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Uremic Syndrome

Acute Kidney Injury Chronic Kidney Disease

Lecture 3: Genito-urinary system.

10 – 08 – 2009.



Uremic Syndrome

Acute Kidney Injury Chronic Kidney Disease



nephron

the functional unit of the kidney

•capable of forming urine

•has two major components:

glomerulus

tubule:proximalloop of Henledistal

collecting

Interstitium



renal parenchymacortex

medulla

nephronscortical

juxtamedullary

structural organization



Renal Function:

Excretory

Regulatory

Endocrine

Excretory Function:

Glomerular

Glomerular Filtration Rate GFR! Creatinin Clearance"

Ux#$% ml$min



GFR:

inulin clearance

EDTA isotop

99 Tc isotop Iohexal High Performance

liquid chromatography

Clinical setting: e!": Coc#roft$ault !ormula

%D"D !ormula



Coc#roft$ault !ormula

%ale: &'() x *&+, - age . x /0 *#g. Ccr 1 $$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$ ml2min

3cr *4 mol2min.

5r &+, - age *yrs. x /0 *#g. Ccr 1 $$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$ ml2min

6(x 3cr *mg2dl.

!emale: &+, - age *yrs. x /0 *#g.

Ccr 1 $$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$ ml2min 6, x 3cr *mg2dl.

5r Ccr* male. x o787



NKF-KDO! recommen"ationNKF-KDO! recommen"ation

AdultsCockcroft-Gault equation:

GFR (ml/min) = (140-ae) ! "ei#t /$% & 'cr !(0* if female)

+,R, (modification of diet in renal disease) equation:

GFR (ml/min/1$ m%) = 1. ! ('Cr) -11*4 ! (Ae) -0%0 !

(0$4% if female) ! (1%10 if lack)

C#ildren'c#art equation: GFR (ml/min) = 0** & lent#/'cr

Couna#an-2arratt equation: GFR (ml/min/1$m%)= 04 ! 3ent#/'cr



Renal Function:

Excretory

Regulatory

Endocrine

Regulatory Function:

&u'ulo(interstitial

) *ater and electrolyte 'alance) acid('ase 'alance



Renal Function:

Excretory

Regulatory

Endocrine

Endocrine Function:

renal +arenchymal

renin, +rostaglandin,erythro+oietin, calcitriol



#remic $o%icity#remic $o%icity



#remia-1#remia-1

Gree- *ords : urine . 'lood / uremia

Uremia is the retention o0 excessi1e 'y

+roducts o0 +rotein meta'olism in the 'lood

and the toxic condition +roduced there'y"



#remia-2#remia-2

Uremia is a toxic syndrome caused 'y se1ere

glomerular insu00iciency, associated *ith

distur'ances in tu'ular and endocrine 0unctions o0the -idney"

It is characteri2ed 'y retention o0 toxic

meta'olites, associated *ith changes in 1olume

and electrolyte com+osition o0 the 'ody 0luids andexcess or de0iciency o0 1arious hormones uremic

syndrome!"



$o%ic e&&ects o& uremic '(asma$o%ic e&&ects o& uremic '(asma

1ariety distur'ances:

anemia, immunologic de0iciency,

'leeding tendency, disorders o0

car'ohydrate and li+id meta'olism,

and 1arious mem'rane trans+ortdistur'ances"



#remia#remia

General 3 Fatigue, *ea-ness

3 %ruritus

4ental$neurologic status change 3 Uremic ence+halo+athy

3 Sei2ures

3 Asterixis

GI distur'ance 3 Anorexia, early satiety, 5$#,

remic 5ericarditisremic 5ericarditis

%latelet dys0unction$'leeding

An excess in the 'lood o0 urea, creatinine and other

nitrogenous end +roducts *ith signs and sym+toms listed "



#remic to%ins#remic to%ins

)ma((* mi""(e-si+e"* an" (ar,e mo(ecu(es)ma((* mi""(e-si+e"* an" (ar,e mo(ecu(es

Si2e: Small : 6 788 or 978 ! Da

4iddle : 788 7,888 Da

;arge : < 7,888 Da



$o%icity o& inor,anic sustances$o%icity o& inor,anic sustances

in uremiain uremia=ater

Sodium

%otassium>ydrogen ions

4agnesium

%hos+hate

Sul0ate

&race elements



Or,anic com'oun"s o& LoOr,anic com'oun"s o& Lo

mo(ecu(ar ei,/tmo(ecu(ar ei,/tUrea

Creatinine

Guanidines other than creatinine!4ethylguanidine

Guanidinosuccinic Acid GSA!

4ethylated Arginine 4eta'olites?ther guanidines

%roducts o0 5ucleic Acid 4eta'olism

O i " & L ( ( i /t



#rea 1#rea 1

&he most im+ortant end +roduct o0 nitrogen

meta'olism in mammals and account 0or

@7 o0 the urinary nitrogen excretion"Blood concentration: glomerular 0iltration

rate, nitrogen inta-e, 'alance 'et*een

endogenous +rotein synthesis and 'rea-do*n"

Or,anic com'oun"s o& Lo mo(ecu(ar ei,/t

O i " & L ( ( i /t



#rea3#rea3

>igh concentration: headache, 0atigue,

nausea, 1omiting, glucose intolerance, and

'leeding"&he most se1ere uremic GI, C#, mental and

neurologic changes *ere not seen"

Considered mild uremic toxin "

Role in the +atho+hysiology o0 uremia is not

*ell de0ined"




)erum reatinine)erum reatinine

Serum creatinine is a re0lection o0 creatinineclearance

Creatinine +roduction is determined 'y muscle massand must 'e inter+reted *ith res+ect to +ts age,*eight and sex"

Creatinine is 0iltered and secreted and tends to o1erestimate GFR"

Certain diseases and medications inter0ere *ithcorrelation 'et*een serum Cr and GFR" i"e"" Acuteglomerulone+hritis, trimetho+rim, cimetidine!



)erum reatinine cont.)erum reatinine cont.

5one o0 the euations accurately determine

GFR in ARF" Assume Cr is sta'le!

4ore accurate techniues in1ol1e nuclear

medicine studies and GFR scans"

5e* 'iochemical mar-ers in1estigated i"e""

Cystatin C!




Ot/er ,uani"inesOt/er ,uani"ines

&he concentrations o0 1arious guanidinecom+ounds are higher in uremic +atients"

Some toxic in 1itro e00ects seem to ha1e 'eeno'tained at concentrations similar to those inuremic 'ody 0luids"

4ost in 1itro and in 1i1o toxic e00ects ha1e 'eeno'ser1ed at much higher concentrations than are

0ound in uremic +atients&he role o0 guanidines as uremic toxins is still not

*ell de0ined"




ro"uct o& Nuc(eic 4ci"ro"uct o& Nuc(eic 4ci"

5etao(ism5etao(ism Uric acid and other +urine deri1ati1es

Cyclic A4%

%yridine deri1ati1es

Amino acids, di+e+tides, and tri+e+tides Sul0ur amino acids

Ali+hatic amines

Aromatic amines

%olyamines Indoles

%henols

Car'onhyrate deri1ati1es



5i""(e mo(ecu(es as uremic5i""(e mo(ecu(es as uremic

to%insto%ins&he middle molecule hy+othesis:

%eritoneal mem'rane *as more lea-y and thus

more e00ecti1e at remo1ing middle molecules thanthe hemodialysis mem'ranes"

It is *ell esta'lished that CA%D +atients may

sur1i1e and thri1e as *ell as >D +atients do, e1en

though their a1erage *ee-ly clearance o0 urea is

considera'ly lo*er than that 0or >D +atients"



$o%ic e&&ects o& cru"e 55$o%ic e&&ects o& cru"e 55

&ractions&ractions Inhi'ition o0 +roli0eration o0 undi00erentiated cell

lines and hemato+oietic cell lines, de+ression o0

se1eral immmune 0unction, increase hemolysis,cardiotoxicity, inhi'ition o0 +latelet aggregation,

inhi'ition o0 glucose utili2ation, inhi'it +rotein

synthesis and amino acid trans+ort, inhi'ition o0

mitochondrial res+iration Inhi'it osteoclast mitogenesis

Some en2yme acti1ities are also inhi'ited



arat/yroi" /ormonearat/yroi" /ormone

Incresed in uremic +atients as conseuence o0

+hos+hate retention, decreasing ioni2ed calcium

stimulate +arathyroid glands to increase %&>secretion

%&> hy+ersecretio+n in uremic +atients :

ence+halo+athy, neuro+athy, dementia, 'one

disease, so0t tissue calci0ication, hy+ertension,cardiomegaly, car'ohydrate intolerance, anemia,

sextual dys0unction



6i,/-mo(ecu(ar-ei,/t 'e'ti"es6i,/-mo(ecu(ar-ei,/t 'e'ti"es

an" 'roteinsan" 'roteinsRi'onuclease

Granulocyte(inhi'iting +roteins

Com+lement 0actors

Beta(4icroglo'ulin and Dialysis(related

amyloidosis



#remic )yn"rome#remic )yn"rome

4cute Ki"ney !n7ury 4cute Ki"ney !n7ury /ronic Ki"ney Disease/ronic Ki"ney Disease

Lecture 3: Genito-urinary system.

10 – 08 – 2009.



acute kidney injury: definition

ARF is an abrupt decline in glomerular andtubular function, resulting in the failure of the

kidneys to excrete nitrogenous waste productsand to maintain fluid and electrolytehomeostasis



'i"emio(o,y'i"emio(o,y

7 o0 hos+itali2ed +atients de1" ARF"

8"7 o0 these +atients reuire dialysis"

8 o0 critical care admissions de1" ARF"

>os+ital acuired ARF usually de1elo+s in

the setting o0 ICU secondary to multisystem

organ 0ailure"



R!FL (assi&icationR!FL (assi&ication

%004 A,67 rou8 classification

Ris- R! (Increase Cr xH"7 or Decrease GFR x 7 or U?68"7 ml$-g$hr x hrs

Injury I!( Increase Cr x"8 or Decrease GFR x 78 or U?68"7 ml$-g$hr x Hhrs

Failure F!( Increase Cr x9"8 or Decrease GFR xJ7 oranuria x H hours

;oss ;!( %ersistent ARF, com+lete loss o0 -idney 0unction

x *ee-s needing RR&!End Stage Kidney Disease E!( ;oss o0 -idney 0unction x 9

months



The Second International Consensus Conference of

the Acute Dialysis Quality Initiative (ADQI) Group



A K I

PRE RENAL RENAL POST RENAL

Loss of intra-vas. vol

Reduced cardiac-output Periferal #asodilatation

Increased reno-vasc resistenceReduced intra-glomerular pressure

ACE-i



;oss o0 intra(1asc 1ol"" Reduced cardiac(out+ut B;EEDI5G C>F

%?;LURIA, SA;&(;??SI5G G5 CARDI?GE5IC S>?CK

G(I &RAC& F;UIG ;?SS %ERICARDIA;$&A4%?5ADE

%R?FUSE S=EA&I5G 4ASSI#E ;U5G E4B?;I

&ISSUE &AU4A E&C

%eri0er #asodilatation Increase reno(1asc"resistence

SE%SIS SURGERL

A5&I(>I%ER&E5SI#E DRUGS A5ES&EL>ICS

A5A%>L;AMIS >E%A&?RE5A; SL5DR

#AS?C?5S&RIC& DRUGS

Reduced intraglom" +ressure ACE(i

ACU&E KID5EL I5NURL

%re(renal



A K I

PRERENAL RENAL POST RENAL

I! "ESSELS

S#ALL "ESSELS!LO#ER$LARINTERSTITI$#

T$$LAR

BIG VSS!S S"A!! VSS!S



BIG VSS!S S"A!! VSS!S

STENOSIS A.RENALIS VASCULITIS, ATHEROEMBOLIC

DIS. THROMBOSIS/EMBOLI THROMBOTIC

MICROANGIOPATHY

G!#"$%!A$& I'T$STITI%" Ix deposit !o". Dise#se A$%te i&te'stiti#!&ep('itis

ps&, !%p%s &ep('itis, MPGN et$ AB, Di%'eti$s,NSAID,

RPGN #!!op%'i&o! d!! Goodp#st%'e s)&d'

No& Ix deposit *ee&e'+s '#&%!o"#tosis, Po!)#'te'iitis

&odos#, Idiop. C'es$.GN

T%B%!A$&

Re&#! is$(e"i# s(o$-, !eedi&, t'#%"#, '#" 01 #$te'i#,



A K I

PRERENAL RENAL POST RENAL

Stone% Cr&stals Prostate% $reteric

Stricture 'ilateral or uni-lateral in singlefunctioning (idne&

#E)ICAL S$R!ICAL

auses o& 4RF in 6os'ita(i+e"auses o& 4RF in 6os'ita(i+e"



auses o& 4RF in 6os'ita(i+e"auses o& 4RF in 6os'ita(i+e"

atientsatients4*9 A;

7sc#emia< ;e8#roto&ins

%19 5rerenal CF< >olume de8letion< se8sis

109 rinar? ostruction

49 Glomerulone8#ritis or >asculitis

%9 Acute 7nterstitial ;e8#ritis

19 At#eroemoli

etc



re Rena( 4+otemiare Rena( 4+otemia

Im+aired renal 'lood 0lo* as a result o0 trueintra1ascular de+letion, decreased e00ecti1ecirculating 1olume to the -idneys, or agents that

im+air renal 'lood 0lo*"Urine and 'lood studies are hel+0ul in diagnosing

+re renal ARF"

>yaline casts can 'e seen 5ot an a'normal0inding!"

&reat *ith 0luid 'oluses or continuous I#F, monitorurine out+ut"



ost Ostructie #ro'at/yost Ostructie #ro'at/y

?ccurs i0 'oth urinary out0lo* tracts are o'structed orout0lo* tract o0 solitary -idney is o'structed"

%atients *ith SUDDE5 ?5SE& o0 anuria are li-ely toha1e +ost o'structi1e uro+athy"

%rimary causes include B%>, +rostate and cer1ical cancer,stones, strictures and retro+eritoneal 0i'rosis"

Bladder catheteri2ation and Renal U$S to assesshydrone+hrosis"

Can ha1e o'struction *$o hydrone+hrosis on U$S

4onitor 0or +ost o'structi1e diuresis, hemorrhagic cystitisO



!ntrinsic 4cute Ki"ney !n7ury!ntrinsic 4cute Ki"ney !n7ury

H" &u'ular A&5!

" Interstitial AI5!

9" Glomerular Glomerulone+hritis!

" #ascular



4$N 4$N

4ost common cause o0 ARF in hos+itali2ed +atientsContrast and aminoglycosides most o0ten associated *ith

nonischemic A&5"

9 +hases:

H! Initiation +hase( Renal injury lasting hours to days"! 4aintenance +hase( ;asts days to *ee-s" GFR andU"? at lo*est"

9! Reco1ery %hase( %ostacute tu'ular necrosis diuresis"Can still ex+" uremia and hy+o1olemia as tu'ular 0unction

not com+letely restored"



4cute !nterstitia( Ne'/ritis 4cute !nterstitia( Ne'/ritis

J8 Drug hy+ersensiti1ity 98 Anti'iotics: %C5s 4ethicillin!, Ce+halos+orins, Ci+ro Sul0a drugs 5SAIDs Allo+urinol"""

H7 In0ection Stre+, ;egionella, C4#, other 'act$1iruses

@ Idio+athic

Autoimmune D2 Sarcoid, &u'ulointerstitial ne+hritis$U1eitis!



4!N &rom Dru,s 4!N &rom Dru,s

Renal damage is 5?& dose(de+endent

4ay ta-e *-s a0ter initial ex+osure to drug U+ to H@ mos to get AI5 0rom 5SAIDSP

But only 9(7 d to de1elo+ AI5 a0ter second ex+osure to drug

Fe1er J! Serum Eosino+hilia 9! 4aculo+a+ular rash H7!

Bland sediment or =BCs, sterile +yuria most commonly seen =BC Casts are common

Urine eosino+hils on =rights or >ansels Stain( Also see urine eos in R%G5, renal atheroem'oli"""

&reatment is to remo1e o00ending agents" 4ost +atients reco1er com+lete -idney0unction *$I one year"



Ne'/ritic )yn"romesNe'/ritic )yn"romes&y+e H: Anti(GB4 d2 Anti GB4 A' +ositi1e!( Good+astures Disease( Anti(GB4

&y+e : Immune com+lex ;o* com+liment, ele1ated ESR! IgA ne+hro+athy 5ormal Com+liment le1els! %ostin0ectious glomerulone+hritis ;u+us ne+hritis 4ixed cryoglo'ulinemia 4%G5 IBE

&y+e 9: %auci(immune A5CA +ositi1e, assoc *ith 1asculitis! =egners Disease 4icrosco+ic %olyangitis Churg(Strauss



Ne'/ritic )yn"romesNe'/ritic )yn"romes

Fe1er

?liguria

>ematuria>tn

RBC casts

%roteinuria H(grams usually!&reatment 1aries 'ased on underlying disease



Rena( 4t/eroemo(ic D%Rena( 4t/eroemo(ic D%

H o0 Cardiac caths: atheromatous de'ris scra+ed 0rom theaortic *all *ill em'oli2e

3 Retinal

3 Cere'ral 3 S-in ;i1edo Reticularis, %ur+le toes!

3 Renal ARF!

3 Gut 4esenteric ischemia!

Cr *ill 5?& im+ro1e *ith I#F Diagnosis o0 exclusion: *ill 5?& sho* u+ on 4RI or Renal

U$SQ =I;; sho* u+ on renal 'x

&x: su++orti1e



acute rena( &ai(ure:acute rena( &ai(ure: 'reention'reention

recogni2e +atients at ris- +osto+erati1e states, cardiac

surgery, se+tic shoc-!

+re1ent +rogression 0rom +rerenal to renal

+reser1e renal +er0usion 3 iso1olemia, cardiac out+ut, normal 'lood +ressure

3 a1oid ne+hrotoxins aminoglycosides, 5SAIDS, am+hotericin!



$reatment$reatment

Re1erse underlying causes and correct 0luid

and electrolyte 'alances

&reatment is su++orti1e"Drugs such as mannitol, loo+ diuretics,

do+amine and CCB success0ul in +romoting

diuresis in animals 'ut not in humans"Dialysis as needed I>D 1s" CRR&!



acute rena( &ai(ure:acute rena( &ai(ure: mana,ementmana,ement

treat the underlying diseases

strictly monitor inta-e and out+ut *eight, urine out+ut,

insensi'le losses, I#F!monitor serum electrolytes

adjust medication dosages according to GFR

a1oid highly ne+hrotoxic drugs



nutritionnutrition

8ro>ide adequate caloric intake

limit +rotein inta-e to control increases in BU5

minimi2e +otassium and +hos+horus inta-e

;imit 5a$0luid inta-e

If adequate caloric intake can not be achieved

due to fluid limitations, some form of dialysisshould be considered



acute rena( &ai(ure:acute rena( &ai(ure: &(ui" t/era'y&(ui" t/era'y7f 8atient is fluid o>erloaded

0luid restriction insensi'le *ater losses!

attem+t 0urosemide H( mg$-g not e1idence('ased!

Renal re+lacement$su++ort thera+y see later!

7f 8atient is de#?drated: restore intra1ascular 1olume 0irst

then treat as eu1olemic 'elo*!

7f 8atient is eu>olemic: restrict to insensi'le losses 98(97 ml$H88-cal$ hours! .

other losses urine, chest tu'es, etc!



Daily fluid alloance:Daily fluid alloance:

A;;50A<CEA;;50A<CE 1 =olume Excreted > I 0 ;1 =olume Excreted > I 0 ;

(+ hrs(+ hrs

=olume Excreted :=olume Excreted : ?rine' @omitus' diarhea'?rine' @omitus' diarhea'

drain' etcdrain' etc

I 0 ; :I 0 ; : ,, ml 2 (+ hrs,, ml 2 (+ hrs , #g /0 T )6, #g /0 T )6 ,,CC & B & B increment of &increment of & ,,CC

%onitor daily /0 %onitor daily /0



so"iumso"ium

most +atients ha1e dilutional hy+onatremia *hich

should 'e treated *ith 0luid restriction

se1ere hy+onatremia 5a6 H7 mE$;! or

hy+ernatremia 5a< H78 mE$;!: dialysis or

hemo0iltration



$reatment o& 6y'era(emia$reatment o& 6y'era(emia

Calcium Gluconate

Glucose and InsulinSodium Bicar'onate

Diuretics ;asix!

Cation(exchange resins Kayexalate!Dialysis



4cute !n"ications &or Dia(ysis 4cute !n"ications &or Dia(ysis

AIUE?Acidosis meta'olic!

Ingestion o0 drugs$Ischemia

Uremic syndrome

Electrolytes hy+er-alemia!?1erload 0luid!



"A'AG"'TA K I

*L$I)

)IET

)R$!

RRT+S$PPORT

Severe uremic s&mptoms $rea , mg/%Cr ,0 mg/ 1 , 2 mg/ Pericarditis Severe Asidosis

Pulmonar& Oedema

)IAL3SIS

PERITONEAL 4E#O

INDIKASI :

"#I!T$ATI#'

CA"4 5d6% C""4 5d6

SC% (d)* S!DD



5orta(ity;5ori"ity5orta(ity;5ori"ity

4ortality rates range 0rom J(@8 de+ending on +atients other co mor'idities"

&his rate has remained unchanged since the ad1ento0 dialysis 'ecause o0 increasing age and comor'id conditions"

4ost common cause o0 death associated *ith ARF

are se+sis, cardiac 0ailure and res+iratory 0ailure"4ortality rates are lo*er 0or nonoliguric

<88ml$day! then oliguric ARF 688 ml$day!"



Take Home PointsTake Home Points

Features of the history and physical examination

in addition to relevant lab and radiologic

investigations help to determine the most likelycause(s) of ARF in a given patient



Take Home PointsTake Home Points

anagement of a patient !ith ARF involves"

# Treating potentially life$threatening complications

# Reversing pre$renal and post$renal causes# inimi%ing further hemodynamic and toxic insults to

the kidney

# Admission and appropriate consultation# &ack of evidence for converting oliguric to non$

oliguric ARF





#remic )yn"rome#remic )yn"rome

4cute Ki"ney !n7ury 4cute Ki"ney !n7ury /ronic Ki"ney Disease/ronic Ki"ney Disease





CKD

PARENC43#AL OSTR$CTI"E

G' Dia+etic 'ephropathy 'ephrosclerotic,hypertension

Polic&stic Lupus TC

urolit7iasis Prostate

$reteric Stricture





De&inition o& De&inition o&

/ronic Ki"ney Disease/ronic Ki"ney Disease

4<KD 2002: 392







NKF-KDO! recommen"ationNKF-KDO! recommen"ation

Adults

+,R, (modification of diet in renal disease) equation:

GFR (ml/min/1$ m%) = 1. ! ('Cr) -11*4 ! (Ae) -0%0 !

(0$4% if female) ! (1%10 if lack)

C#ildren

'c#art equation: GFR (ml/min) = 0** & lent#/'cr

Couna#an-2arratt equation: GFR (ml/min/1$m%)= 04 !3ent#/'cr

iota( Rote o& G(omeru(ar 6y'ertensioniota( Rote o& G(omeru(ar 6y'ertensionin t/ein t/e !nitiation!nitiation an"an" ro,ressionro,ression



in t/ein t/e !nitiation!nitiation an"an" ro,ressionro,ression

o& )tructura( !n7uryo& )tructura( !n7ury..

4n"erson ). =renner. < 5e" 1989 > ?0 : 18@-189.

)ystemic

6y'ertension

4,in,* Diaetes

5e(itus* Dietary

Factors

E<D5THE;IA; I<?"

Re(ease o& asoactie

&actors

Aascu(ar (i'i" "e'osition

!ntraca'i((ary t/romosis

%E3A<IA; I<?"

4ccumu(ation o& macromo(ecu(es↑5atri% 'ro"uction

↑ e(( 'ro(i&eration

EPITHE;IA; I<?"

Proteinuria

↓ ermeai(ity to ater

GLO5R#L4R 6BR$N)!ON

GLO5R#L4R )LRO)!)

rimary Rena(

Disease Rena(

4(ation

5 i i



5rotein leakae

5roteinuria

5rotein load to5ro&imal tuules

Gene e&8ression

for inflamationransdifferentiation

to m?ofilolast

Glomerular ?8ertension Firosis

An 77 GF @ 1< etc

5roliferation?8ertension

+atri& s?nt#esis

%R?GRESSI?5 o0 CKD

Interstitium



kno?an G< A'; '?m8<5#iladel8#ia<%00%



KD re"icts ADKD re"icts AD

Go* et a(.* 200C

4 , e - )

t a n " a r " i + e " R a t e

o & 2 a r " i o 9 a s c u ( a r

8 9 e n t s ' e r 1 0 0

' e r s o n - y r

stimate" GFR mL;min;1.?3 m2

)ta,e@ N 3?2 0003tage and



)ta,e 1

)ta,e 2

)ta,e 3

)ta,e C

)ta,e@

N@*900*000

GFRE90

N@*300*000

GFR 0-89

N?*00*00

GFR 30-@9

GFR 1@-29

GFR H1@

N3?2*000

NC00*000

!" measurement in m;2min2&76) m(

3tage and

pre@alence of CFD

in indi@iduals older

than (, years

J



.

6eert et aL: K! 2001 @9:1211-2

E S R D



In normal healthy indi1iduals, the eGFR *ill 0all

'y u+ to H8 ml$min ie H8! +er decade

An @8 year old man *ill ha1e an e&8ected eGFR o0

78(8 ml$min



"I3F !ACT5"3 !5" CFD

P"5"E33I5<

GN$!

HPE";CE%IA

R44) 4$!A!$B

HPE"TE<3I5<

P"5TEI<?"IA

6BRL!!D5!4

CIA"ETTE3

6O5OB)$!N

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Kidney International Vol 66 (2004), pp: 753-760



Ki"ney !nt 200C : ?@3 - 0



Ki"ney !nt 200C : ?@3 - 0



Ki"ney !nt 200C : ?@3 - 0

Early Treatment %a#es a DifferenceEarly Treatment %a#es a Difference



Early Treatment %a#es a DifferenceEarly Treatment %a#es a Difference

"A'AG"'T



CKD

C#'S$VATIV $$T

)iet = >ater ? saltProteinCalori

P7osp7ate% 1?

Ris(-factors management

S&mptomatic #edicament =

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DIA!0SIS

"A'AG"'T

CKD

Consernative

TRANSPLANT

4emodialisa Peritoneal

CAP) IP) 4emoltration 4emodialtration

Indication = vide A1I

$$T

Diaetes:Diaetes:

$/ 5 t & )RD$/ 5 t & )RD



$/e 5ost ommon ause o& )RD$/e 5ost ommon ause o& )RD

Primary Diagnosis for Patients 0ho 3tart Dialysis

DiaKetes

,7&B

Hypertension

(6B

lomerulonephritis

&)B

5ther

&,B

#nite" )tates Rena( Data )ystem. 4nnua( "ata re'ort. 2000.

<o7 of patients

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CONSER"ATI"E )IAL3SIS T$A'S1!A'T

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a. )ial&sis:. Peritoneal dial&sis 5continuous am'ulator& peritoneal

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;ong term use o0 imuno(su++ressi1e drugs

to co+e *ith rejection

5 t $ 6



5essa,es to $ae 6ome5essa,es to $ae 6ome

Kidney Disease is a silent -iller(no signs or

sym+toms until you loose <J8 o0 your -idney

0unction,

&he ris- o0 dying 0rom a cardio1ascular e1ent, i0

you1e lost 78 or more o0 your -idney 0unction,

is similar to that ha1ing had a heart attac-"

5roteinuria reduction needs to e a ke? 8art oflood 8ressure manaement"

J(,,7 American College of Physicians7 All "ights "eser@ed7



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