Early RRT Late RRT

IHD
Recover Die
without RRT without RRT
•  IniHate&RRT&emergently&when&lifeLthreatening&changes&in&&fluid,&
electrolyte,&and&acidLbase&balance&exist&
•  Consider&the&broader&clinical&context,&the&presence&of&condiHons&that&
can&be&modified&with&RRT,&and&trends&of&laboratory&testsLrather&than&
single&BUN&and&creaHnine&&thresholds&aloneLwhen&making&the&decision&
to&start&RRT&
•  VenKlator%or%dialysis%first%?????%
 Management&CRS4&&

•  Follow%KDOQI%guidelines%for%CKD%management,%%
•  Exclude%precipitaKng%causes%(cardiac%
tamponade).%%
•  Treat%heart%failure%according%to%ESC%guidelines%
•  Consider%early%renal%replacement%support%
%
Summary&&