Acute Renal Failure and Treatment

8/19/2019 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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;' 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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: cr or children - (K)(


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: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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? 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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'd&erse e,ect o Ca gluconateHh+potension3 tingling sensations

renal calculus

1H ma+ increase digoin toicit+

Treatment of


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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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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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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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;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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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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;/; 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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'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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ncrease intracellular a throughacti&ating a!


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'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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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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'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



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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



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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



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g ymanifestations

nteractionsH aminogl+cosides;'1s probenecidthacr+nic acid ma+ potentiate the

anticoagulant e,ect o ararin



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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



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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



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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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Acute Renal Failure and Treatment