BAB I PENDAHULUAN Chronic kidney disease (CKD) is a common condition in which there is a loss of kidney function over time.

It is associated with an increased risk of cardiovascular disease and chronic renal failure. Kidney disease is the ninth leading cause of death in the United State. It was historically termedis a term that encom asses all degrees of decreased renal function! from damaged"at risk through mild! moderate! and severe chronic kidney failure. CKD is a worldwide u#lic health ro#lem. In the United States! there is a rising incidence and revalence of kidney failure! with oor outcomes and high cost. $he Kidney Disease %utcomes &uality Initiative (KD%&I) defines CKD as either kidney damage or a decreased glomerular filtration rate ('()) of less than *+ m,-min-../0 m1 for 0 or more months. 2hatever the underlying etiology! once the loss of ne hrons and reduction of functional renal mass reaches a certain oint! the remaining ne hrons #egin a rocess of irreversi#le sclerosis that leads to a rogressive decline in the '().

BAB II DASAR TEORI 1. DEFINITION $he Kidney Disease %utcomes &uality Initiative (KD%&I) defines CKD as either kidney damage or a decreased glomerular filtration rate ('()) of less than *+ m,-min-../0 m1 for 0 or more months. 2hatever the underlying etiology! once the loss of ne hrons and reduction of functional renal mass reaches a certain oint! the remaining ne hrons #egin a rocess of irreversi#le sclerosis that leads to a rogressive decline in the '(). 2. PATHOPHYSIOLOGY 3 normal kidney contains a ro4imately . million ne hrons! each of which contri#utes to the total glomerular filtration rate ('()). In the face of renal in5ury (regardless of the etiology)! the kidney has an innate a#ility to maintain '()! des ite rogressive destruction of ne hrons! as the remaining healthy ne hrons manifest hy erfiltration and com ensatory hy ertro hy. $his ne hron ada ta#ility allows for continued normal clearance of lasma solutes. 6lasma levels of su#stances such as urea and creatinine start to show measura#le increases only after total '() has decreased to 7+8. $he hy erfiltration and hy ertro hy of residual ne hrons! although #eneficial for the reasons noted! has #een hy othesi9ed to re resent a ma5or cause of rogressive renal dysfunction. $he increased glomerular ca illary ressure may damage the ca illaries! leading initially to secondary focal and segmental glomerulosclerosis ((S'S) and eventually to glo#al glomerulosclerosis. $his hy othesis is su orted #y studies of five:si4ths ne hrectomi9ed rats! which develo lesions identical to those o#served in humans with chronic kidney disease (CKD) ;aker et al found a strong association #etween e isodes of acute kidney in5ury (3KI) and cumulative risk for the develo ment of advanced CKD in multi le hos itali9ed atients with dia#etes mellitus.</= 3ny 3KI versus no 3KI was a risk factor for stage > CKD! and each additional 3KI e isode dou#led that risk.</= (indings from the 3therosclerosis )isk in Communities (3)IC) Study! a <?= $his study used data from ./?/ cases of CKD that develo ed #etween .@?/ and 1++>. ros ective o#servational cohort! suggest that inflammation and hemostasis are antecedent athways for CKD.

3. HISTORY 6atients with chronic kidney disease (CKD) stages .:0 (glomerular filtration rate <'()= A0+ m,-min-../0 mB) are freCuently asym tomaticD in terms of ossi#le EnegativeF sym toms related sim ly to the loss of glomerular filtration rate ('()). 'enerally! these distur#ances #ecome clinically manifest with CKD stages >:7 ('() G 0+ m,-min-../0 mB). 6atients conditions associated with E ositiveF sym toms (eg! olyuria! hematuria! edema) are more likely to develo signs of disease at earlier stages. Uremic manifestations in atients with CKD stage 7 are #elieved to #e rimarily secondary to an accumulation of multi le to4ins! the full s ectrum and identity of which is generally not known. Heta#olic acidosis in stage 7 may manifest as rotein:energy malnutrition! loss of lean #ody mass! and muscle weakness. 3ltered salt and water handling #y the kidney in CKD can cause ulmonary edema and hy ertension. 3nemia! which in CKD develo s rimarily as a result of decreased renal synthesis of erythro oietin! manifests as fatigue! reduced e4ercise ca acity! im aired cognitive and immune function! and reduced Cuality of life. %ther manifestations of uremia in end:stage renal disease (IS)D)! many of which are more likely in atients who are inadeCuately dialy9ed! include the followingJ 6ericarditisJ Can #e com licated #y cardiac tam onade! ossi#ly resulting in death Ince halo athyJ Can rogress to coma and death 6eri heral neuro athy )estless leg syndrome 'astrointestinal sym tomsJ 3nore4ia! nausea! vomiting! diarrhea Skin manifestationsJ Dry skin! ruritus! ecchymosis (atigue! increased somnolence! failure to thrive Halnutrition Irectile dysfunction! decreased li#ido! amenorrhea 6latelet dysfunction with tendency to #leed eri heral edema and! not uncommonly!

4. PHYSICAL EXAMINATION AND APPROACH CONSIDERATION 3 careful hysical e4amination is im erative. It may reveal findings characteristic of the condition that is underlying chronic kidney disease (CKD). ;owever! the lack of findings on hysical e4amination does not e4clude kidney disease. In fact! CKD is freCuently clinically silent! so screening of atients without signs or sym toms at routine health visits is im ortant.

a. Screen n! "#r $e%re&& #n (orty:five ercent of adult atients with CKD have de ressive sym toms may em hasi9e somatic sym toms : s ecifically! slee distur#ance! fatigue! and anore4ia : that can coe4ist with chronic disease sym toms. '. La'#ra(#r) $esting in atients with chronic kidney disease (CKD) ty ically includes a com lete #lood count (CKC)! #asic meta#olic anel! and urinalysis! with calculation of renal function. Lormochromic normocytic anemia is commonly seen in CKD. %ther underlying causes of anemia should #e ruled out. $he #lood urea nitrogen (KUL) and serum creatinine levels will #e elevated in atients with CKD. ;y erkalemia or low #icar#onate levels may #e resent. atients may have hy oal#uminemia as a result of urinary rotein loss or malnutrition. 3 li id rofile should #e erformed in all atients with CKD #ecause of their risk of cardiovascular disease. Serum hos hate! 17:hydro4yvitamin D! alkaline hos hatase! and intact arathyroid hormone (6$;) levels are o#tained to look for evidence of renal #one disease.. serum cystatin:C levels is gaining a greater role in the estimation of kidney function. <0/= Cystatin:C is a small rotein that is e4 ressed in all nucleated cells! roduced at a constant rate! and freely filtered #y the glomerulusD it is not secreted #ut is instead rea#sor#ed #y tu#ular e ithelial cells and cata#oli9ed! so it does not return to the #loodstream. $hese ro erties make it a valua#le endogenous marker of renal function. <0?= c. Ur na*)& & In adult atients who are not at elevated risk for chronic kidney disease (CKD)! screening with total rotein can #e done with a standard urine di stick! according to guidelines from the Lational Kidney (oundationMs Kidney Disease %utcomes &uality Initiative (KD%&I). If the di stick test is ositive (.N or greater)! atients should undergo testing for confirmation of roteinuria.<0@= In children! teenagers! and young adults in articular! a first morning urine s ecimen is refera#le to a random s ecimen! as so:called orthostatic roteinuria (considered #enign) can #e e4cluded.

3lthough 1>:hour urine collection for total rotein and creatinine clearance (CrCl) can #e erformed! s ot urine collection for total a rotein"to:creatinine (6-C) ratio allows relia#le ro4imation (e4tra olation) of total 1>:hour urinary rotein e4cretion. 6atients with a 6-C ratio

a#ove 1++ mg-mg should undergo a full diagnostic evaluation.<0@= 3 value of greater than 0++: 07+ mg-mg is within the ne hrotic range. ;owever! a total 6-C ratio is acce ta#le if the al#umin: to:creatinine ratio is high (A7++ to .+++ mg-g).<0@= (or screening atients at elevated risk! the KD%&I recommends using an al#umin: s ecific di stickD this is #ecause al#uminuria is a more sensitive marker than total rotein for CKD from dia#etes! hy ertension! and glomerular diseases. 3 ositive di stick test should #e followed #y calculation of the al#umin:to:creatinine ratio! with a ratio greater than 0+ mg-mg followed #y a full diagnostic evaluation.<0@= $he urine sediment finding of red #lood cells ()KCs) and )KC casts suggests roliferative glomerulone hritis. 6yuria and-or white #lood cell casts suggest interstitial ne hritis ( articularly if eosino hiluria is resent) or urinary tract infection. $. Rena* F+nc( #n F#r,+*a& $he Cockcroft:'ault formula for estimating creatinine clearance (CrCl) should #e used routinely as a sim le means to rovide a relia#le a ro4imation of residual renal function in all atients with chronic kidney disease (CKD). $he formulas are as followsJ CrC* -,a*e. / -01412a!e3 4 5e !6( n 7!.8-&er+, crea( n ne 4 92. CrC* -"e,a*e. / CrC* -,a*e. 4 1.:;

e. I,a! n! U*(ra&#n#!ra%6)

)enal ultrasonogra hy is useful to screen for hydrone hrosis! which may not #e o#served in early o#struction! or involvement of the retro eritoneum with fi#rosis! tumor! or diffuse adeno athy. Small! echogenic kidneys are o#served in advanced renal failure. Re(r#!ra$e %)e*#!ra, Hay #e indicated if a high inde4 of clinical sus icion for o#struction e4ists des ite a negative finding on renal ultrasonogra hy. Intravenous this rocedure is often used to diagnose renal stones. C#,%+(e$ (#,#!ra%6) -CT. &cann n! Can #etter define renal masses and cysts usually noted on ultrasonogra hy. 3lso! C$ scanning is the most sensitive test for identifying renal stones. Intravenous (IO) contrast" enhanced C$ scans should #e avoided in atients with renal im airment to avoid acute renal failureD this risk significantly increases in atients with moderate to severe CKD. Dehydration also markedly increases this risk. Ma!ne( c re&#nance ,a! n! -MRI. yelogra hy is not commonly erformed! #ecause of the otential for renal to4icity from the intravenous contrastD however!

Oery useful in atients who would otherwise undergo a C$ scan #ut who cannot
receive IO contrast. Hagnetic resonance angiogra hy (H)3) is #ecoming more useful for the diagnosis of renal artery stenosis! although renal arteriogra hy remains the criterion standard. ;owever! H)I contrast is systemic fi#rosis. Rena* ra$ #n+c* $e &can ro#lematic in atients with e4isting chronic kidney disease (CKD) #ecause they have a low! #ut otentially fatal! risk of develo ing ne hrogenic

Can #e used to screen for renal artery stenosis when erformed with ca to ril
administrationD it also Cuantitates differential renal contri#ution to total glomerular filtration rate ('()). ;owever! radionuclide scans are unrelia#le in atients with a '() of less than 0+ m,-min-../0 mB. Rena* B #%&) $his a rocedure is generally indicated when renal im airment and-or roteinuria ro riate roaching the ne hrotic range are resent and the diagnosis is unclear after an a

worku . Kio sies are also indicated to guide management in already:diagnosed conditions! such as lu us! in which the rognosis is highly de endent on the degree of kidney involvement. Kio sy is not usually indicated when renal ultrasonogra hy reveals small!

echogenic kidneys on ultrasonogra hy! #ecause this finding re resents severe scarring and chronic! irreversi#le in5ury. $he most common com lication of this rocedure is #leeding! which can #e life: threatening in a minority of cases. Surgical o en renal #io sy can #e considered when the risk of renal #leeding is felt to #e great! occasionally with solitary kidneys! or when ercutaneous #io sy is technically difficult to erform. )enal histology in chronic kidney disease (CKD) reveals findings com ati#le with the underlying rimary renal diagnosis. In some cases! a #io sy may show nons ecific changes! with the e4act diagnosis remaining in dou#t.

;. TREATMENT
Iarly diagnosis and treatment of the underlying cause and-or the institution of secondary reventive measures are im erative in atients with chronic kidney disease (CKD). Iarly referral to a ne hrologist is of e4treme im ortance. $he medical care of atients with CKD should focus on the followingJ .. Delaying or halting the rogression of CKD 3ggressive #lood ressure control to target values er current guidelines $he Point Lational Committee on 6revention! Detection! Ivaluation! and $reatment of ;igh Klood 6ressure (PLC OII) and the Lational Kidney (oundationMs Kidney Disease %utcomes &uality Initiative (KD%&I) suggest a target #lood ressure of less than .0+-?+ mm

;g.

$reatment of hy erli idemia to target levels er current guidelines 3ggressive glycemic control er the 3merican Dia#etes 3ssociation (3D3) recommendations (target hemoglo#in 3.c <;#3.C= G /8)

3voidance of ne hroto4ins! including intravenous (IO) radiocontrast media! nonsteroidal anti:inflammatory agents (LS3IDs)! and aminoglycosides Use of renin:angiotensin system ()3S) #lockers among atients with dia#etic kidney disease (DKD) and roteinuria

Use of angiotensin:converting en9yme inhi#itors (3CIIs) or angiotensin:rece tor #lockers (3)Ks) in atients with roteinuria

1. $reating the athologic manifestations of CKD 3nemiaJ 2ith erythro oietin treatment! the goal is a hemoglo#in level of .+:.1 g-d,! as normali9ation of hemoglo#in in atients with CKD stages >:7 has #een associated with an increased risk of adverse outcomes
;y ocalcemiaJ $reat with calcium su lements with or without calcitriol ;y er arathyroidismJ $reat with calcitriol! vitamin D analogues! or calcimimetics Oolume overloadJ $reat with loo diuretics or ultrafiltration Heta#olic acidosisJ $reat with oral alkali su lementation . I4 erts recommend alkali thera y

to maintain the serum #icar#onate concentration a#ove 11 mIC-, Uremic manifestationsJ $reat with long:term renal re lacement thera y (hemodialysis! eritoneal dialysis! or renal trans lantation) Cardiovascular com licationsJ $reat as a ro riate

0. $imely lanning for long:term renal re lacement thera y. Indications for renal re lacement
thera y in atients with chronic kidney disease (CKD) include the followingJ Severe meta#olic acidosis ;y erkalemia

6ericarditis Ince halo athy Intracta#le volume overload (ailure to thrive and malnutrition 6eri heral neuro athy Intracta#le gastrointestinal sym toms Iarly atient education regarding natural disease rogression! different dialytic

Consider the followingJ modalities! renal trans lantation! and o tion to refuse or discontinue chronic dialysis

$imely lacement of ermanent vascular access (arrange for surgical creation of rimary arteriovenous fistula! if ossi#le! and refera#ly at least * mo in advance of the antici ated date of dialysis for atients in whom trans lantation is not imminent) $imely elective eritoneal dialysis catheter insertion $imely referral for renal trans lantation

>. 6atients with CKD acutely resenting with indications for dialytic thera y should #e transferred to a hos ital center where acute dialysis can #e erformed. CALCIUM SALTS Ca*c +, ace(a(e Ca*c +, car'#na(e <ITAMIN D ANALOGUES
Ca*c (r #* D#=erca*c "er#* Par ca*c (#* #inding of hos hate! ty ically with calcium! to reduce

hy er hos hatemia recommended in atients with CKD stages 0:7 who are not on dialysis and in whom the serum arathyroid hormone (6$;) level is elevated or has #een ersistently rising. Oitamin D increases the a#sor tion of calcium in the intestines and hel s to revent secretion of calcium in the kidneys. Ky increasing calcium levels in serum! it hel s to decrease hos hate and 6$; levels! as well as #one resor tion Iron salts are nutritionally essential inorganic su#stances used to treat anemia.

IRON SALTS
Ferr#+& &+*"a(e Ir#n $e=(ran c#,%*e= Ir#n &+cr#&e

>. DIET a. Pr#(e n re&(r c( #n 6rotein restriction early in chronic kidney disease (CKD) as a means to delay a decline in the glomerular filtration rate ('()) is controversialD however! as the atient a roaches CKD stage 7! this strategy is recommended in adults (#ut not in children) to delay the onset of uremic sym toms.
'. Sa*( re&(r c( #n

)eduction in salt intake may slow the rogression of dia#etic CKD! at least in art #y lowering #lood ressure. $he dietary sodium recommendation for the general o ulation in u#lic health guidelines is less than 7:* g daily.

9. PROGNOSIS 6atients with chronic kidney disease (CKD) generally e4 erience rogressive loss of kidney function and are at risk for end:stage renal disease (IS)D). $he rate of rogression de ends on age! the underlying diagnosis! the success of im lementation of secondary reventive measures! and the individual atient. $imely initiation of chronic renal re lacement thera y is im erative to revent the uremic com lications of CKD that can lead to significant mor#idity and death. H#&% (a* ?a( #n Unad5usted rates of hos itali9ation in the CKD o ulation! reflecting its total disease #urden! are 0:7 times higher than those of atients without CKD.<17= D a*)& & In the United States! hemodialysis and eritoneal dialysis atients average 1 hos ital admissions er yearD atients who have a renal trans lant average . hos ital admission er year. 3dditionally! atients with IS)D who undergo renal trans lantation survive longer than those on long:term dialysis.<1/= ;emodialysis erformed * times er week significantly increased the risk of vascular access com lications com ared with a conventional 0:day regimen in one study.<1?! 1@= %f .17 atients who received hemodialysis * days er week! >? e4 erienced the com osite rimary end oint event of vascular re air! loss! or related hos itali9ation! com ared with only 1@ of the .1+ atients undergoing conventional treatment. )esults indicated that overall risk for a first access event was /*8 higher with daily hemodialysis than with the conventional regimen.<1?! 1@= M#r(a* () $he mortality rates associated with CKD are striking. Hortality in atients with CKD in 1++@ was 7*8 greater than that in atients without CKD.<17= (or atients with stages >:7 CKD! the ad5usted mortality rate is /*8 greater. $he highest mortality rate is within the first * months of initiating dialysis. Hortality then tends to im rove over the ne4t * months! #efore increasing gradually over the ne4t > years. $he 7:year survival rate for a atient undergoing long:term dialysis in the United States is a ro4imately 078! and a ro4imately 178 in atients with dia#etes.

$he most common cause of sudden death in atients with IS)D is hy erkalemia! which often follows missed dialysis or dietary indiscretion. $he most common cause of death overall in the dialysis o ulation is cardiovascular diseaseD cardiovascular mortality is .+:1+ times higher in dialysis atients than in the general o ulation.<0.= Se=+a* an$ re%r#$+c( @e &&+e& 6u#erty is often delayed among males and females with significant CKD. (emale atients with advanced CKD commonly develo amenorrheic and infertile. :. PATIENT EDUCATION 6atients with chronic kidney disease (CKD) should #e educated a#out the followingJ Im ortance of avoiding factors leading to increased rogression menstrual irregularities. 2omen with IS)D are ty ically

Latural disease rogression 6rescri#ed medications (highlighting their otential #enefits and adverse effects) 3voidance of ne hroto4ins Diet )enal re lacement modalities! including trans lantation $imely lacement of vascular access for hemodialysis eritoneal dialysis! hemodialysis! and

BAB III LAPORAN AASUS 1. IDENTITAS PASIEN

a. Lama #. Usia J $n. ) J ** tahun

c. Penis Kelamin J laki:laki d. 3gama J Islam

e. 3lamat J $unire5o 0-/ f. 6eker5aan J 6etani J +7.10.7+ J ICU J .0 Se tem#er 1+.0 J .7 Se tem#er 1+.0

g. Lo. CH h. )uang i. 5. Hasuk Keluar

2. RIBAYAT PENYAAIT a. ANAMNESA Keluhan Utama J sesak

)iwayat enyakit sekarang J asien mengeluh sesak se5ak 0 hari yang lalu. Se#elumnya asien mengeluh demam se5ak 7 hari yang lalu. Keluarga asien menye#utkan #ahwa se#elumnya asien ergi ke Kalimantan 1 minggu yang lalu. Se#elum di#awa ke rumah sakit! asien muntah darah satu kali se#anyak setengah gelas #elim#ing. )iwayat #atuk lama (:). 3namnesa sistemati7

: : : : : : : : : : : : : :

Keadaan umum J sesak Kulit Ke ala Hata $elinga ;idung Hulut $enggorokan ,eher $hora4 Pantung Saluran cerna Huskuloskeletal Ikstremitas J ikterik (:)! ucat (:) J mesose hal J ka#ur (:) J discharge (:)! kurang endengaran (:) J sekret (:)! nafas cu ing hidung (:) J sianosis (:) J nyeri dan sulit menelan (:)! serak (:) J simetris! em#esaran K'K (:) J dys neu (N)! #atuk (:) J nyeri dada (N)! al itasi (N) J mual (:)! muntah (:)! nyeri ulu hati (:)! J nyeri inggang (:) J oedem ekstremitas (N)

)iwayat enyakit dahulu J asien tidak ernah sakit seru a : : : : : )iwayat hi ertensi (N) tidak terkontrol )iwayat asma (:) )iwayat dia#etes mellitus (:) )iwayat $K (:) )iwayat merokok (N)

Riwayat enyakit keluarga J tidak ada keluarga yang sakit seru a asien menggunakan Pamkesmas se#agai #iaya

)iwayat social ekonomi J engo#atan. Kesan J kurang

#. PEMERIASAAN FISIA Keadaan umum J gelisah dan dys neu

Kesadaran Status 'i9i Oital Sign : : : : J

J Com os mentis J #aik

$D J .7/-@7 mm;g ;) J .+/ 4 - menit )) J 0> 4 - menit $ J 0?!@ C

6emeriksaan sistematik : : : : : : : : Ke ala Hata $elinga J mesose hal J sklera ikterik (:)! kon5ungtiva anemis (N-N) J discharge (:)

;idung J sekret (:)! nafas cu ing hidung (:) Hulut $enggorokan ,eher Ikstremitas J sianosis (:) J nyeri telan (:) J simetris! em#esaran K'K (:) J oedem ekstremitas su erior (:) dan inferior (:)

6emeriksaan $horak : : 6aru Pantung : : : : : : Ins eksi J ictus cordis tidak tam ak 6al asi J Ictus cordis tera#a di ICS OI linea mid clavicula sinistra! thrill (:). 6erkusi J ekak Katas atas J ICS II linea sternalis sinistra 6inggang 5antung J ICS III linea arasternalis sinistra Katas kanan #awah J ICS OI linea arasternalis de4tra J suara dasar vesicular (N) L! suara tam#ahan (:)

Katas kiri #awah J ICS OII 1 cm lateral linea mid clavicula sinistra

6emeriksaan a#domen : : : : : Ins eksi J datar! sikatrik (:)! striae(:)! ca ut medusa (:). 3uskultasi J eristaltic (N) L 6erkusi J tym ani! shifting dullness (:)! area trou#e(N) tym ani ;e ar J ekak (N)! liver s an de4tra .. cm! liver s an sinistra * cm 6al asi .. Su erfisial J su el! massa (:) 1. dalam J nyeri tekan (:)! he ar! lien dan gin5al tidak tera#a

Ikstremitas Ikstremitas su erior Inferior

%edem 3kral dingin )eflek fisiologis Ikterik c. PEMERIASAAN PENUNCANG

:-: :-: N-N :-:

N-N :-: N-N :-:

,a#oratorium tanggal .0 se tem#er 1+.0

;# ;t /!@ g-dl 1> 8 .1++ */.+++ 1>

,eukocyte 6latelet S'%$ S'6$ IK'

11

tanggal .0 se tem#er 1+.0

3. ABNORMALITAS DATA

: :

3L3HLIS3 6IHI)IKS33L (ISIK Dys neu : Dys neu dengan )) 01 : %edem ekstremitas kali er menit inferior : ;i ertensi

6ILULP3L' ,a#oratorium J 3nemia

4. DAFTAR MASALAH Chronic Kidney (ailure

;. INITIAL PLAN ASSESMENT I6 diagnosis A7+( $an 7r#n 7 : ,a#oratorium J ;t! factor koagulasi! K'3 : )adiologi J foto $hora4 : IK' : ekokardiografi : Su ly oksigen J target saturasi A ?? 8

I6 tera i

I6 monitoring I6 edukasi

Heningkatkan fungsi ventrikel kanan J diuretic! digitalis dan walfarin : Henurunkan vasokonstriksi aru J CCK! Keta selektif agonis dan $heo hyline : Invasif J hle#otomy Honitoring kadar %1 dan kondisi klinis Henyam aikan #ahwa engo#atan ini sangat enting dan vital. Hen5elaskan rognosis.

>. FOLLOB UP Ae&a$aran Aea$aan U,+, Tan$a @ (a* TD HR RR S S%O2 La'#ra( H' Le+7#& ( Tr#,'#& ( H( SGOT SGPT Ure+, Crea( n n GDS Na(r +, Aa* +, Aa*& +, Ma!ne& +, C*#r $a Pr#(e n A*'+, n G*#'+* n $ a!n#&a 138D813 UGD I>H*O7 'elisah Sesak .7/-@7 .+/ 0> 0?!@ .++ /!@ .1++ */.+++ 1> 1> 11 0*> .0!@ 7. /. ..?!* 7!07 /!0> .!@ ??!@ *!? 1!7 >!0 CKD gr O 3nemia Insefalo ati uremic : ), .1 t m : In5 Cefota4im 14. gr : In5 (urosemid 0>1 .+!1/ @> 138D813 ICU I>H*O7 'elisah Sesak .>+-?@ .1+ 0> 0/ .++ 148D813 ICU I>H*O7 Somnolen Sesak .1?-/0 ..1 01 0*!? .++ 1;8D813 ICU I0H7O7 Somnolen ?*->0 ..@ 10 0* ?*

(e#ris 7 hari dengan anemia : %1 ?:.+ l-mt : ), 0+ tts-mt : In5. Cefota4im 14. gr

CKD gr O CC$ >!7 :Inf D78 1 flash :Kicnat dri 17+ mg D78 lus .++ cc #icnat! .1

CKD gr O 3nemia Insefalo ati uremic $era i lan5ut

Tera%

: In5. )anitidine *4.3 : In5 vit K 04. : 6aracetamol dri . gr : 6asang L'$! DC : Usaha transfuse 6)C 1 kolf

tts-mnt

14. : In5 )anitidine *4. : Kicnat 047+ : 3sam folat .4.

Tan!!a* 1;8D813 19.11 TD HR &% O2 RR & 10 0* 1* 11 0* 1? 1@ 77!? 1* 0* 1+ 0* @en( * a(#r 1/ 10 .* 11 10 ?*->0 ..@ ?* 1:.11 .+.7. .1+ @? .0+ ?+ .1> @+ ../ .++ 1D.11 @1-7/ 11.11 @.->/ 11.11 //-7. 12.11 .+07/ .1* @> ... @* .1> .++ 13.11 *0-1. 14.11 @0-71 1;.11 .++>7 .+/ .++ ../ ?/ @1 .++ 7> @? *7 /* 1>.11 ?+-1/ 19.11 *+-10 1:.11 *+->+ 1D.11 .1/-71

BAB I< AESIMPULAN

In chronic kidney disease (CKD)! doses and dosing intervals of drugs that are e4creted or meta#oli9ed renally should #e ad5usted according to the residual glomerular filtration rate ('()). Some drugs are contraindicated in moderate to severe renal im airment #ecause of otentially serious effects from drug or meta#olite accumulation. )outine consultation of the a undertaken when rescri#ing any new drug to a atient with CKD. (or atients undergoing dialysis! it is e4tremely im ortant to carefully check dosing guides or monitor levels when ossi#le. $hese modalities differ in their clearance of drugs. ;os itali9ed atients undergoing other ty es of continuous renal re lacement thera y also reCuire close monitoring. 3n e4 erienced clinical harmacist can #e invalua#le in assisting to design individuali9ed dosing regimens. $reatments for the athologic manifestations of CKD include the followingJ ;y er hos hatemiaJ Dietary hos hate #inders and dietary hos hate restriction ;y ocalcemiaJ Calcium su lements and ossi#ly calcitriol ro riate references should #e

;y er arathyroidismJ Calcitriol or vitamin D analogues

DAFTAR PUSTAAA

.. Douglas D. Oitamin D Cur#s 3l#uminuria in Kidney Disease. Hedsca e Hedical Lews.

3vaila#le athtt J--www.medsca e.com-viewarticle-?.+?+*. 3ccessed Se tem#er .*! 1+.0. 1. Holina 6! 'Qrri9 P,! Holina HD! 6eris 3! KeltrRn S! Kanter P! et al. $he effect of cholecalciferol for lowering al#uminuria in chronic kidney diseaseJ a ros ective controlled study. Le hrol Dial $rans lant. 3ug 1> 1+.0D<Hedline=. 0. ,ameire L! Oan Kiesen 2. $he initiation of renal:re lacement thera y::5ust:in:time delivery. L Ingl P Hed. 3ug .1 1+.+D0*0(/)J*/?:?+. <Hedline=. >. 2aknine S. Kidney Disease Classification to Include 3l#uminuria Hedsca e Hedical Lews. Dec 0. 1+.1. 3vaila#le at htt J--www.medsca e.com-viewarticle-//*@>+. 3ccessed Pan @ 1+.0. 7. <'uideline= KDI'%. Kidney Int Su . Pan 1+.0D0(.)J.:.7+. <(ull $e4t=. *. $hakar CO! Christianson 3! ;immelfar# P! ,eonard 3C. 3cute kidney in5ury e isodes and chronic kidney disease risk in dia#etes mellitus. Clin P 3m Soc Le hrol. Lov 1+..D*(..)J17*/: /1. <Hedline=. /. <Kest Ividence= Kash ,D! Irlinger $6! Coresh P! Harsh:Han9i P! (olsom 3)! 3stor KC. Inflammation! hemostasis! and the risk of kidney function decline in the 3therosclerosis )isk in Communities (3)IC) Study. 3m P Kidney Dis. 3 r 1++@D70(>)J7@*:*+7. <Hedline=. <(ull $e4t=. ?. ;allan SI! Hatsushita K! Sang S! Hahmoodi KK! Klack C! Ishani 3! et al. 3ge and association of kidney measures with mortality and end:stage renal disease. P3H3. Dec .1 1+.1D0+?(11)J10>@: *+. <Hedline=.<(ull $e4t=. @. de Koer I;. Chronic kidney diseasea challenge for all ages. P3H3. Dec .1 1+.1D0+?(11)J1>+.:1.<Hedline=. <(ull $e4t=. .+. (riedman DP! Ko9litina P! 'enovese '! Pog 6! 6ollak H). 6o ulation:Kased )isk 3ssessment of 36%,. on )enal Disease. P 3m Soc Le hrol. Lov 1+..D11(..)J1+@?:.+7. <Hedline=. ... Isakova $! Tie ;! Sang 2! Tie D! 3nderson 3;! Scialla P! et al. (i#ro#last growth factor 10 and risks of mortality and end:stage renal disease in atients with chronic kidney disease. P3H3. Pun .7 1+..D0+7(10)J1>01:@. <Hedline=. <(ull $e4t=.

.1. Illis P2! Chen H;! (oster HC! ,iu C$! ,arson H'! de Koer I! et al. Oalidated SL6s for e'() and their associations with al#uminuria. ;um Hol 'enet. Pul .7 1+.1D1.(.>)J01@0: ?. <Hedline=. <(ull $e4t=.

.0. 6attaro C! KUttgen 3! $eumer 3! et al. 'enome:wide association and functional follow:u
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.>. Lordfors ,! ,uttro

K! Carrero PP! 2itas 3! Stenvinkel 6! ,indholm K! et al. 'enetic studies in

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.7. Su S,! ,u KC! ,in S(! ;su SP! ,ee 6S! Sang ;S! et al. 'ene olymor hisms of angiotensin:
converting en9yme and angiotensin II ty e . rece tor among chronic kidney disease atients in a Chinese o ulation.P )enin 3ngiotensin 3ldosterone Syst. Har 1+.1D.0(.)J.>?:7>. <Hedline=. .*. Kidney Disease Statistics for the United States. Lational Kidney and Urologic Diseases Information Clearinghouse (LKUDIC). 3vaila#le at htt J--kidney.niddk.nih.gov-kudiseases- u#s-kustats-V./. 3ccessed Se tem#er 7! 1+.1. ./. Centers for Disease Control and 6revention. Deaths and Hortality. 3vaila#le

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.@. <Kest Ividence= Choi 3I! )odrigue9 )3! Kacchetti 6! Kertenthal D! ;ernande9 '$! %W;are 3H.
2hite-#lack racial differences in risk of end:stage renal disease and death. 3m P Hed. Pul 1++@D.11(/)J*/1:?. <Hedline=. <(ull $e4t=.

1+. Schold PD! Srinivas $)! Kraun 2I! et al. $he relative risk of overall graft loss and acute
re5ection among 3frican 3merican renal trans lant reci ients is attenuated with advancing age. Clin $rans lant. Se 1+..D17(7)J/1.:0+. <Hedline=.

1.. ;icks 6P! ,angefeld CD! ,u ,! Kleyer 3P! Divers P! Lachman 6;! et al. Sickle cell trait is not
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10. Lorris KC! 3godoa ,S. Unraveling the racial dis arities associated with kidney disease. Kidney
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1>. United

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1*. 2olfe )3! 3sh#y OK! Hilford I,! %5o 3%! Ittenger )I! 3godoa ,S! et al. Com arison of
mortality in all atients on dialysis! atients on dialysis awaiting trans lantation! and reci ients of a first cadaveric trans lant. L Ingl P Hed. Dec 1 .@@@D0>.(10)J./17:0+. <Hedline=.

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1?. HcLamara D. Hore freCuent dialysis increases risk for com lications. (e#ruary .0! 1+.0.
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1@. Sens (! Schott:6ethela9 3H! ,a#eeuw H! Colin C! Oillar I. Survival advantage of hemodialysis
relative to eritoneal dialysis in atients with end:stage renal disease and congestive heart failure. Kidney Int. Lov 1+..D?+(@)J@/+:/. <Hedline=.

0+. 2ald )! San 3$! 6erl P! et al. )egression of left ventricular mass following conversion from
conventional hemodialysis to thrice weekly in:centre nocturnal hemodialysis. KHC Le hrol. Pan .@ 1+.1D.0(.)J0.<Hedline=.

0.. )a hael K,! 2ei '! Kaird KC! 'reene $! Keddhu S. ;igher serum #icar#onate levels within the
normal range are associated with #etter survival and renal outcomes in 3frican 3mericans. Kidney Int. (e# 1+..D/@(0)J07*:*1. <Hedline=.

01. Lavaneethan SD! Schold PD! 3rrigain S! et al. ,ow 17:;ydro4yvitamin D ,evels and Hortality
in Lon:Dialysis:De endent CKD. 3m P Kidney Dis. %ct 1+..D7?(>)J70*:>0. <Hedline=. <(ull $e4t=.

00. Kendrick P! Cheung 3K! Kaufman PS! 'reene $! )o#erts 2,! Smits '! et al. 3ssociations of
lasma 17:hydro4yvitamin D and .!17:dihydro4yvitamin D concentrations with death and rogression to maintenance dialysis in atients with advanced kidney disease. 3m P Kidney Dis. %ct 1+.1D*+(>)J7*/:/7. <Hedline=.<(ull $e4t=.

0>. Lavaneethan SD! Schold PD! 3rrigain S! Polly SI! Pain 3! Schrei#er HP Pr! et al. ,ow 17:
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07. <Kest Ividence= ;edayati SS! Hinha5uddin 3$! $oto )D! Horris D2! )ush 3P. Oalidation of
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0*. Inker ,3! Schmid C;! $ighiouart ;! Ickfeldt P;! (eldman ;I! 'reene $! et al. Istimating
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0/. ,ater9a %(! 6rice C6! Scott H'. Cystatin CJ an im roved estimator of glomerular filtration
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0?. Lational Kidney (oundationWs Kidney Disease %utcomes &uality Initiative. Chronic Kidney
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0@. ,evey 3S! Kosch P6! ,ewis PK! 'reene $! )ogers L! )oth D. 3 more accurate method to
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>+. <Kest Ividence= Stevens ,3! Schmid C;! 'reene $! Zhang S,! Keck 'P! (roissart H! et al.
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>.. Silveiro S6! 3ra[5o 'L! (erreira HL! Sou9a (D! Samaguchi ;H! Camargo I'. Chronic Kidney
Disease I idemiology Colla#oration (CKD:I6I) eCuation 7. <Hedline=. <(ull $e4t=. ronouncedly underestimates glomerular filtration rate in ty e 1 dia#etes. Dia#etes Care. Lov 1+..D0>(..)J1070:

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>7. ,evey 3S! 3dler S! Caggiula 32! et al. Iffects of dietary rotein restriction on the rogression
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>*. Kasiske K,! ,akatua PD! Ha PZ! ,ouis $3. 3 meta:analysis of the effects of dietary rotein
restriction on the rate of decline in renal function. 3m P Kidney Dis. Pun .@@?D0.(*)J@7>: *.. <Hedline=.

>/. <Kest Ividence= (ish#ane S! Chittineni ;! 6ackman H! Dutka 6! 3li L! Durie L. %ral aricalcitol
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>?. 6lantinga ,! 'ru##s O! Sarkar U! et al. Lonsteroidal 3nti:Inflammatory Drug Use 3mong
6ersons 2ith Chronic Kidney Disease in the United States. 3nn (am Hed. Se tem#er:%cto#er 1+..D@(7)J>10:>0+.<Hedline=. <(ull $e4t=.

>@. ;allan SI! %rth S). Smoking is a risk factor in the rogression to kidney failure. Kidney Int. Se
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7+. Kusko H. ,:thyro4ine dam ens renal function decline in CKD with SC;. Pune .@! 1+.0.
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7.. Shin D;! ,ee HP! ,ee ;S! %h ;P! Ko KI! Kim C;! et al. $hyroid hormone re lacement thera y
attenuates the decline of renal function in chronic kidney disease hy othyroidism. $hyroid. Pun 1+.0D10(*)J*7>:*.. <Hedline=. <(ull $e4t=. 71. US (ood and Drug 3dministration. SafetyJ %montys ( eginesatide) In5ection #y 3ffyma4 and $akedaJ recall of all lots : serious hy ersensitivity reactions. (e#ruary 10! 1+.0. 3vaila#le atients with su#clinical