Acute Renal Failure_2

8/6/2019 Acute Renal Failure_2

1/56

Acute Renal FailureAcute Renal Failure

Matthew L. Paden, MDMatthew L. Paden, MD

Pediatric Critical CarePediatric Critical Care

Emory UniversityEmory UniversityChildrens Healthcare of Atlanta at EglestonChildrens Healthcare of Atlanta at Egleston


2/56

Structure and Function of theStructure and Function of the

KidneyKidney Primary unit of thePrimary unit of the

kidney is the nephronkidney is the nephron

1 million nephrons per1 million nephrons per

kidneykidney

Composed of aComposed of a

glomerulus and aglomerulus and a

tubuletubule Kidneys receive 20%Kidneys receive 20%

of cardiac outputof cardiac output

Renal Lecture Required Picture #1


3/56

Renal blood flowRenal blood flow

AortaAorta Renal arteryRenal artery interlobar arteriesinterlobar arteries interlobular arteriesinterlobular arteries afferent arteriolesafferent arterioles

glomerulusglomerulus

efferentefferentarteriolesarterioles

In the cortexIn the cortex peritubularperitubularcapillariescapillaries

In the juxtamedullaryIn the juxtamedullaryregionregion vasa rectavasa recta

Back to the heart throughBack to the heart throughthe interlobularthe interlobularintralobarintralobar renal veinsrenal veins


4/56

Glomerular Filtration RateGlomerular Filtration Rate

Determined by the hydrostatic and oncoticDetermined by the hydrostatic and oncoticpressure within the nephronpressure within the nephron

Hydrostatic pressure in the glomerulus isHydrostatic pressure in the glomerulus is

higher than in the tubule, so you get a nethigher than in the tubule, so you get a netoutflow of filtrate into the tubuleoutflow of filtrate into the tubule

Oncotic pressure in the glomerulus is theOncotic pressure in the glomerulus is theresult of nonresult of non--filterable proteinsfilterable proteins

Greater oncotic pressure as you progress throughGreater oncotic pressure as you progress throughthe glomerulusthe glomerulus

GFR = Kf (hydrostaticGFR = Kf (hydrostatic oncotic pressure)oncotic pressure)


5/56

Renal Lecture Required

Picture #2


6/56

Glomerular Filtration RateGlomerular Filtration Rate

The capillary endothelium is surroundedThe capillary endothelium is surroundedby a basement membrane and podocytesby a basement membrane and podocytes

Foot processes of the podocytes formFoot processes of the podocytes formfiltration slits that :filtration slits that :

Allow for ultrafiltrate passageAllow for ultrafiltrate passage

Limit filtration of large negatively chargedLimit filtration of large negatively charged

particlesparticles Less than 5,000 daltons = freely filteredLess than 5,000 daltons = freely filtered Large particles (albumin 69,000 daltons) notLarge particles (albumin 69,000 daltons) not

filteredfiltered


7/56

Tubular FunctionTubular Function

ProximalProximal

Most of reabsorption occurs hereMost of reabsorption occurs here

Fluid is isotonic with plasmaFluid is isotonic with plasma 6666--70% of sodium presented is reabsorbed70% of sodium presented is reabsorbed

Glucose and amino acids are completelyGlucose and amino acids are completely

reabsorbedreabsorbed


8/56

Tubule FunctionTubule Function

Loop of HenleLoop of Henle

Urine concentration and dilution via changesUrine concentration and dilution via changes

in oncotic pressure in the vasa rectain oncotic pressure in the vasa recta

Descending tubuleDescending tubule permeable to water,permeable to water,

impermeable to sodiumimpermeable to sodium

Ascending tubuleAscending tubule actively reabsorbsactively reabsorbs

sodium, impermeable to watersodium, impermeable to water


9/56


Medullary thick ascending limbMedullary thick ascending limb criticalcritical

for urinary dilution and most oftenfor urinary dilution and most often

damaged in ARFdamaged in ARF

ADH stimulates Na reADH stimulates Na re--absorption in this areaabsorption in this area

Most sensitive to ischemiaMost sensitive to ischemia

Low oxygen tension, high oxygen consumptionLow oxygen tension, high oxygen consumption

Lasix use here inhibits the NaLasix use here inhibits the Na--KK--2Cl ATPase2Cl ATPasewhich in the face of ARF, may decreasewhich in the face of ARF, may decrease

oxygen consumption and ameliorate theoxygen consumption and ameliorate the

severity of the ARFseverity of the ARF


10/56


All of those studies done in an in vitroAll of those studies done in an in vitro

modelmodel

In vivo, if you drop oxygen concentration evenIn vivo, if you drop oxygen concentration evensubsub--atmospheric you do not get tubularatmospheric you do not get tubular

damage even with increased tubular workloaddamage even with increased tubular workload

In vivo models exist where you do see thatIn vivo models exist where you do see that

damage, but appears to need a second hitdamage, but appears to need a second hit


11/56

Tubule FunctionTubule Function

Distal TubuleDistal Tubule

ReRe--absorption of another ~12% of NaClabsorption of another ~12% of NaCl

Proximal segmentProximal segment impermeable to waterimpermeable to water Distal segment is the cortical collecting ductDistal segment is the cortical collecting duct

and secretes K and HCO3and secretes K and HCO3


12/56


Collecting DuctCollecting Duct

Aldosterone acts here to increase NaAldosterone acts here to increase Na

reuptake and K wastingreuptake and K wasting

ADH enhances water reADH enhances water re--absorptionabsorption

Urea reUrea re--absorption to maintain the medullaryabsorption to maintain the medullary

interstitial concentration gradientinterstitial concentration gradient


13/56


14/56

Acute Renal FailureAcute Renal Failure -- DefinitionsDefinitions

70% Non70% Non--oliguric , 30% Oliguricoliguric , 30% Oliguric

NonNon--oliguric associated with betteroliguric associated with better

prognosis and outcomeprognosis and outcome Overall, the critical issue is maintenanceOverall, the critical issue is maintenance

of adequate urine output and prevention ofof adequate urine output and prevention of

further renal injury.further renal injury.

Are we converting nonAre we converting non--oliguric to oliguric witholiguric to oliguric with

our hemofilters?our hemofilters?


15/56

Acute Renal FailureAcute Renal Failure -- DiagnosisDiagnosis

PrePre--renalrenal Decrease in RBFDecrease in RBF constriction of afferent arterioleconstriction of afferent arteriole

which serves to increase systemic blood pressurewhich serves to increase systemic blood pressure

by reducing the shunt through the kidney, butby reducing the shunt through the kidney, but

does so at a cost of decreased RBFdoes so at a cost of decreased RBF

At the same time, efferent arteriole constricts toAt the same time, efferent arteriole constricts to

attempt to maintain GFRattempt to maintain GFR

As GFR decreases, amount of filtrate decreases.As GFR decreases, amount of filtrate decreases.

Urea is reabsorbed in the distal tubule, leading toUrea is reabsorbed in the distal tubule, leading toincreased tubular urea concentration and thusincreased tubular urea concentration and thus

greater regreater re--absorption of urea into the blood.absorption of urea into the blood.

Creatinine cannot be reabsorbed, thus leading to aCreatinine cannot be reabsorbed, thus leading to a

BUN/Cr ratio of > 20BUN/Cr ratio of > 20


16/56

PrePre--Renal vs. Renal FailureRenal vs. Renal Failure

PrerenalPrerenal RenalRenal

BUN/CrBUN/Cr >20>20 1.020 500 mOsm/L 1.3


17/56

Acute Renal FailureAcute Renal Failure -- DiagnosisDiagnosis

DiagnosisDiagnosis

UltrasoundUltrasound Structural anomaliesStructural anomalies polycystic, obstruction, etc.polycystic, obstruction, etc.

ATNATN poor corticomedullary differentiationpoor corticomedullary differentiation

Increased Doppler resistive indexIncreased Doppler resistive index

(Systolic Peak(Systolic Peak Diastolic peak) / systolic peakDiastolic peak) / systolic peak

Nuclear medicine scansNuclear medicine scans DMSADMSA StaticStatic -- anatomy and scarringanatomy and scarring DTPA/MAG3DTPA/MAG3 DynamicDynamic renal function, urinaryrenal function, urinary

excretion, and upper tract outflowexcretion, and upper tract outflow


18/56

Acute Renal FailureAcute Renal Failure

Overall, renal vasoconstriction is the majorOverall, renal vasoconstriction is the major

cause of the problems in ARFcause of the problems in ARF

Suggested ARF be replaced with vasomotorS

uggested ARF be replaced with vasomotornephropathynephropathy

Insult to tubular epithelium causes releaseInsult to tubular epithelium causes release

of vasoactive agents which cause theof vasoactive agents which cause the

constrictionconstriction Angiotensin II, endothelin, NO, adenosine,Angiotensin II, endothelin, NO, adenosine,

prostaglandins, etc.prostaglandins, etc.


19/56

Regulation of Renal Blood FlowRegulation of Renal Blood Flow

In adults autoIn adults auto--regulated over a range ofregulated over a range of

MAPs 80MAPs 80--160160

Developmental changesDevelopmental changes Doubling of RBF in first 2 weeks of lifeDoubling of RBF in first 2 weeks of life

Triples by 1 yearTriples by 1 year

Approaches adult levels by preschoolApproaches adult levels by preschool

Renal blood flow regulation is complexRenal blood flow regulation is complex

No one system accounts for everything..No one system accounts for everything..


20/56

ReninRenin--Angiotensin AxisAngiotensin Axis

For the one millionth time.For the one millionth time.

Hypovolemia leads to decreased afferentHypovolemia leads to decreased afferentarteriolar pressure which leads to decreasedarteriolar pressure which leads to decreasedNaCl reNaCl re--absorption which leads to decreased Clabsorption which leads to decreased Clpresentation to the macula densa whichpresentation to the macula densa whichincreases the amount of renin secreted from theincreases the amount of renin secreted from theJGA which increases conversionJGA which increases conversionangiotensinogen to AGI to AGII which increasesangiotensinogen to AGI to AGII which increases

Aldosterone secretion from the adrenal cortexAldosterone secretion from the adrenal cortexand ADH which leads to increased sodium andand ADH which leads to increased sodium andthus water rethus water re--absorption from the tubule whichabsorption from the tubule whichincreases your blood pressurewhewincreases your blood pressurewhew


21/56

Renin Angiotensin AxisRenin Angiotensin Axis

Renal Lecture Required

Picture #4


22/56


Renins role in pathogenesis of ARFRenins role in pathogenesis of ARF

Hyperplasia of JGA with increased reninHyperplasia of JGA with increased reningranules seen in patients and experimentalgranules seen in patients and experimental

models of ARFmodels of ARF Increased plasma renin activity in ARFIncreased plasma renin activity in ARF

patientspatients

Changing intraChanging intra--renal renin content modifiesrenal renin content modifies

degree of damagedegree of damage Feed animals high salt diet (suppress reninFeed animals high salt diet (suppress renin

production)production) renal injuryrenal injury less renal injury thanless renal injury thanthose fed a low sodium dietthose fed a low sodium diet


23/56


Not the only thing going on thoughNot the only thing going on though

You can also ameliorate renal injury byYou can also ameliorate renal injury by

induction of solute diuresis with mannitol orinduction of solute diuresis with mannitol or

loop diuretics (neither affect the RAS)loop diuretics (neither affect the RAS)

No change in renal injury in animals givenNo change in renal injury in animals given

ACE inhibitors, competitive antagonist toACE inhibitors, competitive antagonist to

angiotensin IIangiotensin IIOverall, role of RAS in ARF is uncertainOverall, role of RAS in ARF is uncertain


24/56

ProstaglandinsProstaglandins

PGE 2 and PGIPGE 2 and PGI

Very important for renal vasodilation,Very important for renal vasodilation,especially in the injured kidneyespecially in the injured kidney

Act as a buffer against uncontrolled A2Act as a buffer against uncontrolled A2mediated constrictionmediated constriction

If you constrict the afferent arteriole, you willIf you constrict the afferent arteriole, you willdecrease GFRdecrease GFR

The RAS and Prostaglandin pathwaysThe RAS and Prostaglandin pathwaysaccount for ~60% of RBF autoaccount for ~60% of RBF auto--regulationregulation


25/56

AdenosineAdenosine

Potent renal vasoconstrictorPotent renal vasoconstrictor

Peripheral vasodilatorPeripheral vasodilator

Infusion of methylxanthines (adenosineInfusion of methylxanthines (adenosinereceptor blockers) inhibits the decrease inreceptor blockers) inhibits the decrease in

GFR that is seen with tubular damageGFR that is seen with tubular damage

Some animal models show that infusion ofSome animal models show that infusion of

methylxanthines lessen renal injury in ARFmethylxanthines lessen renal injury in ARF


26/56

AdenosineAdenosine

But. Likely not a major factor in ARFBut. Likely not a major factor in ARF

Methylxanthines have lots of other actionsMethylxanthines have lots of other actionsbesides adenosine blockadebesides adenosine blockade

Adenosine is rapidly degraded afterAdenosine is rapidly degraded afterproductionproduction

IntraIntra--renal adenosine levels diminish veryrenal adenosine levels diminish veryrapidly after reperfusion, but therapidly after reperfusion, but thevasocontriction remains for a longer periodvasocontriction remains for a longer period

Finally, if you block ADA, creating higherFinally, if you block ADA, creating highertissue adenosine levels, and then createtissue adenosine levels, and then createischemiaischemia you actually get an enhancementyou actually get an enhancementof renal recoveryof renal recovery


27/56

EndothelinEndothelin

21 amino acid peptide that is one of the most21 amino acid peptide that is one of the mostpotent vasoconstrictors in the bodypotent vasoconstrictors in the body Can be used as a pressorCan be used as a pressor

Its role in unclear in normal stateIts role in unclear in normal state

In ARF, overproduction by cells (both in andIn ARF, overproduction by cells (both in andoutside of the kidney) leads to decreasedoutside of the kidney) leads to decreasedafferent flow and thus decreased RBF and GFRafferent flow and thus decreased RBF and GFR Endothelin increases mesangial cell contraction whichEndothelin increases mesangial cell contraction which

reduces glomerular ultrafiltrationreduces glomerular ultrafiltration

Stimulates ANP release at low doses and canStimulates ANP release at low doses and canincrease UOPincrease UOP

AntiAnti--endothelin antibodies or endothelin receptorendothelin antibodies or endothelin receptorantagonists decrease ARF in experimentalantagonists decrease ARF in experimental

modelsmodels


28/56

Nitric OxideNitric Oxide

Produced by multiple isoProduced by multiple iso--enzymes of NOSenzymes of NOS

In addition to its role in vasodilation, likelyIn addition to its role in vasodilation, likelyhas a role in sodium rehas a role in sodium re--absorptionabsorption

Give a NOS blocker and you get naturesisGive a NOS blocker and you get naturesis

Important in the overall homeostasis ofImportant in the overall homeostasis ofRBFRBF

Exact mechanisms not worked outExact mechanisms not worked outcompletelyat least when Rogers wascompletelyat least when Rogers waswritten.written.


29/56


30/56


Confusing resultsConfusing results

Ischemic rat kidney modelIschemic rat kidney model inducing NOSinducing NOS

causes increasing injurycauses increasing injury

Hypoxic tubular cell culture modelHypoxic tubular cell culture model inducinginducing

NOS causes increasing injuryNOS causes increasing injury

But if you block NOS production, you getBut if you block NOS production, you get

worsening of renal function and severeworsening of renal function and severevasoconstrictionvasoconstriction


31/56


So stimulation of NO in the renalSo stimulation of NO in the renal

vasculature will modulate vasoconstrictionvasculature will modulate vasoconstriction

and lead to lesser injurybutand lead to lesser injurybut

That same induction of NO in the tubularThat same induction of NO in the tubular

cells will cause increased cytotoxic effectscells will cause increased cytotoxic effects


32/56

DopamineDopamine

Dopamine receptors in the afferentDopamine receptors in the afferent

arteriolearteriole

Dilation of renal vasculature at low doses,Dilation of renal vasculature at low doses,constriction at higher dosesconstriction at higher doses

Also causes naturesis (? Reason forAlso causes naturesis (? Reason for

increased UOP after starting)increased UOP after starting)

Renal dose dopamine controversy.Renal dose dopamine controversy.


33/56

Renal Hemodynamics and ARFRenal Hemodynamics and ARF

Conclusions.Conclusions.

Renal vasoconstriction is a well documentedRenal vasoconstriction is a well documented

cause of ARFcause of ARF

Renal vasodilation does not consistentlyRenal vasodilation does not consistently

reduce ARF once establishedreduce ARF once established

Although renal hemodynamic factors play aAlthough renal hemodynamic factors play alarge role in initiating ARF, they are not thelarge role in initiating ARF, they are not the

dominant determinants of cell damagedominant determinants of cell damage


34/56

ARFARF -- PathophysiologyPathophysiology

Damage is caused mostly by renalDamage is caused mostly by renal

perfusion problems and tubularperfusion problems and tubular

dysfunctiondysfunction

Usual causesUsual causes

HypoHypo--perfusion and ischemiaperfusion and ischemia

Toxin mediatedToxin mediated

InflammationInflammation


35/56

ARFARF PathophysiologyPathophysiology

HypoHypo--perfusionperfusion

Well perfused kidneyWell perfused kidney 90% of blood to cortex90% of blood to cortex

IschemiaIschemia increased blood flow to medullaincreased blood flow to medulla

Outcome may be able to be influenced byOutcome may be able to be influenced by

restoration of energy/supply demandsrestoration of energy/supply demands

Lasix exampleLasix example

Leads to tubular damageLeads to tubular damage


36/56


Oxidative damageOxidative damage

Especially during reperfusion injuriesEspecially during reperfusion injuries

Main playersMain players

SuperSuper--oxide anion, hydroxyl radicaloxide anion, hydroxyl radical highlyhighly

ionizingionizing

Hydrogen peroxide, hypochlorous acidHydrogen peroxide, hypochlorous acid not asnot as

reactive, but because of that have a longer half lifereactive, but because of that have a longer half life

and can travel farther and cause injury distal to theand can travel farther and cause injury distal to the

site of productionsite of production


37/56


IschemiaIschemia

Damage to mitochondrial membrane andDamage to mitochondrial membrane and

change of xanthine dehydrogenase (NADchange of xanthine dehydrogenase (NAD

carrier) to xanthine oxidase (produces O2carrier) to xanthine oxidase (produces O2

radicals)radicals)

Profound utilization of ATPProfound utilization of ATP 55--10 minutes of10 minutes of

ischemia you use ~90% of your ATPischemia you use ~90% of your ATP Make lots of adenosine, inosine, hypoxanthineMake lots of adenosine, inosine, hypoxanthine


38/56

ATP

ADP

AMP

Adenylosuccinate Adenosine

InosineIMP Hypoxanthine

Xanthine

Uric Acid

Allantoin

H20 O2

H20 O2

H20 O2

H2O2

H2O2

CO2


39/56


Once you get reperfusion, the hypoxanthine getsOnce you get reperfusion, the hypoxanthine gets

metabolized to xanthine and uric acidmetabolized to xanthine and uric acid eacheach

creating one Hcreating one H22OO22 and one superand one super--oxide radicaloxide radical

intermediateintermediate Reactive oxygen species oxidize cellularReactive oxygen species oxidize cellular

proteins resulting in:proteins resulting in:

Change in function/inactivation/activationChange in function/inactivation/activation

Loss of structural integrityLoss of structural integrity

Lipid peroxidation (leads to more radical formation)Lipid peroxidation (leads to more radical formation)

Direct DNA damageDirect DNA damage


40/56


41/56

Obligatory

Incomprehensible Pathway

for Jim #2


42/56

ARF PathophysiologyARF Pathophysiology

Amount of damage depends on ability toAmount of damage depends on ability to

replete ATP storesreplete ATP stores

Continued low ATP leads to disruption of cellContinued low ATP leads to disruption of cell

cytoskeleton, increased intracellular Ca,cytoskeleton, increased intracellular Ca,

activation of phospholipases andactivation of phospholipases and

subsequently the apoptotic pathwayssubsequently the apoptotic pathways

This endothelial cell injury sparks anThis endothelial cell injury sparks animmune response.that cant be good.immune response.that cant be good.


43/56


44/56


45/56

ARFARF -- PreventionPrevention

LasixLasix

May have uses early in ARFMay have uses early in ARF

MannitolMannitol

May work byMay work by Increasing flow through tubules, preventingIncreasing flow through tubules, preventing

obstructionobstruction

Osmotic action, decreasing endothelial swellingOsmotic action, decreasing endothelial swelling

Decreased blood viscosity with increased renalDecreased blood viscosity with increased renalperfusion (???)perfusion (???)

Free radical scavengingFree radical scavenging


46/56


Renal dose dopamine.Renal dose dopamine.

Endothelin antibodiesEndothelin antibodies

No human trialsNo human trials ThyroxineThyroxine

More rapid improvement of renal function inMore rapid improvement of renal function in

animalsanimals

Increased uptake of ADP to form ATP or cellIncreased uptake of ADP to form ATP or cell

membrane stabilization as a possible causemembrane stabilization as a possible cause


47/56


ANPANP Improve renal function and decrease renalImprove renal function and decrease renal

insufficiencyinsufficiency

? Nesiritide role? Nesiritide role

TheophylineTheophyline Adenosine antagonistAdenosine antagonist prevents reduction in GFR.prevents reduction in GFR.

Growth FactorsGrowth Factors

After ischemic insult, infusion of IG

FAfter ischemic insult, infusion of IG

F--I, EpidermalG

F,I, EpidermalG

F,Hepatocyte GF improved GFR, diminishedHepatocyte GF improved GFR, diminishedmorphologic injury, diminished mortalitymorphologic injury, diminished mortality

None of these things are well tested..None of these things are well tested..


48/56

ARFARF Prevention in Specific CasesPrevention in Specific Cases

Hemoglobinuria/MyoglobinuriaHemoglobinuria/Myoglobinuria

Mechanism of toxicityMechanism of toxicity Disassociation to ferrihemate, a tubular toxin, inDisassociation to ferrihemate, a tubular toxin, in

acidic urineacidic urine Tubular obstructionTubular obstruction

Inhibition of glomerular flow by PGE inhibition orInhibition of glomerular flow by PGE inhibition orincreased renin activationincreased renin activation

Treatments (?)Treatments (?) Aggressive hydration to increase UOPAggressive hydration to increase UOP Alkalinization of urineAlkalinization of urine

Mannitol/Furosemide to increase UOPMannitol/Furosemide to increase UOP

?Early Hemofiltration?Early Hemofiltration


49/56

ARFARF Prevention in Specific CasesPrevention in Specific Cases

Uric Acid NephropathyUric Acid Nephropathy

A thing of the past thanks to Rasburicase?A thing of the past thanks to Rasburicase?

TreatmentsTreatments

Aggressive hydration to drive UOPAggressive hydration to drive UOP

Alkalinization of the urineAlkalinization of the urine

Xanthine oxidase inhibitorsXanthine oxidase inhibitors


50/56

ARFARF -- ManagementManagement

Electrolyte managementElectrolyte management

SodiumSodium

HyponatremiaHyponatremia fluid restriction first, 3% NaCl iffluid restriction first, 3% NaCl if

AMS or seizingAMS or seizing

PotassiumPotassium

Calcium/Bicarb/Glucose/Insulin/KayexalateCalcium/Bicarb/Glucose/Insulin/Kayexalate

HemodialysisHemodialysis


51/56

ARFARF -- ManagementManagement

Nutrition managementNutrition management

Initially very catabolicInitially very catabolic

Goals:Goals:

Adequate caloriesAdequate calories

Low proteinLow protein

Low K and PhosLow K and Phos

Decreased fluid intakeDecreased fluid intake


52/56

Renal Replacement TherapyRenal Replacement Therapy

Peritoneal DialysisPeritoneal Dialysis

Acute Intermittent HemodialysisAcute Intermittent Hemodialysis

Continuous HemofiltrationContinuous Hemofiltration CAVHCAVH

SCUFSCUF

CVVH, CVVHDCVVH, CVVHD

And others.And others.


53/56

Peritoneal dialysisPeritoneal dialysis

Simple to set up &Simple to set up &

performperform

Easy to use in infantsEasy to use in infants

Hemodynamic stabilityHemodynamic stability No antiNo anti--coagulationcoagulation

Bedside peritoneal accessBedside peritoneal access

Treat severe hypothermiaTreat severe hypothermia

or hyperthermiaor hyperthermia

Unreliable ultrafiltrationUnreliable ultrafiltration

Slow fluid & solute removalSlow fluid & solute removal

Drainage failure & leakageDrainage failure & leakage

Catheter obstructionCatheter obstruction Respiratory compromiseRespiratory compromise

HyperglycemiaHyperglycemia

PeritonitisPeritonitis

Not good forNot good forhyperammonemia orhyperammonemia or

intoxication with dialyzableintoxication with dialyzable

poisonspoisons

Advantages Disadvantages


54/56

Intermittent HemodialysisIntermittent Hemodialysis

Maximum soluteMaximum solute

clearance of 3clearance of 3

modalitiesmodalities Best therapy for severeBest therapy for severe

hyperkalemiahyperkalemia

Limited antiLimited anti--coagulationcoagulation

timetime Bedside vascularBedside vascular

access can be usedaccess can be used

HemodynamicHemodynamic

instabilityinstability

HypoxemiaHypoxemia

Rapid fluid andRapid fluid and

electrolyte shiftselectrolyte shifts

Complex equipmentComplex equipment

Specialized personnelSpecialized personnel

Difficult in small infantsDifficult in small infants



55/56

Continuous HemofiltrationContinuous Hemofiltration

Easy to use in PICUEasy to use in PICU

Rapid electrolyteRapid electrolyte

correctioncorrection

Excellent soluteExcellent solute

clearancesclearances

Rapid acid/base correctionRapid acid/base correction

Controllable fluid balanceControllable fluid balance

Tolerated by unstable pts.Tolerated by unstable pts.

Early use of TPNEarly use of TPN

Bedside vascular accessBedside vascular access

routineroutine

SystemicSystemic

anticoagulationanticoagulation

(except citrate)(except citrate)

Frequent filter clottingFrequent filter clotting

Vascular access inVascular access in

infantsinfants



56/56

Indications for RRTIndications for RRT

Still evolving.Generally acceptedStill evolving.Generally accepted Oliguria/AnuriaOliguria/Anuria

HyperammonemiaHyperammonemia

HyperkalemiaHyperkalemia

Severe acidemiaSevere acidemia Severe azotemiaSevere azotemia

Pulmonary EdemaPulmonary Edema

Uremic complicationsUremic complications

Severe electrolyte abnormalitiesS

evere electrolyte abnormalities Drug overdose with a filterable toxinDrug overdose with a filterable toxin

AnasarcaAnasarca

RhabdomyolysisRhabdomyolysis

Acute Renal Failure_2

Documents

Transcript of Acute Renal Failure_2