Chronic Renal Failure

CLINICAL
History: Patients whose renal adaptation maintains a GFR of 70-100 cc/min and those with CRI
(GFR >30 cc/min !enerall" are entirel" as"mptomatic and do not e#perience clinicall" e$ident
dist%r&ances in water or electrol"te &alance or endocrine/meta&olic deran!ements' (hese
dist%r&ances !enerall" &ecome clinicall" manifest thro%!h the sta!es of CRF (GFR )30 cc/min
and *nd +a!e Renal ,iseases/*+R, (GFR )10 cc/min''
-"per.alemia
/eta&olic acidosis often is mi#ed0 non1anion !ap and anion !ap0 the latter o&ser$ed
!enerall" with se$ere CRF that is approachin! or at *+R, &%t with the anion !ap
!enerall" not hi!her than 20 m*3/4'
*#tracell%lar $ol%me e#pansion and total-&od" $ol%me o$erload res%lts from fail%re of
sodi%m and free water e#cretion'
5ormochromic normoc"tic anemia principall" de$elops from decreased renal s"nthesis of
er"thropoietin0 the hormone responsi&le for &one marrow stim%lation for red &lood cell
(R6C prod%ction
+econdar" h"perparath"roidism de$elops &eca%se of h"pocalcemia0 decreased renal
s"nthesis of 1027-dih"dro#"cholecalciferol (1027-dih"dro#"$itamin ,0 or calcitriol0 and
h"perphosphatemia'
Physical: (he ph"sical e#amination often is not $er" helpf%l &%t ma" re$eal findin!s characteristic
of the condition %nderl"in! CRF (e!0 l%p%s0 se$ere arteriosclerosis0 h"pertension or
complications of CRF (e!0 anemia0 &leedin! diathesis0 pericarditis'
Causes:
8asc%lar disease - Renal arter" stenosis0 c"toplasmic pattern antine%trophil c"toplasmic
anti&od" (C-95C91positi$e and perin%clear pattern antine%trophil c"toplasmic anti&od"
(P-95C91positi$e $asc%litides0 antine%trophil c"toplasmic anti&od" (95C91ne!ati$e
$asc%litides0 atheroem&oli0 h"pertensi$e nephrosclerosis0 renal $ein throm&osis
Primar" !lomer%lar disease - /em&rano%s nephropath"0 imm%no!lo&%lin 9 (I!9
nephropath"0 focal and se!mental !lomer%losclerosis (F+G+0 minimal chan!e disease0
mem&ranoproliferati$e !lomer%lonephritis0 rapidl" pro!ressi$e (crescentic
!lomer%lonephritis
+econdar" !lomer%lar disease - ,ia&etes mellit%s0 s"stemic l%p%s er"thematos%s0
rhe%matoid arthritis0 mi#ed connecti$e tiss%e disease0 scleroderma0 Goodpast%re
s"ndrome0 :e!ener !ran%lomatosis0 mi#ed cr"o!lo&%linemia0 postinfectio%s
!lomer%lonephritis0 endocarditis0 hepatitis 6 and C0 s"philis0 h%man imm%nodeficienc"
$ir%s (-I80 parasitic infection0 heroin %se0 !old0 penicillamine0 am"loidosis0 li!ht chain
deposition disease0 neoplasia0 throm&otic throm&oc"topenic p%rp%ra (((P0 hemol"tic-
%remic s"ndrome (-;+0 -enoch-+ch<nlein p%rp%ra0 9lport s"ndrome0 refl%#
nephropath"
(%&%lointerstitial disease - ,r%!s (e!0 s%lfa0 allop%rinol0 infection ($iral0 &acterial0
parasitic0 +=<!ren s"ndrome0 chronic h"po.alemia0 chronic h"percalcemia0 sarcoidosis0
m%ltiple m"eloma cast nephropath"0 hea$" metals0 radiation nephritis0 pol"c"stic .idne"s0
c"stinosis
;rinar" tract o&str%ction - ;rolithiasis0 &eni!n prostatic h"pertroph"0 t%mors0
retroperitoneal fi&rosis0 %rethral strict%re0 ne%ro!enic &ladder
TREATMENT
Diet:
Protein restriction earl" in CRF as a means to dela" decline in GFR is contro$ersial>
howe$er0 as the patient approaches *+R,0 this is recommended to dela" onset of %remic
s"mptoms' Patients with CRF who alread" are predisposed to &ecomin! malno%rished
are at hi!her ris. for maln%trition with o$erl" a!!ressi$e protein restriction' /aln%trition is
a well-esta&lished predictor of increased mor&idit" and mortalit" in the *+R, pop%lation
and m%st &e a$oided if possi&le'
Phosphate restriction startin! earl" in CRF
Potassi%m restriction
+odi%m and water restriction as needed to a$oid $ol%me o$erload
,r%! Cate!or"? Phosphate-lowering agents -- -"perphosphatemia is treated with dietar"
phosphate &inders and dietar" phosphate restriction' -"pocalcemia is treated with calci%m
s%pplements and possi&l" calcitriol' -"perparath"roidism is treated with calcitriol or $itamin ,
analo!s'
Calci%m acetate (Calphron0 Phos4o -- For treatment of h"perphosphatemia in CRF' Com&ines
with dietar" phosphor%s to form insol%&le calci%m phosphate0 which is e#creted in feces
Calci%m car&onate (Caltrate0 @"stercal -- For treatment of h"perphosphatemia or as a calci%m
s%pplement in CRF' +%ccessf%ll" normaliAes phosphate concentrations in patients with CRF'
Com&ines with dietar" phosphate to form insol%&le calci%m phosphate0 which is e#creted in feces'
/ar.eted in a $ariet" of dosa!e forms and is relati$el" ine#pensi$e'
Calcitriol (Rocaltrol0 Calci=e# -- ;sed to s%ppress parath"roid prod%ction and secretion in
secondar" h"perparath"roidism and for treatment of h"pocalcemia in CRF &" increasin! intestinal
calci%m a&sorption'
,o#ercalciferol (-ectorol -- 9 $itamin , analo! (1-alpha-h"dro#"er!ocalciferol that does not
re3%ire acti$ation &" the .idne"s' Indicated for the treatment of secondar" h"perparath"roidism in
end-sta!e renal disease'
4anthan%m car&onate (Fosrenal -- 5oncalci%m0 nonal%min%m phosphate &inder indicated for
red%ction of hi!h phosphor%s le$els in patients with end-sta!e renal disease' ,irectl" &inds
dietar" phosphor%s in %pper GI tract0 there&" inhi&itin! phosphor%s a&sorption
+e$elamer (Rena!el -- Indicated for the red%ction of ser%m phosphoro%s in patients with *+R,'
6inds dietar" phosphate in the intestine0 th%s inhi&itin! its a&sorption' In patients on
hemodial"sis0 it decreases the fre3%enc" of h"percalcemic episodes relati$e to patients on
calci%m acetate treatment'
Paricalcitol (Bemplar -- For treatment of secondar" h"perparath"roidism in *+R,' Red%ces P(-
le$els0 stim%lates calci%m and phosphoro%s a&sorption0 and stim%lates &one mineraliAation
*poetin alfa (*po!en0 Procrit -- +tim%lates di$ision and differentiation of committed er"throid
pro!enitor cells' Ind%ces release of retic%loc"tes from &one marrow into &lood stream
Ferro%s s%lfate (Feosol0 Ferata&0 +low F* -- ;sed as a &%ildin! &loc. for hemo!lo&in s"nthesis
in treatin! anemia of CRF with er"thropoietin
Iron de#tran (,e#Ferr%m0 InFed -- ;sed to treat microc"tic0 h"pochromic anemia res%ltin! from
iron deficienc" when oral administration is %nfeasi&le or ineffecti$e'
;tiliAed to replenish iron stores in indi$id%als on er"thropoietin therap" who cannot ta.e or
tolerate oral iron s%pplementation'
9 0'7-m4 (0'27 m4 in children test dose sho%ld &e administered prior to startin! therap"'
9$aila&le as 70 m! iron/m4 (as de#tran'
Iron s%crose (8enofer -- ;sed to treat iron deficienc" (in con=%nction with er"thropoietin d%e to
chronic hemodial"sis' Iron deficienc" is ca%sed &" &lood loss d%rin! the dial"sis proced%re0
increased er"thropoiesis0 and ins%fficient a&sorption of iron from the GI tract' Iron s%crose has
shown a lower incidence of anaph"la#is than other parenteral iron prod%cts'
Gagal ginjal ronis

!LINI"
Ri#ayat: +a&ar siapa adaptasi renal memelihara sat% GFR dari 70 - 100 cc / min dan it% den!an
CRI (GFR>30 cc / min %m%mn"a sel%r%hn"a as"mptomatic dan tida. men!alami !an!!%an =elas
clinicall" di air ata% .eseim&an!an ele.trolit ata% endo.rin / !an!!%an meta&olic' Gan!!%an ini
%m%mn"a men=adi clinicall" men=elma melal%i lan!.ah dari CRF (GFR )30 cc/min and *nd +a!e
Renal ,iseases/*+R, (GFR )10 cc/min''
-"per.alemia
/eta&olic acidosis serin! dicamp%r0 non1anion =%ran! pemisah dan celah anion0 diamati
"an! &ela.an!an %m%mn"a den!an =en!.el.an CRF &ahwa sedan! mende.ati ata% di
*+R, tapi den!an celah anion %m%mn"a tida. le&ih tin!!i di&andin!.an 20 m*3 / l'
8ol%me m%aian *#tracell%lar dan $ol%me t%&%h pen=%mlahan &e&an terlal% &erat a.i&at
oleh .e!a!alan dari air sodi%m dan &e&as e.sresi'
9nemi 5ormochromic normoc"tic ter%tama .em&an!.an dari men"%s%t sintese renal dari
er"thropoietin0 hormon &ertan!!%n! =awa& %nt%. ran!san!an s%ms%m t%lan! %nt%.
darah sel merah (R6C pen!hasilan
+e.%nder h"perparath"roidism men!em&an!.an .arena a.i&at h"pocalcemia0 sintese renal
pen%r%nan dari 1027 - dih"dro#"cholecalciferol (1027 - dih"dro#"$itamin ,0 ata% calcitriol0 dan
h"perphosphatemia
Fisi: Pen!%=ian fisi. serin! adalah tida. terlal% san!at menolon! tapi m%n!.in men!%n!.ap.an
.ara.teristi. penem%an dari .ondisi mendasari CRF (e!0 l%p%s0 pen!ap%ran pem&%l%h darah
=en!.el.an0 hipertensi ata% .er%mitan dari CRF (e!0 anemi0 &erdarah diathesis0 radan! .ant%n!
=ant%n!'
Lantaran:
Pen"a.it $as.%ler renal nadi stenosis0 c"toplasmic memola anti&odi antine%trophil
c"toplasmic (C 95C91positif dan perin%clear memola anti&odi antine%trophil
c"toplasmic (P 95C91$asc%litides positif0 anti&odi antine%trophil c"toplasmic (95C91
$asc%litides ne!atif0 atheroem&oli0 h"pertensi$e nephrosclerosis0 pem&%l%h darah
trom&osa renal
Pen"a.it !lomer%lar primer +eperti +elap%t nephropath"0 imm%no!lo&%lin sat% (I!9
nephropath"0 focal dan !lomer%losclerosis terdiri &e&erapa &a!ian (F+G+0 pen"a.it
per%&ahan minimal0 mem&ranoproliferati$e !lomer%lonephritis0 den!an cepat pro!resif
(crescentic !lomer%lonephritis
Cencin! /anis se.%nder pen"a.it !lomer%lar mellit%s0 s"stemic l%p%s er"thematos%s0
artritis rhe%matoid0 mencamp%r =arin!an h%&%n!.an pen"a.it0 scleroderma0 +indrom
Goodpast%re0 :e!ener !ran%lomatosis0 cr"o!lo&%linemia camp%ran0 postinfectio%s
!lomer%lonephritis0 endocarditis0 radan! hati & dan c0 ra=a sin!a0 $ir%s imm%nodeficienc"
man%sia (-I80 =an!.itan seperti parasit0 pen!!%naan heroin0 emas0 penicillamine0
am"loidosis0 meneran!i pen"a.it pemecatan ran!.ai0 neoplasia0 throm&otic
throm&oc"topenic p%rp%ra (((P0 sindrom hemol"tic %remic (-;+0 -enoch p%rp%ra
+ch<nlein0 +indrom 9lport0 alir .em&ali nephropath"
Pen"a.it @&at (%&%lointerstitial (e!0 camp%ran &eleran!0 allop%rinol0 =an!.itan (.arena $ir%s0
hasil &a.teri0 seperti parasit0 +indrom +=<!ren0 h"po.alemia .ronis0 h"percalcemia .ronis0
sarcoidosis0 &e&erapa m"eloma mem&ent%. nephropath"0 &erat lo!am0 radan! &%ah pin!!an!
pancaran0 &%ah pin!!an! pol"c"stic0 c"stinosis
Pen!halan! sal%ran .and%n! .emih ;rolithiasis0 prostatic h"pertroph" dermawan0 t%mor0
retroperitoneal fi&rosis0 .riti.an %rethral0 p%ndi ne%ro!enic
PERLA!$AN
Diet:
Pem&atasan protein awal di CRF seperti &erma.na %nt%. men%nda .emerosotan di GFR
adalah !emar &erten!.ar> &a!aimanap%n0 se&a!ai pasien mende.ati *+R,0 ini
dire.omendasi.an %nt%. men%nda seran!an dari !e=ala %remic' +a&ar den!an CRF
siapa telah dipen!ar%hi %nt%. men=adi malno%rished ada di risi.o le&ih tin!!i %nt%.
&%stin! lapar den!an san!at pem&atasan protein a!resif' 6%stin! lapar adalah sat%
peramal mapan den!an .eadaan tida. sehat ditin!.at.an dan an!.a .ematian pada
pop%lasi *+R, dan har%s dihindari .ala% m%n!.in'
Perm%laan pem&atasan fosfat awal di CRF
Pem&atasan .ali%m
Pem&atasan sodi%m dan air =i.a di&%t%h.an %nt%. men!hindari &e&an terlal% &erat $ol%me
P%.a% Cate!ori? Agen penurunan fosfat -- -"perphosphatemia diperla.%.an den!an fosfat
&inder dietar" dan fosfat pem&atasan dietar"' -"pocalcemia diperla.%.an den!an pelen!.ap
.alsi%m dan m%n!.in calcitriol' -"perparath"roidism diperla.%.an den!an calcitriol ata% $itamin ,
analo!'
9sam c%.a .alsi%m (Calphron0 Phos4o -- ;nt%. perla.%an dari h"perphosphatemia di CRF'
Com&inasi.an den!an fosfor dietar" %nt%. mem&ent%. fosfat .alsi%m tida. dapat lar%t0 "ait%
di.el%ar.an di tin=a
Calsi%m .ar&onat (Caltrate0 @"stercal -- ;nt%. perla.%an dari h"perphosphatemia ata% se&a!ai
sat% pelen!.ap .alsi%m di CRF' ,en!an s%.ses mem&%at normal .onsentrasi fosfat di pasien
den!an CRF' Com&inasi.an den!an fosfat dietar" %nt%. mem&ent%. fosfat .alsi%m tida. dapat
lar%t0 "ait% di.el%ar.an di tin=a' /ar.eted di &er&a!ai &ent%. dosis dan secara relatif m%rah'
Calcitriol (Rocaltrol0 Calci=e# -- ,iper!%na.an %nt%. !encet pen!hasilan parath"roid dan
pen!el%aran di se.%nder h"perparath"roidism dan %nt%. perla.%an dari h"pocalcemia di CRF
den!an menin!.at &atas serapan .alsi%m %s%s'
,o#ercalciferol (-ectorol -- +at% $itamin , analo! (1 - h"dro#"er!ocalciferol alfa it% tida.
memerl%.an a.ti$asi oleh &%ah pin!!an!' ,itandai %nt%. perla.%an dari se.%nder
h"perparath"roidism di dalam &era.hir lan!.ah pen"a.it renal'
Car&onat 4anthan%m (Fosrenal -- 5oncalci%m0 fosfat &inder nonal%min%m ditandai %nt%.
pen!%ran!an dari taraf fosfor .etin!!ian di pasien den!an lan!.ah a.hir pen"a.it renal' +ecara
lan!s%n! men!i.at fosfor dietar" di &a!ian atas &idan! GI0 &atas serapan fosfor inhi&itin! den!an
demi.ian
+e$elamer (rena!el -- ,itandai %nt%. pen!%ran!an dari ser%m men!and%n! fosfor di pasien
den!an *+R,' I.at fosfat dietar" pada %s%s0 den!an demi.ian inhi&itin! &atas serapann"a' ,i
pasien pada hemodial"sis0 pen"%s%tan ini fre.%ensi dari episode h"percalcemic seh%&%n!an
den!an sa&ar pada perla.%an asam c%.a .alsi%m'
Paricalcitol (Bemplar -- ;nt%. perla.%an dari se.%nder h"perparath"roidism di *+R,' C%ran!i
P(- tin!.at0 ran!san! .alsi%m dan &atas serapan men!and%n! fosfor0 dan ran!san!
mineraliAation t%lan!
*poetin alfa (*po!en0 Procrit -- Ran!san! di$isi dan pem&edaan den!an sel &erpendirian lel%h%r
er"throid' Pen!ar%hi pelepasan dari retic%loc"tes dari s%ms%m t%lan! .e dalam aliran darah
s%lfate men!and%n! &esi (Feosol0 Ferata&0 4am&at F* -- ,iper!%na.an se&a!ai sat% &lo.
&an!%nan %nt%. sintese hemo!lo&in di perla.%.an anemi dari CRF den!an er"thropoietin
+etri.a de#tran (,e#Ferr%m0 InFed -- ,iper!%na.an %nt%. perla.%an microc"tic0 anemi
h"pochromic a.i&at oleh .e.%ran!an &esi .eti.a administrasi lisan adalah tida. m%n!.in ata%
tida. efe.tip'
,imanfaat.an %nt%. men!isi pen"impanan setri.a di indi$id% pada er"thropoietin pen!o&atan
"an! tida. dapat men!am&il ata% mema.l%mi &esi lisan s%pplementation'
+at% 0'7 - m4 (0' 27 m4 di ana.-ana. men!%=i dosis har%s di%r%s %tama %nt%. m%lai
pen!o&atan'
+iap se&a!ai 70 m! men"etri.a / m4 (seperti de#tran'
+etri.a s%crose (8enofer -- ,iper!%na.an %nt%. perla.%an men"etri.a .e.%ran!an (di .ata
pen!h%&%n! den!an er"thropoietin seh%&%n!an den!an hemodial"sis .ronis' /en"etri.a
.e.%ran!an dise&a&.an oleh r%!i darah selama prosed%r dialisis0 er"thropoiesis ditin!.at.an0 dan
&atas serapan tida. c%.%p dari &esi dari &idan! GI' +etri.a "an! s%crose telah memperlihat.an
sat% sin!!%n! pe!awai rendahan dari anaph"la#is di&andin!.an lain parenteral men"etri.a
prod%.'