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C hronic renal fail u re C hronic renal fail u re q iubo q iub
C hronic renal fail u re
C hronic renal fail u re
q iubo
q iub o
TE L :15 1537 01 8 81
T EL :15 1537 018 81
ch ronic renal fai lure chronic renal fai lure definit ion: definit ion: - a pathophysiologic
ch ronic renal fai lure
chronic renal fai lure
definit ion:
definit ion:
-
a pathophysiologic process with m ultiple etiologies
a pathophys iologic process with m ultiple etiologies
-
reduced of neph ron number and function
reduced of neph ron num ber and function
-
A state, in w hich there has been an irr eversible loss of
A state, in w hich there has been an irreversible loss of
rena l function , m ust d epend upon dialysis or
renal function , must d epend upon dialysis or
transplantatio n
tra nsplantati on
-
““The wor ld kidney day”, the second tuesd ay in March
The w orld kidney day ”, the second tuesd ay in March
every ye ar
ev ery year
-
B e a great soci a l and economic burden on the whole
Be a great soci a l and economic bur den on the whole
world, in USA, the cost on thera py for chronic kidney
world, in USA, the cost on therapy for chronic kidney
disease has been rised to 20,000 ,000,000 dollars
disease has been rised to 20,000 ,000, 000 dollars
-
Be the lea ding killer to m ankinds health
Be the lea ding killer to mankinds health
defi n ition defin it ion 1.Azote mia - elevated blood urea nitrogen (BUN 1.Azote m
defi n ition
defin it ion
1.Azote mia - elevated blood urea nitrogen (BUN
1.Azote m ia - elevated blood urea nitrogen (BUN
>28 m g/dL) and crea tini n e (Cr>1.5 mg/dL)
>28 m g/dL) and crea ti nin e ( C r>1.5 mg/dL)
2.Uremia - azotem ia w ith sym ptoms or si g ns of renal
2.Uremia - azotem ia w ith sym ptoms or sig ns of renal
failure
failure
3.End Stage Rena l Diseas e (ESRD) - u remia requiring
3.End Stage Rena l Diseas e (ESRD) - u rem ia requiring
transplantation or dialysis
transplantation or dialysis
4.Chronic Renal Failure (CRF ) - irrevers ibl e kidney
4.Chronic Renal Failure (CRF ) - ir revers ible kidney
dysfun ction with azotemia >3 month s
dysfunc tion w ith azotemia > 3 m onth s
5.Creatinine Clea rance (CCr) - the rate o f filtration of
5.Cr eatinine Clea rance (CCr) - the rate of filtration of
crea tinine by the ki dney (GFR marke r)
creatinine by the ki dney (GFR mark e r)
6.Glo merular Filtra tion Rate (GFR) - the total r ate of
6.Glo merular Filtra tion Rate (GFR) - the total r ate of
filtration of blood by the kidney
filtration of blood by the kidney
7.Chronic kidney disease (CKD)
7.Chronic kidney disease (CKD)
from National Kid ney founda tion, K-DOQI ,
from National Ki dney foundati on, K-DOQI ,
chro nic kidney disease gu idelines
chro nic kidney dis ease guidelines
difference difference CChronic re nal failure? hronic re nal failure? c h ro nic k i
difference
difference
CChronic re nal failure?
hronic re nal failure?
c h ro nic k i d ney disease ?
c h ronic kid ne y disea se ?
CC hro nic ki d n e y d ise ae inclu ding pa tie nts in
hronic ki d n e y d ise ae includin g pa tient s in
stag e 1 , G FR is n orm a l or elev ated
stag e 1 , G FR is n orma l or ele vate d
AAims: to a p pe al more atte n tio n to the
ims: t o a p pe al more atte n tion to the
kidn e y d ise a se, p rev e n t t he patie nts
kidn ey d isea s e, p reve n t t h e p atie nts
dev elop renal fa ilu re quic k ly
d evelop ren al fa ilu re quic k ly
difference difference CChronic re nal failure? hronic re nal failure? c h ro nic k i
M ajor Ca uses of CRF M ajor Causes of CRF In c hina , g
M ajor Ca uses of CRF
M ajor Causes of CRF
In c hina , g lo meruloneph ritis, d iab etic,
In china , g lo me rulone ph ritis, d iab etic,
h yp erte nsion,and polycystic ren al d isease
h y p ert ens ion,and polycystic ren al d is ease
a re th e le adin g u nd erl ying eti olog ies of CRD
a re th e le ading und e rl ying eti olo gies o f CRD
o r ESR D
o r ESR D
B ut in th e ad van ce d co u ntries, s uch as th e
B ut in the a d van ce d c o untries, such as th e
USA , dia betic is the le ad in g ca use, and then
USA , d ia betic is the lead in g c aus e, an d then
h yp erte nsion, g lomerulo n eph rit is an d
h y p ert ens ion, g lomerulo nephrit is an d
po lycytic kid n ey d is ease
po lycytic kid n ey d is ea se
M ajor Ca uses of CRF M ajor Causes of CRF In c hina , g
Etiol ogy Etiol ogy 1 .P rima ry glo me ru lar d isease s 1
Etiol ogy
Etiol ogy
1 .P rima ry glo me ru lar d isease s
1 . P rimary glo m e r u lar d isea s es
a .fo c al a nd se gm e ntal GN
a.foc a l a n d seg me ntal GN
b .me m bra no p roliferative G N
b.me mbra no p roliferativ e G N
c .IgA nep h rop ath y
c .IgA ne p h ropathy
d .me m bra no u s n e ph ropa thy
d .me mbra no u s n eph ro pa thy
Etiol ogy Etiol ogy 2 .S econ dary g lome rular d iseases 2 .S econ
Etiol ogy
Etiol ogy
2 .S econ dary g lome rular d iseases
2 .S econ da ry glome ru lar d ise ase s
a.d iabe tic nep hropathy
a.d i ab etic n ephropathy
b .Am yloid osis
b.Am yloid osis
c .po st-i n fectio u s GN
c .post-i n fectio us GN
d .HIV-as s ocia te d n e ph ropa thy
d .HIV -as sociate d n eph r opa thy
e .Co llage n va s c ul a r dis e ase
e.Co llage n va s c ula r dise ase
f.Sickle cell nephropathy
f.Sickle cell neph rop athy
Etiol ogy Etiol ogy 3 .Tu bulo interstitial nep h ritis 3 .Tu bulo interstitial ne
Etiol ogy
Etiol ogy
3 .Tu bulo interstitial nep h ritis
3 .Tu bulo interstitial ne p hritis
a .Drug hyp erse nsitivity
a.Drug hyperse nsitiv ity
b .h eav y me tals
b.h ea vy me tals
c .an alg esic neph rop a th y
c .an a lg es ic neph rop a thy
d .Re flux/chro nic py elo nephritis
d .Reflu x/chron ic p yelo n eph ritis
e.Id iop ath ic
e.Id iop ath ic
Etiol ogy Etiol ogy 4.He reditary diseases 4.Heredita ry diseases a.polycys tic k idney disease a.polycys
Etiol ogy
Etiol ogy
4.He reditary diseases
4.Heredita ry diseases
a.polycys tic k idney disease
a.polycys tic kidney disease
b.medullary cystic disease
b.medul lary cystic diseas e
c.Alports syndrom e
c.Alports sy ndrom e
5.O bstuctiv e nephropathies
5.Obst uctive nephropathies
a.prostatic disease
a.pr ostatic disease
b.retroper itoneal fibrosis /tumor
b.retroper itoneal fibrosis/tum or
6.Vasc ular diseases
6.Vasc ular diseases
a.hypertensive nephrosclerosis
a.hypertensive nephrosclerosis
b.renal artery stenosis
b.renal artery stenosi s
Etiol ogy Etiol ogy 4.He reditary diseases 4.Heredita ry diseases a.polycys tic k idney disease a.polycys
Com mon causes of Chronic Com mon causes of Chronic Renal F ailure Renal Failure G
Com mon causes of Chronic
Com mon causes of Chronic
Renal F ailure
Renal Failure
G lom e rulo n eph ritis
G lom e rulonep h ritis
2
25%
5 %
D iabetes Mellitus
D iabetes Mellitus
2
25%
5 %
Hypertensi on
H ypertensi on
1
1
0 %
0%
C hronic pylonephr itis/reflux
C hr onic pylonephritis/r eflux
1
1
0 %
0%
P olyc ysti c kidney disease
Polycysti c ki dney disease
1
1
0 %
0%
Interstitial nephri tis
Interstitial nephri tis
5
5
%
%
O bstruction
Obstructi on
3
3
%
%
U nk nown
U nknow n
12%
1
2%
pathophy sio l ogy pathophysiol ogy in iti atin g m ec hanisms -- in itiatin
pathophy sio l ogy
pathophysiol ogy
in iti atin g m ec hanisms --
in itiatin g m e chanisms --
specific to un d relying
s pecific to un drelying
etiolog etiologyy
prog ressive mech an is ms ---
p rog re ssiv e m ech an is ms ---
non-specific
non-specific
com pensatory hy pertrophy of s u rviv ing nephrons
com pens atory hypertrophy of s u rvivi ng nephrons
-
-
adapt ive hype rfiltra ti on
adapt ive h ype rfiltrati on
-
-
med iated by v aso active m olecules , cytokines, growt h fac tors
med iat e d by v as o active m olecule s , cytokines, growt h factors
-
-
incre ased g lo m erul ar capillary pressure and flow
incre as ed g lo m erular cap illary pressure and flow
(hyp erperfusion, hype rtens ion, hyperfil tration )
(hyperperfusion, hype rt ension, hy perfil trati on )
– but, cannot last lon g
but, cannot last long
sclerosis of remaining nephrons
sclerosis of remaining nephrons
ch ronic renal fai lure chronic renal fai lure diabetes damage to kid ney hypertensi on
ch ronic renal fai lure
chronic renal fai lure
diabetes
damage to kid ney
hypertensi on
glomeru lonephritis
loss of renal mass (ne phrons)
hy pertro phy & hyp erfiltration o f
rem a ining nephrons
“hypertension” of remaining nephrons
glomerulosclerosis
PPathophysiology and biochemistry athophysiology and biochemistry of urem ia of urem ia PP resent ly, the
PPathophysiology and biochemistry
athophysiology and biochemistry
of urem ia
of urem ia
PP resent ly, the mai n toxins responsible for urem ic
resently, the m ai n toxins responsible for urem ic
syndrom e re main elusive
syndrome re main elusive
UU rea may contribute to som e sy m ptom s, including:
rea may contribute to som e symp toms, including:
anorexia, malaise, vomiting
anorexia, malaise, vo miting
AA ddi tional cat egories of nit rogenous excretory products
dditi onal categories of n itrogen ous excretory products
i n clude urates , poly am ines, etc. which molecular m ass
i nclude urates, poly amines, etc. which molecular m ass
(500 -12 000 Da, so-called m idd le m olecules)
(500-12 000 Da, so-called m idd le m olecules)
PP oly peptide h orm ones, including par athyriod
olypeptide hormone s, including parathy riod
hormo ne(PT H ) , insulin, g l ucagon, and prolactin rise w ith
hormo ne(PT H) , insulin, g lucagon, and p rolactin rise w ith
rena l failure, production of erythr opoiet in(EP O) and 1,25-
renal failure, pro duction of erythropoiet in(EP O) and 1,25-
dihydrox ycholecalciferol are reduced
dihydroxycholecalcifero l are reduced
RResulting in anemia, ma lnutrition , im paired m etabolism
esulting in anemia, malnutrition , im paired m etabolism
of carbohydrate s, fats, and metabo lic bone disease
of carbohydrates, fa ts, and metabolic bone disease
Clinical m anifestat ion of CRF Clinical manifestation of CRF Dis turba nce in eve ry
Clinical m anifestat ion of CRF
Clinical manifestation of CRF
Dis turba nce in eve ry orga n syste m
Dis turba nce in eve ry orga n sys tem
Dev e l o p slowly and a symptoma ti c u ntil
Deve l o p slow ly an d a symptom atic u ntil
ren al failure is fa r-ad van ced
ren a l failure is fa r-ad v an ced
Dia lysis ca n reduc e th e s e verity of the
Dialys is ca n red uce th e s everity of the
d istu rba n c e b ut is not a pana cea
d i stu rban ce b ut is n ot a pana cea
Some dis turb a nce re s ulting fro m im pa ire d
Som e dis turb a nce re s ulting from im pa ire d
renal functio n fa il to respon d fu lly .
rena l fu nction fa il to respon d fu
Sodiu m and water homeostas is So diu m and water homeostas is Disru pt gl
Sodiu m and water homeostas is
So diu m and water homeostas is
Disru pt gl om eru lotubular ba lance and promote
Disrupt glom eru lotubular ba lance and p romote
sod ium re ten tion
sod ium re ten tion
Exc ess iv e sodiu m i ngestio n
Exces s ive s odiu m i ngestio n
Lea d to cu mulative pos itive Na
L ead to c u m ulativ e pos itiv e Na
++
ba lan ce a nd
balan ce and
extrac e llular flu id volu m e expansio n (ECFV)
e xtrac ellula r fluid vo lu me expa nsio n( ECFV)
Pa tients w it h C RD also ha ve im pa i red ren al
Pa tients w it h C RD also hav e im pa i re d ren al
mec ha n is m s for fluid co ns e rving Na
mec ha n ism s for fl u id co nse rv ing N a
++
a n d
a n d
HH 22 OO ,,
wil l be prone to v o lu me de ple tion,im pa ir
will be prone to volu me de ple tion,im pa ir
res idual rena l fuction
res idua l rena l fuction
Sodiu m and water homeostas is So diu m and water homeostas is Disru pt gl
Potass iu m ho me ostasis Po tas siu m ho me ostasis Hy perkal emia
Potass iu m ho me ostasis
Po tas siu m ho me ostasis
Hy perkal emia
Hy perkalemia
Ca use ::
Ca use
c o nstipation
c onstip atio n
augmen te d d ie tary intake
aug me n te d d i eta ry intake
p rote in ca tabo lis m
p rote in ca ta bo lis m
h e m o lys is
h e mo l ys is
h emorrh a ge
h em orrha ge
trans fus i on of sto red RBC
transfusi on of sto red RBC
me tab o lic ac i d o sis
me ta bo lic aci d o sis
me d ica tion (beta-b loc ke rs, ACE in h ib ito rs
me d ication (beta-blockers, AC E i n h ib i to rs
ARB, K -s par ing d i u re tics)
ARB, K -sp ar ing d i u retic s )
++
Potass iu m ho me ostasis Po tas siu m ho me ostasis Hy perkal emia
Metabolic ac idosis Metabo lic a cidosis Is commom i n CRF o r ESRD Is
Metabolic ac idosis
Metabo lic a cidosis
Is commom i n CRF o r ESRD
Is commom in CRF o r ESRD
Ca u se:
Ca use:
a.re du ced a bil ity to produ ce am mo nia
a.reduce d a bility to produ ce am monia
b .h y pe rka le mia fu rt he r d e p res ses ammon ia
b .hy pe rka le m ia fu rt her d e p resses am mon ia
exc retio n
e xc retio n
c.with tu b ul o in terstitia l dis e ase
c .with tu b u lo inters titia l dis e ase
I n m ost pa ti e n ts , th e a c idos is is m ild, s evere
I n m os t p atie nts , th e a c idos is is m ild , s eve re
acid osis m ay occur when th e pa ti ent is
acidosis may occu r when th e p a tie nt is
challenged with a n excess ive end o g en ous or
challenge d wit h a n exc e s s ive e nd o g enous or
exogenous acid loa d or lose s excessive alkali
exoge nous acid load or loses exces sive alka li
Renal osteo dy strophy Renal osteo dystro phy OOsteitis fibrosis steitis fi brosis high bone turnov
Renal osteo dy strophy
Renal osteo dystro phy
OOsteitis fibrosis
steitis fi brosis
high bone turnov er and high PT H levels
high bo ne turnov er and high P TH levels
OOsteom al acia and adynam ic bone disease
steom al acia and adynam ic bone disease
low bone turnover with low or normal PT H levels,
low bone turnov er w ith l ow or normal P TH levels,
excessive active vitam ine D, which supp ress
excess ive activ e v itam ine D, w hich s u ppress
production of parathyroid hormone
production of parathyroid horm one
SSym ptom s : bony pain and pr oxima l m usc le
ymptoms : bony pain and proxima l m usc le
weakness, spontaneous bone fractures ca n
w eak n e ss, spontaneous bone fr actures ca n
occur that are slow to heal
occur that are slow to heal
CCalcification of soft tissue and blood vessels
al cificati on of soft tissue and blood v ess els
Renal osteo dy strophy Renal osteo dystro phy OOsteitis fibrosis steitis fi brosis high bone turnov
sign s of CRF/E SRD signs of CRF/ ESRD 1 1 . osteodystrop hy o steo
sign s of CRF/E SRD
signs of CRF/ ESRD
1 1 . osteodystrop hy
o steo dystrop hy
failing kidney func tion
electrolyte im balanc e
second ary h yperparathy roidism
“r enal” osteodystrophy
also GFR 1 -hydroxy lase activity phosphorus excretion vit D activation Ca 2+ inta ke in
also
GFR
1
-hydroxy lase activity
phosphorus excretion
vit D activation
Ca 2+ inta ke in gastr
hyperphosphatemia
Ca 2+ & PO 4 3- reabsorption
≠ PTH produ ction
i n distal tubules
Seconda ry hyperparathyro id is m
≠ oste oclast activity
oste itis fibrosis cys tica
renal
slow bo ne mineral iza tion
osteodystropy
osteomalacia
Cardiovas cula r a bn or m a lities Cardio vascula r a bn orma litie
Cardiovas cula r a bn or m a lities
Cardio vascula r a bn orma litie s
The l eading caus e of morbility and m ortality in
T he l eading cause of mor bili ty and m ortality in
patien ts wi th C RD at al l s tages!
patients wi th C RD at al l s tages!
Is chemic c ardio vascular disease Is chemic c ardiovascular disease risk factors risk fa ctors
Is chemic c ardio vascular disease
Is chemic c ardiovascular disease
risk factors
risk fa ctors
traditio n a l
traditio na l
CK D-re l ate d
CK D-relate d
h y pe rte n tion
hy pe rte ntion
a n emia
a n em ia
h y pe rvo lemia
hy pe rvo lem ia
h yperph osp h a temia
h yperp h osp hatemia
d yslipid em i a
dy slipid em i a
hype rp arath yro id ism
hyperparath yroid ism
s m ok in g
smok ing
m icroin fla mm at ion
m icroinfla mmatio n
alcoh ol
alco h ol
d ialysis
d ialysis
a g e
a ge
over-weight
over-weight
Co ngestive heart failu re Conges tive heart fail ure Cause: Cause: a.m yo c ardial
Co ngestive heart failu re
Conges tive heart fail ure
Cause:
Cause:
a.m yo c ardial is chemic disea se
a.m yo cardial is chemic disea se
b.left ve ntricula r hyp ertrophy
b.left ve ntricular hyp ertroph y
c.s a lt and wate r retentio n
c .s a lt a nd w ate r reten tion
h eart fai lure and pu lmo na ry ed e m a
h e art fai lu re a nd pu lm ona ry e d e m a
usu a lly respond pro mptly to vi g o rou s dia lysis
usua lly re sp on d promptly to vigorous dia lysis
Co ngestive heart failu re Conges tive heart fail ure Cause: Cause: a.m yo c ardial
Hy perte ntion a nd left ve ntr icu lar Hy pertention a nd left v
Hy perte ntion a nd left ve ntr icu lar
Hy pertention a nd left v entr icu lar
hyp ertrop hy
hyp ertrop hy
ca u s e: (h ype rtenyion)
ca u se: (hypertenyion)
a.v olu m e o verlo a d is the majo r cause
a.volu m e overload is the maj or c ause
b .eleva t io n leve l of serum re n in
b .eleva t ion level o f seru m re n in
ca u s e: (LV F)
ca u se: (L V F)
a .is th e m o st om inou s ri s k fator for morbil ity
a .is th e m ost om inous ri s k fator for m orbility
and morta l ity in CRF
an d m orta l ity in CRF
b .prolonged hype rte ntion
b .p rolonged hype rte ntio n
c .fluid volum e ove rload
c .fluid volum e ov e rload
Hy perte ntion a nd left ve ntr icu lar Hy pertention a nd left v
Pericardit is Pe ricardit is a.Pericard ial pa in with respi ratory a.Pe ricard ial p
Pericardit is
Pe ricardit is
a.Pericard ial pa in with respi ratory
a.Pe ricard ial p ain with respira tory
b.Acc o mpa n ied with a friction ru b
b .Ac co mpa nied w ith a frictio n rub
c.Electro cardio gr aphi c a bnorma li ties incl u de:
c.Electroca rdiographic a bnorm ali ties incl u de:
P R-inte rva l de pression
P R-inte rva l de p ression
S T-seg m e nt ele vation
S T-segm e n t e levation
d .D e te cte d b y ech oca r dio grap h y
De te cted by ec h ocardiograp h y
e.So metim es le a d to card iac tam po n ade
e .So m etim es le a d to card ia c tam po n ade
Pericardit is Pe ricardit is a.Pericard ial pa in with respi ratory a.Pe ricard ial p
H em ato log ic ab normalitie s H em a to log ic ab nor
H em ato log ic ab normalitie s
H em a to log ic ab nor m alities
Anemia Anemia Observed beginni n g a t sta ge 3 CRD a n d Observed
Anemia
Anemia
Observed beginni n g a t sta ge 3 CRD a n d
Observed beginni ng a t sta ge 3 CRD a n d
univers al at stage 4
univers al at stage 4
Reasons:
Reaso ns :
a .in su fficien t pro ductio n of E P O
a .in sufficien t prod uction o f E P O
b .iron and fo late d efic ie n cy
b .iron an d fo late d eficie n cy
c.s e ve re h yperp arathy ro id is m
c .s eve re h yperp arath yro id i s m
d
d
.in f lam matio n
.in fla m m ation
e.alumin um toxic it y
e.aluminum toxicity
f.shorte n red cell su rvial
f.shorte n red cell su rvial
Anemia Anemia Observed beginni n g a t sta ge 3 CRD a n d Observed
Ne uromuscular abnorma lit ies Ne uromuscula r abnorm alit ies Ca u se: retained nitroge
Ne uromuscular abnorma lit ies
Ne uromuscula r abnorm alit ies
Ca u se: retained nitroge nous me tab olities vt6
Ca use: retaine d n itrog enous m eta b olities vt6
. a n d mid d l e m o le c u les as w ell a s PTH
an d midd l e m o le cu les as w ell as P TH
con tribu te to
con tribu te to
Man ifes tati on s:
Man ifestati ons :
m ind d is turban ce
m in d d isturba n ce
sleep d istu rb an ce
sle ep d istu rb an ce
neuromu s cular irrita bility: hiccu ps ,c ramp s,c ho rea
neuromu scula r irrita bility: hicc u ps ,cramps,cho re a
Periphe ral n e urop athy
Peripheral n e uropathy
initi ally,sensory nerves are involved t han m otor
in iti ally,senso ry nerves are involved tha n m otor
Endocrine me ta bolic disturbance En docrine m eta bolic disturbance a.Parathyroid function a.Pa rathyroid function
Endocrine me ta bolic disturbance
En docrine m eta bolic disturbance
a.Parathyroid function
a.Pa rathyroid function
b.Blood gluc ose slig htly elevate d
b .B lood g lucos e slig ht ly ele vated
c.Plasma insu lin s lightly elev ated
c.Plasma in sulin slightly ele vate d
d. M an y h ypo glyc e m ic d rugs require d ose
d .M an y h ypo gly ce m ic dru gs re quire d ose
redu ctio n
reducti o n
e. M etform in a re co n tra ind i ca ted whe n
e .M etfo rm in a re co n tra ind i c ated whe n
GFR dim ini s h ed by 25 %-50 %
GFRdim in is h ed by 25% -50%
f.In women,estro g en leve ls are low, inabi lity to
f.In women,estro gen leve ls are low , ina b i lity to
carry preg nancies to te rm
carry preg nancies to te rm
g.In men, im pote nce, testosteron e are
g.In men, im pote nce, testosteron e are
low,growth, sexual maturation is often impaired
low,growth, sexual maturation is often impaired
De rmatology abnormalitie s De rmatology abnormalities a.Ca lci u mp hosphate depos it ion, s
De rmatology abnormalitie s
De rmatology abnormalities
a.Ca lci u mp hosphate depos it ion, s econdary
a.Ca lci u m p hosphate depos ition, s econda ry
hyperp arath yroid ism, and d ep osition of
hyp e r pa rat h yroid ism, an d d e p ositio n of
pi g m e nted metabol ities or u roc h ro me and urea
pi g me nte d metabol ities or u ro c hro me and urea
itse lf .
itse
b .P ru ri tu s
Pru ritu s
c.Skin ne cros is
c.Sk in n ecros is
De rmatology abnormalitie s De rmatology abnormalities a.Ca lci u mp hosphate depos it ion, s
Evalu a tion an d man ag ement Evalu a tion a n d m a
Evalu a tion an d man ag ement
Evalu a tion a n d m a n agem ent
History and physical examinati on History and physical examinati on a.history: hype rtension, d iabetes,systemic a.his
History and physical examinati on
History and physical examinati on
a.history: hype rtension, d iabetes,systemic
a.his tory: hyp ertension, d iabetes,system ic
infec tio n ,i nflamm a tion, metaboli c d ise a se,
infe ctio n ,inflamm ation, meta b olic d isease,
expo su re to d rugs an d toxin s, an d fa mily
expos u re to d rug s an d toxin s, and fa m ily
h i s to ry of re n al disea se
h i s to ry of re n al disea se
b .q ue stio ns : app etite , d ie t, n a usea , vomi ting,
q ue stio n s : ap petite, d ie t , n a us ea , vomi ting,
sho rt o f b rea th, e d ema, w e ig ht loss , mus c ule
sho rt of b rea th , e dem a, we ig ht loss , mus cule
cram p s, p ru ritu s
cram ps, p ru ritu s
c.Physica l examin at ion:blood pressu re,
c.Ph ysica l examin at ion :blood pressu re,
fu n d uscopy, ab dom e n pa lp atio n , pros tate siz e
fu n duscopy, a b dom en p alpat io n , p rostate size
History and physical examinati on History and physical examinati on a.history: hype rtension, d iabetes,systemic a.his
La boratory inv estigation La boratory investig ation a.Focus on a search for clues to a
La boratory inv estigation
La boratory investig ation
a.Focus on a search for clues to a n u n derlying
a.Focu s on a search fo r clue s to an u nderlying
di se ase pro ce ss and its c o ntinued activity
di s ease process and its co ntinued activity
b.Immunolo gi c tests for sy s te mic lu pu s
b .Im mu no lo gic tests for s yste m ic lupus
e rythem a tosu s and vas c u l itis
e ryth em a tos u s and vas c ul itis
c.Se rum a n d u rinary e letropho res is to p reclude
c.Se rum an d u rinary eletrop horesis t o p reclude
parap rote inemia
p arap rotein emia
d .Te s ts fo r de termin e the sta ge a n d com plication :
Tes ts fo r d e te rm in e the sta ge a nd co m plication:
creat in in e, G FR , u re a, eletro lytes , a lk alin e
creat in ine, G FR , urea, eletro lyte s , a lkalin e
phospha tase to asse s s metabo lic bon e disease
phospha tase to asse s s metabo lic bone dise ase
24h u rine col lection for p rotein excretion
2 4h u rine col lection for protein excretion
Imaging studies Im aging studies a.Ultrasou nd exam inatio n: kidney size, a.Ultraso u nd examination:
Imaging studies
Im aging studies
a.Ultrasou nd exam inatio n: kidney size,
a.Ultraso u nd examination: kidney size ,
obstru ctive u rop ath y
obs tru ctive u rop ath y
b.Symmetric smal l kidn eys s u ppo rt dia gnosis o f
b .Symmetric smal l kid n eys s upp ort dia gnos is of
CF R,a nd ind icate i rre vers ib l e
CFR,a n d i nd ica te i rreve rs ib le
c.No rma l s iz e us ually s u gge sts a cute renal fai lure
c.No rma l s i ze u s ually s u g ges ts a cute renal fai lure
d. Asymm etric kidney siz e s ug gests un ilateral
d .As ymme tr ic k idne y s iz e s u gge s ts un ila te ral
develo p me nta l ab n ormality o r ch ro ni c
d ev e lo p m e ntal ab n orm ality or c hro ni c
renova scu lar d isease
renovascu lar d iseas e
e. M RI a nd d opp ler so nography are u se ful in
e.M RI a nd dop p ler so nography are useful in
assess the re nal arteries a nd veins
asse ss the re nal arteries a nd vein s
Renal b iopsy Renal biopsy a.Res erve d for patients with norma l kidne y a.Re
Renal b iopsy
Renal biopsy
a.Res erve d for patients with norma l kidne y
a.Re s erv ed for patients with norma l kidn ey
siz e ,diag nosis cannot b e ma de by in va sive
size ,diag nosis c annot be mad e by in vasive
means , or when the po s s ibility of a rev ersible
mean s ,o r wh en th e po ssibility o f a reversib le
u nd e rlying disease
u nd e rlying dis ease .
b .con train d ication:b ilateral s mal l k i dne ys,
con train dication:bilateral s mall k id neys,
polycytic k id n ey di s ease , u ncon tro led
p olycytic k idn ey d i s ease , u nco ntr oled
hyp ertens ion , urin a ry or p e rine ph ri c infe ction,
h yp e rten s ion , u r in a ry o r p e rinep h ric infe ction,
b l e eding d iath es i s , r e s p iratory distres s, and
b l ee ding d iath esi s , r esp iratory d istress, an d
morb id obes ity
morbid obes ity
Renal b iopsy Renal biopsy a.Res erve d for patients with norma l kidne y a.Re
Esta blishing the diagnosis an d e tiology of E sta blishing the diagnosis an d
Esta blishing the diagnosis an d e tiology of
E sta blishing the diagnosis an d etiology of
CRCRDD
a.To distin gu is h ne wly d iagnos ed C RD from
a .To di s tingu is h n e wly d iag no s ed C RD from
acute ren al fa ilure
acu te re n al fa ilure
b .C h ron ic m etab olic b one disea se with
C h ron ic m eta bolic bon e dise ase with
hyp erp h o s ph ate mia, hypocalcem i a, e levated
h yp e r ph o sph ate mia , hypo calcem ia, e levated
PTH le vel,n o r m ocytic a n em ia, bilateral reduce d
PTH lev e l,n o rm o c ytic a n em ia, b ila teral reduce d
kid n ey s iz e, stro ng ly su pport CRF
kid ney s ize, str o ngly s u pport C R F
c.I n a dva n ce d stag es o f C RD , d efinitiv e eti o logy
c.I n a dva nce d s tag es of C RD, d e finitive e ti o lo gy
becomes le s s feas ible and is also o f le s s
beco me s le ss feasible and is a l so o f les s
th e rape utic signific ance
th e ra peutic s igni ficance
trea tm e nt trea tment
trea tm e nt
trea tment
1.Spe cific treatement a im ed at selecte d 1.Spe cific treatement a imed at selected
1.Spe cific treatement a im ed at selecte d
1.Spe cific treatement a imed at selected
unde rlying etiology of CFR ,s uch as lu pus
unde rlying etio logy of CFR ,such as lu pus
vasculitis,o ptimal time fo r suc h th era py ca n
vasc ulitis, optimal time fo r suc h th era p y c a n
made the fu nction of the kid n ey reve rsible
made the fu nction of the kid ney rev ersible
2. To find o ut sup e rimposed a cute p roc esses th at
2 .To f ind o ut s up e rimpos e d a cu t e p rocesses that
lea d to an a c u te a n d re vers ible decl in e i n GFR
lead to a n a c ute a n d re v ers ible dec l in e i n GF R
3. In c lu de volu me d epl e tion, u ncontrole d
3 .In clu de volu m e d epl etio n, u n controled
hyp ertens ion , nep h ro tox in o f m ed ica tio ns,and
h yp e rten s ion , n ep h ro to x in of m ed ic ations,and
so o n
so o n
4.Slowing th e progre ssio n of C RD , a imed to
4.Slowing th e p rogress io n of C RD , a i med to
stabilize the GFR or reduccee tthhee aannnnuuaall raratete ooff
sta bilize the GFR or redu
decline decline
decline
decline
RRev ersible causes of renal failure eversi bl e causes of renal failure rere vers ib
RRev ersible causes of renal failure
eversi bl e causes of renal failure
rere vers ib le
vers ib le fact ors
factors
d iagnos tic clues
d iagnost ic clues
II nfect ion
nfect
ion
urine cu lture a nd s ensitivity tests
urine cu lture and sens itivity tests
obstructio n
obst ruct io
n
cat he teriz ation and renal ul trasound
c athete riz ation a nd re nal ul traso und
EFVD
EFVD
o rt hostati c blood pressure
o rt hostat i c blood pressure
hyper ka lem ia
hyp erka
lem ia
s eru m ele ct rilytes exam inat ion
seru m ele ctr ilytes exa m inat ion
hyperca lcemia
hyp erca
lcem ia
ser um e lectrilytes e xaminatio n
s er um e le ctril ytes e xam in at ion
nep hro toxic ag ents
ne phrotoxic ag ents
d rug history
d rug history
hypertension
hypert ension
blo od pres sure
blood pressure
conges tive heart fail ure
con ges tive heart failure
physical examination chest X-ray
physical exa mination ch est X-ray
P rotein restriction P ro tein restriction 1.Aim :ameliorating the complicatio n s of urem ia
P rotein restriction
P ro tein restriction
1.Aim :ameliorating the complicatio n s of urem ia
1.Aim :ameliorating the complicatio ns o f urem ia
to slow the rate of d ecline of n ep h ro n i nju ry.
to slow the ra te of d ecline of n ep hro n i nju ry.
2. Protein req u irement o f 0.6 g/d .kg is
2 . Prote in re q u irement o f 0.6g/d .kg is
reco m me nd ed
recomme nd e d
3. D ietary pro tein s hou ld b e h igh er i n esse ntial
3 .D ietary pro tein shou ld b e high er i n e s se ntial
a min o acid s
a mino acid s
4. En e rgy req uireme n ts in t he rag e of 3 5kca l/kg.d
4 .E n e rgy req uireme n ts in the rag e o f 3 5 kca l/kg.d
are reco m m en d e d
are reco m mend e d
P rotein restriction P ro tein restriction 1.Aim :ameliorating the complicatio n s of urem ia
Reducing intraglom erular hy perte nsion and Reducing intraglomerular hypertension and proteinuria proteinuria 1.aim :to s
Reducing intraglom erular hy perte nsion and
Reducing intraglomerular hypertension and
proteinuria
proteinuria
1.aim :to s low th e p rog ress ion of neph ro n inj ury
1 .aim :to slow th e p rog re ss io n of neph ro n inj ury
by amelioratin g intr a glo me ru lar hyp ertension
by amelioratin g intr aglo me ru lar hy p e rtens ion
a nd hy p ertro p h y
a nd hyp e rtrop hy
2. Proteinu ria is co nsid e red a risk facto r fo r
2 .P ro tein u ria is co nside red a r is k facto r fo r
p rogress ive ne phro n i nju ry
p rogre ss iv e ne phro n injury
3. ACEI inh ibitors an d (ang io t ens in recep tor
3 .ACEI inh ibitors an d (ang ioten s in recep tor
b l o cke rs (ARB ) a re e ffective to red uce
b l ockers(ARB) are effective to red u c e
prote inu ria, second -line thera peu tic a p p roc h is
proteinu ria, se con d -lin e therapeu tic a p p ro c h i s
calcium cha nn el blo ckers
calc ium cha nn el blockers
Reducing intraglom erular hy perte nsion and Reducing intraglomerular hypertension and proteinuria proteinuria 1.aim :to s
Disorder of water, sodium, potassium, and ac idosis D isorder of water, sodium, pot assium, and
Disorder of water, sodium, potassium, and ac idosis
D isorder of water, sodium, pot assium, and acidosis
1.Restriction of dietary intake and use of l oop di uretics
1.Restriction of dietary intake and use of l oop diuretics
2.Attention : excessive use of diuretics caus e
2.Attention : excessive use of diuretics caus e
hypovol em ia, thus lead to further decline in G FR
hypovol emia, thus lead to further dec line in G FR
3.hyper kalem ia: avoi d potassium-containing or retaining
3.hyper kal em ia: avoi d potass ium-containing or retaining
m edications, and d i etary restrictio n o f
m edications, an d d ietary restriction of
potass ium ,potassium - bi ndi ng resins can pr omote
potass ium,potassium - bi ndi ng resins can promote
gastrointes ti nal potas sium loss
gastrointest inal potassium loss
4.Metabolic acidosi s:ser um bi car b on ate level should be
4.Metaboli c acidosi s:ser um bicar bonate level should be
m aintained at >21mmol/l, sodium bicarbonate and
m aintained at >21mm ol/l, sodium bicarbon at e an d
calcium b icar bonate should be given to th e patients
calcium b icarbonate shoul d be give n to th e patients
Diso rd er of m inera l m etabolis m Disorder of mineral metabolis m 1.Dietary
Diso rd er of m inera l m etabolis m
Disorder of mineral metabolis m
1.Dietary phos phorus restriction sho uld be les s
1.Dietary pho s phorus res triction should be les s
t h an 1 000 m g/d
t h an 1 00 0m g/d
2.O ra l p h osphorus-bindin g ag ents such as
2 .O ra l p hos pho rus-bindin g a gen ts su ch as
calc iu m c arbo n a t e g ive n i n d ivid ed d o s es three
calciu m carbo nate g ive n i n d ivid ed d o ses th ree
o r fou r times dialy w it h mea ls
o r fou r times dialy w it h mea ls
3 .V itam in D s ho uld be g iv en the pa tie n ts with
Vitam in D s h o uld be given the pa tien ts with
hyp erp a rath yroi d is m
h yp e r pa rat h yroid is m
4.Since ady namic bo ne d ise ase is ofte n a
4.S ince adynamic bo ne d ise a s e is o fte n a
conse que n ce o f overzealo u s treatment of
conse que nc e o f overzealo us treatme nt of
hype rparat h yroidis m, P TH should n ot b e
hyperparat h yroidism, PTH should n o t b e
<120p g/ml
<120pg/ml
Hypertension Hypertension 1.Sho u ld be contro led to 1 30/8 0-8 5m mHg 1.Sho uld
Hypertension
Hypertension
1.Sho u ld be contro led to 1 30/8 0-8 5m mHg
1.Sho uld be controled to 1 30/80-85m mHg
2.In CR D pa tien ts w ith d iabe tes o r proteinuria
2 .In CR D pa tients with d ia be tes or proteinuria
>1 .0g/d,fu rthe r reduce d to 125/75mm Hg
>1 .0g/d ,furthe r reduce d to 125 /75m m Hg
3. Vo lu me c on trol with salt restri ction and diuret ics
3 .Vo lume con trol with salt res tri ctio n an d d iuret ics
is th e m ain stay of th e ra p y
is the m ain sta y o f th era p y
4. Be cause of th e va s cu la r-re nal prote ctive
4 .Be cause of th e va s cu la r-re n al prote ctive
ben efit, AC E in h ibitors a n d AR B a re
b en e fi t, ACE in h ibitors a n d ARB a re
recom me nd ed firstly.
recomme nd ed firstly.
Hypertension Hypertension 1.Sho u ld be contro led to 1 30/8 0-8 5m mHg 1.Sho uld
Cardiovascu lar di sease Cardiovascu la r di sease 1.Hyp erh omo cyste inemia may r
Cardiovascu lar di sease
Cardiovascu la r di sease
1.Hyp erh omo cyste inemia may r epond to vita min
1.Hyp erh omocyste inemia may repond to vita min
t h era py
t h erapy
2.Hyp erlip id em ia : HMG -co A red ucta s e inhibitor.
2 .H yp erlip i d emi a : HMG-coA re d uct ase inhibitor.
simva statin and lo v astatin ca n be se l ected
s im v astatin and lo vas tatin ca n b e se l ected
Cardiovascu lar di sease Cardiovascu la r di sease 1.Hyp erh omo cyste inemia may r
Ure mic pericarditis Ure m ic pericarditis 1.Sho u ld be intensify the d ialysis in
Ure mic pericarditis
Ure m ic pericarditis
1.Sho u ld be intensify the d ialysis in those alrea dy
1.Sho uld be intens ify the dia lysis in those alre ady
on dialys is
on dialys is
2.Pe ricard i ectom y s h ould b e cons id ered only if
2 .Pe ricard i ectom y s h ould b e c on s idered only if
more co n s e rv a tive m ea s ures fail
more co n se rva ti ve meas ures fail
Con ge stive he a rt fail ure
Cong e stive he art fa ilu re
1 1 .Sa lt a nd wa te r i ntake sho uld be co ntro l
Sa lt a n d w ate r i nta ke sho uld be co n trol
2 .D iu retics are of v alue , lo o p diu retic s o ften used
D iuretics are of v alue , loo p d iuretic s often u sed
3.D igoxin sh ould b e used with cau tion
3.D igoxin s h ould be used with c aution
4.ACEI and ARB are effective in hear failure,butt
4.AC EI and A RB are effective in he ar fa ilure ,bu
serum creatin ine and potassium shou ld b e serum creatinine and potassium shou ld be
serum creatin ine and potassium shou ld b e
serum creatinine and potassium shou ld be
chcheecckkeded wwithithiinn 55-1-144 ddaayyss
Anemia Anemia 1.Rec omb inan t human EP O 1.Re combinan t human EP O 2.Be
Anemia
Anemia
1.Rec omb inan t human EP O
1.Re combinan t human EP O
2.Be fore tre atmen t of EPO, iro n store s sho uld be
2 .Before tre atm ent of EPO, iron stores sh ould be
ava ila b le
ava il ab le .
3 .A n e mia re sistant to recom m e nde d d os es of
An e mia resis tan t to rec om me n de d dos es of
EP O o ften su gge st:
EPO often su g gest:
in a deq u at e d ia lysis, h ype rpara thy ro idism
in ad eq u ate d ia lysis, hype rparath yro idism
a lu m in u m toxic ity,
a lu m in u m toxicity,
c hron ic b l o o d loss
c hron ic b lo od lo s s
m aln utritio n ,
m alnutritio n ,
ch ronic i n fectio n
ch ro nic i nfe c t io n
Anemia Anemia 1.Rec omb inan t human EP O 1.Re combinan t human EP O 2.Be
Medication dose adjustment Medication dose adjus tment 1.Drugs th at >70 % excretion is by non
Medication dose adjustment
Medication dose adjus tment
1.Drugs th at >70 % excretion is by non ren al ro ute,
1.Drugs that >7 0% excretio n is by non re n al r oute,
adjustment sh oul d n ot be neede d
adjustmen t sh oul d n ot be need ed
2.M eperidine, metfo rmi n , and othe r drugs w ith a
2 .M eperid ine, metfo rmi n, and o the r d rug s with a
renal rou te o f ex cretion
renal ro u te of excretion
3. M an y d rug s hav e n ep hrot oxi city,s uch as
3 .M an y d rugs h ave n eph roto xi city ,s uch as
NSAID s ,sh oul d b e fo rbi d en
NSAIDs ,sh ou l d be forb i de n .
4. D ru gs a ggrava te th e tende ncy to hyperka le mia,
4 .D ru gs aggrava te th e te n de ncy to hyperka le mia,
and fu rth er red uce GF R s hou ld b e us e d wit h
and fu rth er red uce GF R s hou ld b e us ed w ith
cautio n.
cautio n.
Renal re pla cement therapy R ena l r epla ce ment therapy
Renal re pla cement therapy
R ena l r epla ce ment therapy
1.When conse rvative manag ement of ESRD is 1.When conse rvativ e mana g ement of
1.When conse rvative manag ement of ESRD is
1.When conse rvativ e mana g ement of ESRD is
ina dequate,hemodi alysis, peritone al
inadequate,hemodialys is, pe riton eal
di a lys is,an d ki dney tra ns plan t atio n a re needed
di aly s is,an d k i dney tra nspla n tatio n a re needed
2.When G FR <10ml/mi n , re qu ire ren al
2 .Whe n G FR <10 ml/mi n , r equ ire ren al
repla ce me nt th e rapy
repla cem en t th e rapy
3. Ab solu te in dic ation:
3 .A b solu te in d icatio n :
severe volu me overload
sev ere vo lu me overload
severe hyp erkale m ia an d ac idosis
sev ere hyp erka lem ia and ac ido s is
ence ph alop ath y
enc ephalopa th y
perica rd itis
pericard i tis
symptom atic ure mia
symptom atic uremia
• Procedu re for C hro n ic Hemod ialysis Procedu re for C hro nic
Procedu re for C hro n ic Hemod ialysis
Procedu re for C hro nic Hemod ialysis
b.
b.
Bl ood is run through a semi-
Bl ood is run through a semi-
pe rme a ble filte r me m b ra n e bathed in
pe rm ea ble filte r mem b ra n e bath ed in
dialysate
dialysate
c.
c.
Co m po sition of t he d i a lysate is a ltered
Co mpo sition of the d ia lysate is altered
to adjust e l ec tro l yte pa rameters
to adjust e l ectro lyte p arameters
d.
d.
E l ectr olytes an d s o me toxins pass
E l ectrolyte s an d s o me toxins pass
th rou g h filte r
th rou g h filt e r
e.
e.
By controlling flow rates (pressu res),
B y controlling flow rates (pre ssu res),
patient's in travasc u la r v ol um e c a n be
pa tient's in travasc u la r vol ume ca n be
re duced
reduced
f.f.
Most ch ron ic hemodialysis p a t ie n ts
Most chron ic hemodia lysis p a tie n ts
receive 3 hours dialysis 3 d ays per
receive 3 h ours dialysis 3 days per
wweeeekk
Peritoneal di alysis P eritone al di aly sis 1.Place a perito neal catheter that a
Peritoneal di alysis
P eritone al di aly sis
1.Place a perito neal catheter that a llo w infusion
1.Place a peritoneal catheter t hat a llow infusion
of a dialysate solu ti on into th e a bdo minal
of a dialysate solu ti on into t h e abdom inal
cavity.whic h se rved as “artificia l kidn ey”
cavity.wh ic h s erv ed as “artifi c ial kid n ey”
2. Exc ha n ge d ialys ate
2 .Ex ch ang e d ialysate
3. The most comm on complica tion is periton itis
3 .Th e mos t co mm on complica tion i s periton itis
Kid ne y tran s pla ntatio n
Kid ney tran s pla ntatio n
W ith the adve n t of more potent an d well-
With the adv en t of more potent and well-
t o le rated imm u n osup p re ss ive d rug s,kidn e y
to le rated imm u nosup p re s s ive d rug s,kidn e y
tran spla ntation offers the pote ntia l for nearly
tran sp la ntat ion offers the potential for nea rly

complete

complete

rehabil

rehabilitation

itation

Peritoneal di alysis P eritone al di aly sis 1.Place a perito neal catheter that a