acute renal failure and treatment
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Acute Renal Failure
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Acute renal failure
50% increase in baseline serumcreatinine concentration
25% decrease in glomerular fltrationrate (GFR)
Urine output o less than 0.5m!"g!hr or at least # hours
$ o single serum creatinine &aluee isa threshold or 'RF
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RIFLE Classication
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Epidemiology
eteen 5% and 25% o allhospitali*ed patients ma+ de&elop
this dissease
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',erent and e,erent arteriolar&asoconstriction!&asodilation e,ects
on GFR and RF
',erent and e,erent&asoconstriction - 'ngiotensin
',erent &asodilation - /rostaglandin2
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1ecrease GFR RF - s+mpatheticner&es3 angiotensin 3 endothelin
ncrease GFR RF - /G23 43brad+"inin
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Why ACEI is contraindicatedin renal artery stenosis?
/ressure proimal to the renal arter+stenosis is increased hile pressure
distal to it is normal or reduced
oering the /3 loers the pressuredistal to the stenosis loering RF GFR
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Categories
/rerenal670625% o cases
ntrinsic6 50%
/ostrenal 8 70%
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Prerenal ARF
Reduced blood deli&er+ to the "idne+
1ue to intra&ascular &olumedepletion3 reduced cardiac outputand h+potension
o structural damage to the "idne+has occurred
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Prerenal ARF
9ild to moderate decrease in RF3intraglomerular pressure is
maintained b+ dilation o the a,erentartierioles3 constriction o e,erentarterioles and redistribution o RFto the o+gen sensiti&e renalmedulla
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Functional ARF
:aused b+ drugs;'1s impairs prostaglandin6mediated
dilation o the a,erent arterioles': and 'Rs inhibit angiotensin 6
mediated e,erent arteriole &asoconcstriction
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Prerenal ARF
:aused b+ renal arter+ stenosis
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Intrinsic ARF
'lso "non as intrarenal 'RF1amaged is ithin the "idne+s
'cute tubular necrosis ('=)Results rom toic (amphotericin 3
aminogl+cosides3 contrast agents)and ischemic insult to the "idne+
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AT
ecrosis in proimal tubuleepithelium and 93 decreased
glomerular capillar+ permeabilit+and bac"lea" o glomerular fltrateinto the &enous circulation
9ediated b+ intrarenal&asoconstriction
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Intrinsic ARF
Glomerulonephritis3 ;3 interstitialnephritis3 &asculitis
:' be a result o prerenal 'RF i thecondition is not corrected
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Postrenal ARF
1ue to obstruction o urinar+ out>oenign prostatic h+pertroph+ (/
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Assessment of RenalFunction
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!lomerular ltrationrate
?olume o plasma fltered across theglomerulus per unit time
:orrelates ith the fltration3secretion3 absorption3 endocrine andmetabolic unciotn o the "idne+
Used to compute or the properdosing o drugs that undergo renalelimination (e.g. ?ancom+cin)
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!lomerular ltrationrate
@06720 m!min:reatinine clearance (:r:l) is used to
estimate GFR
Urine &olume3 urine creatinine concentrationand serum creatinine concentration
:r:l ma+ underestimate or o&erestimaterenal unction depending on the stage o thedisease
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Estimating creatinineclearance "Coc#roft $ !ault%
:cr or males - (7A06age in +rs)(B in "g)
(m!min) (C2)(;cr in mg&dL)
:cr or emales - (0.D5)(:cr)
;erum creatinine is at stead+ stateand age3 t.3 and gender re>ectsnormal muscle mass
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Estimating creatinineclearance "Coc#roft $ !ault%
:cr or - F (7A06age in +rs)(t.in "g)
(m!min) (;cr in umol&L)
F- 7.0A in emales or 7.2E in males
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Estimating creatinineclearance
B in males ("g) - 50 (2.E
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Estimating creatinineclearance
;' in m2 - (Beight in "g!C0 "g)0.C (7.CE m2)
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Compute for estimatedCrCl
5A +ear6old male3 Bt. @2 "g3 ;:r #.7mg!d
E2 +ear6old emale3 Bt. DD "g3 ;:rE.5 mg!d
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Estimating creatinineclearance
: cr or children - (K)(
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Estimating creatinineclearance
:cr or children - (:cr inm!min!7.CE m2) (m!min)
(;'!7.CEm2
)
:cr or children - (:cr inm!min!7.CE m2)(m!min) (Bt. n "g!C0"g)0.C
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Estimating renal clearance "(odication of)iet in renal disease study or ()R)%
eGFR (m!min!7.CE m2) - 7C0 (;cr)60.@@@ (age)60.7C# (0.C#2 i emale)
(7.7D i blac") (U)60.7C
('lb)0.E7D
Bhere ;:r is in mg!d3 U is inmg!d 'lbumin in g!d
Used to estimate renal unction ithGFR L #0 m!min
A f l
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Assessment of renalfunction
;+mptomatolog+ (signs o uremia3pruritus3 edema3 atigue3 eight
gain)
aborator+ results (blood creatinine3urinal+sis)
Urine output
A f l
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Assessment of renalfunction
4liguria 8 urine output less than A00m! 2A hours
'nuria 8 urine output less than 50m! 2A hours
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Prerenal RenalFea (%) L 7 2
Urine a(mM!) L 20 A0Urine!serumU (umol!)
D L E
Urine!serum:rea (umol!)
A0 L 20
Urine osm
(m4sm!"g)
500 LA00
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Course of AT
4liguric phase (C67A da+s3 # ee"s) 8prerenal 'K
1iuretic phase (7 ee") 8recommencement o tubular unctionReco&er+ phase 8 tubular cells
regenerate slol+ o&er months 3 GFRdoes not return to initial le&els(elderl+ reco&er more slol+ lesscompletel+
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Course of AT
Uremia h+per"alemia;epticemia and acute &ascular
e&ents (9 stro"e) are commoncause o deaths associated ith 'KUremia results in debilit+
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ACEI $ AR*s in ARF
9onitor / because o h+potensionleading to prerenal 'RF
:ontraindicated in renal arter+stenosisloc"s the action o angiotensin
(increasing e,erent arteriolar tone)resulting in decreased GFR
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!oals of treatment
:ontrol an+ identifable underl+ingcause o 'RF (h+po&olemia3
nephrotoic drugs3 ureterobstruction):orrect and maintain proper >uid
electrol+te balance =reat h+per"alemia and metabolic
acidosis hen present mpro&e urine output
=reat s+stemic maniestations o 'RF
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=here is no e&idence that drugtherap+ hastens patient reco&er+3
shorten length o hospital sta+ orimpro&es sur&i&al
/rerenal and postrenal 'RF can bere&ersed i promptl+ treated
ntrinsic 'RF is more supporti&e innature
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Treatment o+,ecti-es
:orrect re&ersible causes o 'RF/re&enting or minimi*ing urther
renal damage or complications1iscontinue nephrotoic drugs =reat underl+ing inectionRemo&e an+ urinar+ tract inections
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Treatment o+,ecti-es
:orrect and maintain proper >uid electrol+te balance
=reat bod+ chemistr+ alterationsespeciall+ h+per"alemia andmetabolic acidosis
mpro&e urine output =reat s+stemic maniestations o 'RF
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:onser&ati&e management ma+suNce in uncomplicated 'RF
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(onitor
Fluid balance (hoO)3 signs ocongestion
:o6morbities!drugs that ma+aggra&ate 'K ons (K3 :a3 phosphate3 bicarbonate)'cid6base balanceB: count!di,erential count
(inection)
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Fluid management
Fluid inta"e should match >uid losses
;ensible losses and insensible losseso 50067!da+ should be included in>uid balance calculations
?olume o&erload should be a&oidedto minimi*e ris" o
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.ptimi/e renal perfusion
:entral line ma+ be used0.@% a:l is ideal
Esta+lishing ade0uate
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Esta+lishing ade0uatediuresis
oop diuretics ma+ be gi&en or 1uido-erload h+per"alemia
oop diuretics decrease renal tubularcell metabolic demands and increaserenal blood >o b+ release oprostaglandin (renal &asodilator)
=ransient deaness ma+ occur at highinusion rates
Esta+lishing ade0uate
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Esta+lishing ade0uatediuresis
1opamine at lo doses is a renal&asodilator in normal "idne+s but in
renal failure it is a renal-asoconstrictoro clinical beneft9annitol is also not benefcial
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Pro+lems in A'I or ARF
Uremia ntra&ascular >uid o&erload
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Treatment of uremia
'ccumulation o toic products oprotein metabolism including urea
ausea3 &omiting3 anoreia:ontrol in the diet
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Fluid management
/atient should be eighed dail+ todetermine >uid &olume status
:ontrol in the inta"e o >uid and lo6salt
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)ietary measures
2igh3calorie4 lo53protein diet
Reduce renal or"load b+ decreasingproduction o end products o proteincatabolism that the "idne+s cannotecrete
/re&ent "etoacidosis'lle&iate maniestations o uremia
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)ietary measures
;odium inta"e should be restricted iedema
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Treatment ofhyper#alemia
ntracellular K is released (esp. insepsis3 tissue damage) and ecretion
is decreasedRegulate the diet and drugs (Ksparing diuretics)
mergenc+ treatment i le&el C.0mmol! or :G changes (tall3 pea"ed
= a&es3 reduced / a&es3 increase
PR; complees)
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Treatment of hyper#alemia
)ialysis
'dminister calcium chloride orgluconate to replace and maintainbod+ calcium and counteract the
cardiac e,ects o acuteh+per"alemia
Treatment of
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Treatment ofhyper#alemia
? calcium is contraindicated inpatients ith &entricular fbrillation
renal calculi
:G should be monitored
Calcium gluconate should not bemied ith solutions containinga
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Treatment ofhyper#alemia
'd&erse e,ect o Ca gluconateHh+potension3 tingling sensations
renal calculus
1H ma+ increase digoin toicit+
Treatment of
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Treatment ofhyper#alemia
6odium +icar+onate ? can begi&en as an emergenc+ measure to
treat h+per"alemia metabolicacidosis
RationaleH Renal tubules cannot
reabsorb orm the glomerular fltrate increase arterial p< shit K intocells
Treatment of
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Treatment ofhyper#alemia
9onitoringH can lead to sodium and>uid o&erload
9a+ precipitate calcium salts
'G and serum electrol+tes must be
monitored
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Treatment of hyper#alemia
Regular insulin I7 "839: u% 5ith ;trose
:auses intracellular shit o potassium
1eposits potassium ith gl+cogen in theli&er
9onitoringH >uid o&erload and serum glucose
6al+utamol ma+ also be gi&en (temporar+emergenc+ measure)3 does not permanentl+loer K
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Treatment of hyper#alemia
;odium pol+st+rene sulonate (;/;)/otassium6remo&ing resin
(echanges sodium or potassium)1istributed in the intestines andecreted in the eces
Route o administrationO oral
Treatment of
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Treatment ofhyper#alemia
9onitoring o ;/;H sodium3bicarbonate3 chloride3 p< and
QQQQQQQQQQQQQQQQ /otassium beteen A65 mM!/otassium depletion irritabilit+3
conusion3 cardiac arrh+thmias3 :G
changes and muscle ea"ness
9onitor or signs o
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Treatment ofhyper#alemia
;/; oral should be mied ith ateror sorbitol not ith orange Juice
's enema ith ater or sorbitol3ne&er ith mineral oil
Treatment of
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Treatment ofhyper#alemia
'd&erse e,ectsH constipation3 ecalimpaction3 &omiting diarrhea
;hould not be used as a sole agent
nteractionsH 9agnesium h+droideand nonabsorbable cation6donating
laati&es antacids ma+ decreasethe e,ects s+stemic al"alosis
Treatment of meta+olic
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Treatment of meta+olicacidosis
nabilit+ o the "idne+s to ecrete
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Treatment of meta+olicacidosis
ncrease intracellular a throughacti&ating a!
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Treatment of meta+olicacidosis
'd&erse e,ectH Fluid o&erload due tosodium
et treatment alternati&e is dial+sis
1o not gi&e simultaneousl+ ith :a
gluconate in a single ? line due toprecipitate ormation
Treatment of
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Treatment ofhyperphosphatemia
/hosphate is normall+ ecreted b+the "idne+s
Treatment of
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Treatment ofhyperphosphatemia
I7 calcium is the frst line o therap+Reduces phosphorus conc. b+
chelation4ral calcium binds to dietar+ / in the
G tract:alcium carbonate is used to treat
acute3 lie6threateningh+perphosphatemia ith acuteh+pocalcemia hen &olume o&erload
is present
Treatment of
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Treatment ofhyperphosphatemia
'luminum h+droide oral can bindecess phosphate in the intestines
4nset o actionH #672 hours;ide e,ectsH anoreia9onitoringH serum phosphate or
calcium:an cause calcium resorption bone
deminerali*ation
Treatment of
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Treatment ofhypocalcemia
1ue to :a malabsorption due todisordered &it 1 metabolism
Calcium gluconate for lo5 le-elsReplaces and maintains bod+
calcium3 raising the serum calciumle&el immediatel+
9ild h+pocalcemiaH oral calcium(carbonate3 chloride3 gluconate or
lactate) supplementation
Treatment of
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Treatment ofhyponatremia
Fluid restriction or moderate oras+mptomatic h+ponatremia
For sodium le&el belo 720 mM!3 QQQQQQQQQQQQQQQQ ?Replaces and maintains sodium and
chloride increasing etracellular
tonicit+
Treatment of
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Treatment ofhyponatremia
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(anagement of systemicmanifestations
=reatment o >uid o&erload edema
9annitol or loop diuretic ma+ beused
=hia*ide diuretics are a&oided
(anagement of systemic
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(anagement of systemicmanifestations
Loop "high3ceiling% diuretics9ore potent and rapid acting than
thia*ide diuretics
(anagement of systemic
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a age e o sys e cmanifestations
9a+ cause o&erdiuresis orthostatich+potension3 >uid and electrol+teabnormalities (QQQQQQcalcemia3
QQQQ"alemia3 QQQQchloremia3 QQQQQnatremia3 QQQQQmagnesemia)and transient ototoicit+ ith rapid
? inJection?ital signs should be monitored9onitor QQQQQQQQQQQQ in diabetics
(anagement of systemic
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g ymanifestations
;ensiti&e to sulonamides ma+ besensiti&e to bumetanide urosemide
Furosemide and ethacr+nic acid ma+produce agranuloc+tosis
(anagement of systemic
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g ymanifestations
nteractionsH aminogl+cosides;'1s probenecidthacr+nic acid ma+ potentiate the
anticoagulant e,ect o ararin
(anagement of systemic
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g ymanifestations
(annitol (routeO)4smotic diuretic94'H increases the osmotic pressure
o the glomerular fltrateFluid rom interstitial spaces is dran
into blood &essels3 epanding
plasma &olume and maintaining orincreasing urine >o
(anagement of systemic
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g ymanifestations
9a+ be gi&en to pre&ent 'RF in high6ris" patients (undergoing surger+3se&ere trauma) or oliguric 'RF
:ontraindicated in anuria3 se&eredeh+dration3 pulmonar+edema!congestion intracranial
hemorrhage
9a+ orsen pulmonar+ edema
circulation o&erload
(anagement of systemic
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g ymanifestations
'd&erse e,ectsH >uid electrol+teabnormalities3 ater intoication3headache3 conusion3 blurred &ision3thirst3 nausea &omiting
9onitoringH &ital signs3 urine output3
dail+ eight3 cardiopulmonar+status3 serum urine a K
Treatment of infections
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Treatment of infections
1ue to bladder catheters3 centralcatheters3 peripheral ? lines shouldbe used ith care
;erum culture sensiti&it+*road spectrum anti+iotic can be
used hile aaiting results
)ialysis
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)ialysis
all strategies ailFor 'RF ith acute >uid o&erload3
anuria3 se&ere h+per"alemia3metabolic acidosis3 U le&el abo&e700 mg!d
Why dialysis?
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Why dialysis?
Remo&e uremic toins rapidl+ hense&ere s+mptoms are present (e.g.altered sensorium)
Resistant to diuretics:orrect electrol+te and acid6base
imbalances (contraindication to
sodium bicarbonate)
2emodialysis
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2emodialysis
For patients ith reduced peritonealmembrane3 h+percatabolism oracute h+per"alemia
n&ol&es shunting o blood through adial+sis membrane containing unitor di,usion3 osmosis ultrafltration
?ascular access &ia arterio&enousfstula or eternal shunt
2emodialysis
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2emodialysis
Recei&es heparin to pre&ent clotting:lotting o the hemoflter3
hemorrhage3 hepatitis3 anemia3septicemia3 cardio&ascular problems3air embolism3 rapid shits in >uid electrol+te balance3 itching3
headache3 sei*ures3 nausea3&omiting3 aluminum osteod+stroph+
2emodialysis
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2emodialysis
2emodialysis
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2emodialysis
2emoltration
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2emoltration
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Peritoneal dialysis
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Peritoneal dialysis
/reerred or patients ith bleedingdisorders and cardio&ascular disease
/eritoneum is used as asemipermeable membrane
/lastic catheter is inserted into theperitoneum pro&ides access or the
dial+sate3 hich dras >uids3 astesand electrol+tes across theperitoneal membrane b+ osmosis
and di,usion
Peritoneal dialysis
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Peritoneal dialysis
Peritoneal dialysis
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Peritoneal dialysis
ntermittent /1 6 automatic c+clingmode lasting D670 hours3 E a ee"3or or"ing patients
:ontinuous ambulator+ /1 8 2Ahours ith A echanges dail+3patient can remain acti&e during
treatment
Peritoneal dialysis
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Peritoneal dialysis
:ontinuous c+clic /1 8 dial+sis ta"esplace at night3 last echange isretained in the peritoneal ca&it+during the da+3 then drained thate&ening
'd&antagesH lac" o seriouscomplications3 retention o normal>uid electrol+te balance3 reduced
cost simplicit+ reduced or no need
Peritoneal dialysis
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Peritoneal dialysis
:omplicationsH h+pergl+cemia3constipuation3 inection o thecatheter site3 high ris" o peritonitis
Ideal drug for use in a patient
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5ith renal failure
o acti&e metabolites1isposition una,ected b+ >uid
balance changes1isposition una,ected b+ protein
binding changesResponse una,ected b+ altered
tissue sensiti&it+Bide therapeutic marginot nephrotoic
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