06 Paden Acute Renal Failure

Acute Renal FailureAcute Renal Failure

Matthew L. Paden, MDMatthew L. Paden, MDPediatric Critical CarePediatric Critical Care

Emory UniversityEmory UniversityChildren’s Healthcare of Atlanta at EglestonChildren’s Healthcare of Atlanta at Egleston

Structure and Function of the Structure and Function of the KidneyKidney

Primary unit of the Primary unit of the kidney is the nephronkidney is the nephron

1 million nephrons per 1 million nephrons per kidneykidney

Composed of a Composed of a glomerulus and a glomerulus and a tubuletubule

Kidneys receive 20% Kidneys receive 20% of cardiac outputof cardiac output

Renal Lecture Required Picture #1

Renal blood flowRenal blood flow Aorta Aorta Renal artery Renal artery

interlobar arteries interlobar arteries interlobular arteries interlobular arteries afferent arterioles afferent arterioles glomerulus glomerulus efferent efferent arteriolesarterioles

In the cortex In the cortex peritubular capillariesperitubular capillaries

In the juxtamedullary In the juxtamedullary region region vasa rectavasa recta

Back to the heart through Back to the heart through the interlobular the interlobular intralobar intralobar renal veins renal veins

Glomerular Filtration RateGlomerular Filtration Rate

Determined by the hydrostatic and oncotic Determined by the hydrostatic and oncotic pressure within the nephronpressure within the nephron

Hydrostatic pressure in the glomerulus is Hydrostatic pressure in the glomerulus is higher than in the tubule, so you get a net higher than in the tubule, so you get a net outflow of filtrate into the tubuleoutflow of filtrate into the tubule

Oncotic pressure in the glomerulus is the Oncotic pressure in the glomerulus is the result of non-filterable proteinsresult of non-filterable proteins Greater oncotic pressure as you progress through Greater oncotic pressure as you progress through

the glomerulusthe glomerulus GFR = Kf (hydrostatic – oncotic pressure)GFR = Kf (hydrostatic – oncotic pressure)

Glomerular Filtration RateGlomerular Filtration Rate

The capillary endothelium is surrounded The capillary endothelium is surrounded by a basement membrane and podocytesby a basement membrane and podocytes

Foot processes of the podocytes form Foot processes of the podocytes form filtration slits that :filtration slits that : Allow for ultrafiltrate passageAllow for ultrafiltrate passage Limit filtration of large negatively charged Limit 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) not Large particles (albumin 69,000 daltons) not

filteredfiltered

Tubular FunctionTubular Function

ProximalProximal Most of reabsorption occurs hereMost of reabsorption occurs here Fluid is isotonic with plasmaFluid is isotonic with plasma 66-70% of sodium presented is reabsorbed66-70% of sodium presented is reabsorbed Glucose and amino acids are completely Glucose and amino acids are completely

reabsorbed reabsorbed

Tubule FunctionTubule Function

Loop of HenleLoop of Henle Urine concentration and dilution via changes Urine concentration and dilution via changes

in oncotic pressure in the vasa rectain oncotic pressure in the vasa recta Descending tubule – permeable to water, Descending tubule – permeable to water,

impermeable to sodiumimpermeable to sodium Ascending tubule – actively reabsorbs Ascending tubule – actively reabsorbs

sodium, impermeable to watersodium, impermeable to water


Medullary thick ascending limb – critical Medullary thick ascending limb – critical for urinary dilution and most often for urinary dilution and most often damaged in ARFdamaged in ARF ADH stimulates Na re-absorption in this areaADH stimulates Na re-absorption 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 Na-K-2Cl ATPase Lasix use here inhibits the Na-K-2Cl ATPase

which in the face of ARF, may decrease which in the face of ARF, may decrease oxygen consumption and ameliorate the oxygen consumption and ameliorate the severity of the ARFseverity of the ARF


All of those studies done in an in vitro All of those studies done in an in vitro modelmodel In vivo, if you drop oxygen concentration even In vivo, if you drop oxygen concentration even

sub-atmospheric you do not get tubular sub-atmospheric you do not get tubular damage even with increased tubular workloaddamage even with increased tubular workload

In vivo models exist where you do see that In vivo models exist where you do see that damage, but appears to need a “second hit”damage, but appears to need a “second hit”

Tubule FunctionTubule Function

Distal TubuleDistal Tubule Re-absorption of another ~12% of NaClRe-absorption of another ~12% of NaCl Proximal segment – impermeable to waterProximal segment – impermeable to water Distal segment is the cortical collecting duct Distal segment is the cortical collecting duct

and secretes K and HCO3and secretes K and HCO3


Collecting DuctCollecting Duct Aldosterone acts here to increase Na Aldosterone acts here to increase Na

reuptake and K wastingreuptake and K wasting ADH enhances water re-absorptionADH enhances water re-absorption Urea re-absorption to maintain the medullary Urea re-absorption to maintain the medullary

interstitial concentration gradientinterstitial concentration gradient

Acute Renal Failure - DefinitionsAcute Renal Failure - Definitions

Renal failureRenal failure is defined as the cessation is defined as the cessation of kidney function with or without changes of kidney function with or without changes in urine volumein urine volume

AnuriaAnuria – UOP < 0.5 cc/kg/hour – UOP < 0.5 cc/kg/hour OliguriaOliguria – UOP “more than 1 cc/kg/hour” – UOP “more than 1 cc/kg/hour”

Less than?Less than?

Acute Renal Failure - DefinitionsAcute Renal Failure - Definitions

70% Non-oliguric , 30% Oliguric70% Non-oliguric , 30% Oliguric Non-oliguric associated with better Non-oliguric associated with better

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

of adequate urine output and prevention of of adequate urine output and prevention of further renal injury.”further renal injury.” Are we converting non-oliguric to oliguric with Are we converting non-oliguric to oliguric with

our hemofilters?our hemofilters?

Acute Renal Failure - DiagnosisAcute Renal Failure - Diagnosis Pre-renalPre-renal

• Decrease in RBF Decrease in RBF constriction of afferent arteriole constriction of afferent arteriole which serves to increase systemic blood pressure which serves to increase systemic blood pressure by reducing the “shunt” through the kidney, but by 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 to At 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 to Urea is reabsorbed in the distal tubule, leading to increased tubular urea concentration and thus increased tubular urea concentration and thus greater re-absorption of urea into the blood.greater re-absorption of urea into the blood.

Creatinine cannot be reabsorbed, thus leading to a Creatinine cannot be reabsorbed, thus leading to a BUN/Cr ratio of > 20 BUN/Cr ratio of > 20

Pre-Renal vs. Renal FailurePre-Renal vs. Renal Failure

PrerenalPrerenal RenalRenalBUN/CrBUN/Cr >20>20 <20<20

FENaFENa <1%<1% >2%>2%

Renal Failure IndexRenal Failure Index <1%<1% >1%>1%

UUNaNa <20 mEq/L<20 mEq/L >40 mEq/L>40 mEq/L

Specific GravitySpecific Gravity >1.020>1.020 <1.010<1.010

UUosmosm >500 mOsm/L>500 mOsm/L <350 mOsm/L<350 mOsm/L

UUosmosm/P/Posmosm >1.3>1.3 <1.3<1.3


Acute Renal Failure - DiagnosisAcute Renal Failure - Diagnosis

DiagnosisDiagnosis UltrasoundUltrasound

• Structural anomalies – polycystic, obstruction, etc.Structural anomalies – polycystic, obstruction, etc.• ATN – ATN –

poor corticomedullary differentiationpoor corticomedullary differentiation Increased Doppler resistive indexIncreased Doppler resistive index

• (Systolic Peak – Diastolic peak) / systolic peak(Systolic Peak – Diastolic peak) / systolic peak

Nuclear medicine scansNuclear medicine scans• DMSA – Static - anatomy and scarringDMSA – Static - anatomy and scarring• DTPA/MAG3 – Dynamic – renal function, urinary DTPA/MAG3 – Dynamic – renal function, urinary

excretion, and upper tract outflowexcretion, and upper tract outflow

Acute Renal FailureAcute Renal Failure

Overall, renal vasoconstriction is the major Overall, renal vasoconstriction is the major cause of the problems in ARFcause of the problems in ARF Suggested ARF be replaced with vasomotor Suggested ARF be replaced with vasomotor

nephropathynephropathy Insult to tubular epithelium causes release Insult to tubular epithelium causes release

of vasoactive agents which cause the of vasoactive agents which cause the constrictionconstriction Angiotensin II, endothelin, NO, adenosine, Angiotensin II, endothelin, NO, adenosine,

prostaglandins, etc.prostaglandins, etc.

Regulation of Renal Blood FlowRegulation of Renal Blood Flow

In adults auto-regulated over a range of In adults auto-regulated over a range of MAP’s 80-160MAP’s 80-160

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…..

Renin-Angiotensin AxisRenin-Angiotensin Axis For the one millionth time….For the one millionth time…. Hypovolemia leads to decreased afferent Hypovolemia leads to decreased afferent

arteriolar pressure which leads to decreased arteriolar pressure which leads to decreased NaCl re-absorption which leads to decreased Cl NaCl re-absorption which leads to decreased Cl presentation to the macula densa which presentation to the macula densa which increases the amount of renin secreted from the increases the amount of renin secreted from the JGA which increases conversion JGA which increases conversion angiotensinogen to AGI to AGII which increases angiotensinogen to AGI to AGII which increases Aldosterone secretion from the adrenal cortex Aldosterone secretion from the adrenal cortex and ADH which leads to increased sodium and and ADH which leads to increased sodium and thus water re-absorption from the tubule which thus water re-absorption from the tubule which increases your blood pressure……whew…increases your blood pressure……whew…

Renin Angiotensin AxisRenin Angiotensin Axis



Renin’s role in pathogenesis of ARFRenin’s role in pathogenesis of ARF Hyperplasia of JGA with increased renin Hyperplasia of JGA with increased renin

granules seen in patients and experimental granules seen in patients and experimental models of ARFmodels of ARF

Increased plasma renin activity in ARF Increased plasma renin activity in ARF patientspatients

Changing intra-renal renin content modifies Changing intra-renal renin content modifies degree of damagedegree of damage• Feed animals high salt diet (suppress renin Feed animals high salt diet (suppress renin

production) production) renal injury renal injury less renal injury than less renal injury than those fed a low sodium dietthose fed a low sodium diet


Not the only thing going on thoughNot the only thing going on though You can also ameliorate renal injury by You can also ameliorate renal injury by

induction of solute diuresis with mannitol or induction 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 given No change in renal injury in animals given ACE inhibitors, competitive antagonist to ACE inhibitors, competitive antagonist to angiotensin IIangiotensin II

Overall, role of RAS in ARF is uncertainOverall, role of RAS in ARF is uncertain

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 A2 Act as a buffer against uncontrolled A2

mediated constrictionmediated constriction• If you constrict the afferent arteriole, you will If you constrict the afferent arteriole, you will

decrease GFRdecrease GFR

The RAS and Prostaglandin pathways The RAS and Prostaglandin pathways account for ~60% of RBF auto-account for ~60% of RBF auto-regulation…regulation…

AdenosineAdenosine

Potent renal vasoconstrictorPotent renal vasoconstrictor Peripheral vasodilatorPeripheral vasodilator

Infusion of methylxanthines (adenosine Infusion of methylxanthines (adenosine receptor blockers) inhibits the decrease in receptor blockers) inhibits the decrease in GFR that is seen with tubular damageGFR that is seen with tubular damage

Some animal models show that infusion of Some animal models show that infusion of methylxanthines lessen renal injury in ARFmethylxanthines lessen renal injury in ARF

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

Methylxanthines have lots of other actions Methylxanthines have lots of other actions besides adenosine blockadebesides adenosine blockade

Adenosine is rapidly degraded after Adenosine is rapidly degraded after productionproduction

Intra-renal adenosine levels diminish very Intra-renal adenosine levels diminish very rapidly after reperfusion, but the rapidly after reperfusion, but the vasocontriction remains for a longer periodvasocontriction remains for a longer period

Finally, if you block ADA, creating higher Finally, if you block ADA, creating higher tissue adenosine levels, and then create tissue adenosine levels, and then create ischemia ischemia you actually get an enhancement you actually get an enhancement of renal recoveryof renal recovery

EndothelinEndothelin 21 amino acid peptide that is one of the most 21 amino acid peptide that is one of the most

potent 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 and In ARF, overproduction by cells (both in and

outside of the kidney) leads to decreased outside of the kidney) leads to decreased afferent flow and thus decreased RBF and GFRafferent flow and thus decreased RBF and GFR Endothelin increases mesangial cell contraction which Endothelin increases mesangial cell contraction which

reduces glomerular ultrafiltrationreduces glomerular ultrafiltration Stimulates ANP release at low doses and can Stimulates ANP release at low doses and can

increase UOPincrease UOP Anti-endothelin antibodies or endothelin receptor Anti-endothelin antibodies or endothelin receptor

antagonists decrease ARF in experimental antagonists decrease ARF in experimental modelsmodels

Nitric OxideNitric Oxide

Produced by multiple iso-enzymes of NOSProduced by multiple iso-enzymes of NOS In addition to its role in vasodilation, likely In addition to its role in vasodilation, likely

has a role in sodium re-absorptionhas a role in sodium re-absorption Give a NOS blocker and you get naturesisGive a NOS blocker and you get naturesis

Important in the overall homeostasis of Important in the overall homeostasis of RBFRBF

Exact mechanisms not worked out Exact mechanisms not worked out completely…at least when Rogers was completely…at least when Rogers was written….written….

Obligatory Incomprehensible Pathway for Jim #1


Confusing resultsConfusing results Ischemic rat kidney model – inducing NOS Ischemic rat kidney model – inducing NOS

causes increasing injurycauses increasing injury Hypoxic tubular cell culture model – inducing Hypoxic tubular cell culture model – inducing

NOS causes increasing injuryNOS causes increasing injury But if you block NOS production, you get But if you block NOS production, you get

worsening of renal function and severe worsening of renal function and severe vasoconstrictionvasoconstriction


So stimulation of NO in the renal So stimulation of NO in the renal vasculature will modulate vasoconstriction vasculature will modulate vasoconstriction and lead to lesser injury…but…and lead to lesser injury…but…

That same induction of NO in the tubular That same induction of NO in the tubular cells will cause increased cytotoxic effectscells will cause increased cytotoxic effects

DopamineDopamine

Dopamine receptors in the afferent Dopamine 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 for Also causes naturesis (? Reason for increased UOP after starting)increased UOP after starting)

Renal dose dopamine controversy……….Renal dose dopamine controversy……….

Renal Hemodynamics and ARFRenal Hemodynamics and ARF

Conclusions….Conclusions…. Renal vasoconstriction is a well documented Renal vasoconstriction is a well documented

cause of ARFcause of ARF Renal vasodilation does not consistently Renal vasodilation does not consistently

reduce ARF once establishedreduce ARF once established

Although renal hemodynamic factors play a Although renal hemodynamic factors play a large role in initiating ARF, they are not the large role in initiating ARF, they are not the dominant determinants of cell damagedominant determinants of cell damage

ARF - PathophysiologyARF - Pathophysiology

Damage is caused mostly by renal Damage is caused mostly by renal perfusion problems and tubular perfusion problems and tubular dysfunctiondysfunction

Usual causesUsual causes Hypo-perfusion and ischemiaHypo-perfusion and ischemia Toxin mediatedToxin mediated InflammationInflammation

ARF – PathophysiologyARF – Pathophysiology

Hypo-perfusionHypo-perfusion Well perfused kidney – 90% of blood to cortexWell perfused kidney – 90% of blood to cortex Ischemia – increased blood flow to medullaIschemia – increased blood flow to medulla Outcome may be able to be influenced by Outcome 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


Oxidative damageOxidative damage Especially during reperfusion injuriesEspecially during reperfusion injuries Main playersMain players

• Super-oxide anion, hydroxyl radical – highly Super-oxide anion, hydroxyl radical – highly ionizing ionizing

• Hydrogen peroxide, hypochlorous acid – not as Hydrogen peroxide, hypochlorous acid – not as reactive, but because of that have a longer half life reactive, but because of that have a longer half life and can travel farther and cause injury distal to the and can travel farther and cause injury distal to the site of productionsite of production


IschemiaIschemia Damage to mitochondrial membrane and Damage to mitochondrial membrane and

change of xanthine dehydrogenase (NAD change of xanthine dehydrogenase (NAD carrier) to xanthine oxidase (produces O2 carrier) to xanthine oxidase (produces O2 radicals)radicals)

Profound utilization of ATP Profound utilization of ATP 5-10 minutes of 5-10 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

ATP

ADP

AMP

Adenylosuccinate Adenosine

InosineIMP Hypoxanthine

Xanthine

Uric Acid

Allantoin

H20 ∙ O2

H20 ∙ O2

H20 ∙ O2

H2O2

H2O2

CO2


Once you get reperfusion, the hypoxanthine gets Once you get reperfusion, the hypoxanthine gets metabolized to xanthine and uric acid – each metabolized to xanthine and uric acid – each creating one Hcreating one H22OO22 and one super-oxide radical and one super-oxide radical

intermediateintermediate Reactive oxygen species oxidize cellular Reactive 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

ARF PathophysiologyARF Pathophysiology

Amount of damage depends on ability to Amount of damage depends on ability to replete ATP storesreplete ATP stores Continued low ATP leads to disruption of cell Continued low ATP leads to disruption of cell

cytoskeleton, increased intracellular Ca, cytoskeleton, increased intracellular Ca, activation of phospholipases and activation of phospholipases and subsequently the apoptotic pathwayssubsequently the apoptotic pathways

Obligatory Incomprehensible Pathway for Jim #2

ARF PathophysiologyARF Pathophysiology

Amount of damage depends on ability to Amount of damage depends on ability to replete ATP storesreplete ATP stores Continued low ATP leads to disruption of cell Continued low ATP leads to disruption of cell

cytoskeleton, increased intracellular Ca, cytoskeleton, increased intracellular Ca, activation of phospholipases and activation of phospholipases and subsequently the apoptotic pathwayssubsequently the apoptotic pathways

This endothelial cell injury sparks an This endothelial cell injury sparks an immune response….that can’t be good….immune response….that can’t be good….

ARF - PreventionARF - Prevention

Maintenance of blood flowMaintenance of blood flow Cardiac output, isovolemia, etcCardiac output, isovolemia, etc

Avoidance of toxinsAvoidance of toxins Aminoglycosides, amphoteracin, NSAIDsAminoglycosides, amphoteracin, NSAIDs

Easy on paper….difficult in practiceEasy on paper….difficult in practice


Lasix Lasix May have uses early in ARFMay have uses early in ARF

MannitolMannitol May work byMay work by

• Increasing flow through tubules, preventing Increasing flow through tubules, preventing obstructionobstruction

• Osmotic action, decreasing endothelial swellingOsmotic action, decreasing endothelial swelling• Decreased blood viscosity with increased renal Decreased blood viscosity with increased renal

perfusion (???)perfusion (???)• Free radical scavengingFree radical scavenging


Renal dose dopamine….Renal dose dopamine…. Endothelin antibodiesEndothelin antibodies

No human trialsNo human trials ThyroxineThyroxine

More rapid improvement of renal function in More rapid improvement of renal function in animalsanimals

Increased uptake of ADP to form ATP or cell Increased uptake of ADP to form ATP or cell membrane stabilization as a possible causemembrane stabilization as a possible cause


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

insufficiencyinsufficiency ? Nesiritide role? Nesiritide role

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

Growth FactorsGrowth Factors After ischemic insult, infusion of IGF-I, Epidermal GF, After ischemic insult, infusion of IGF-I, Epidermal GF,

Hepatocyte GF improved GFR, diminished Hepatocyte GF improved GFR, diminished morphologic injury, diminished mortalitymorphologic injury, diminished mortality

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

ARF – Prevention in Specific CasesARF – Prevention in Specific Cases

Hemoglobinuria/MyoglobinuriaHemoglobinuria/Myoglobinuria Mechanism of toxicityMechanism of toxicity

• Disassociation to ferrihemate, a tubular toxin, in Disassociation to ferrihemate, a tubular toxin, in acidic urineacidic urine

• Tubular obstructionTubular obstruction• Inhibition of glomerular flow by PGE inhibition or Inhibition of glomerular flow by PGE inhibition or

increased 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

ARF – Prevention in Specific CasesARF – Prevention 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

ARF - ManagementARF - Management

Electrolyte managementElectrolyte management SodiumSodium

• Hyponatremia – fluid restriction first, 3% NaCl if Hyponatremia – fluid restriction first, 3% NaCl if AMS or seizingAMS or seizing

PotassiumPotassium• Calcium/Bicarb/Glucose/Insulin/KayexalateCalcium/Bicarb/Glucose/Insulin/Kayexalate• HemodialysisHemodialysis

ARF - ManagementARF - Management

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

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….

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 anti-coagulationNo anti-coagulation Bedside peritoneal accessBedside peritoneal access Treat severe hypothermia Treat 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 for Not good for

hyperammonemia or hyperammonemia or intoxication with dialyzable intoxication with dialyzable poisonspoisons

Advantages Disadvantages

Intermittent HemodialysisIntermittent Hemodialysis

Maximum solute Maximum solute clearance of 3 clearance of 3 modalitiesmodalities

Best therapy for severe Best therapy for severe hyperkalemiahyperkalemia

Limited anti-coagulation Limited anti-coagulation timetime

Bedside vascular Bedside vascular access can be usedaccess can be used

Hemodynamic instabilityHemodynamic instability HypoxemiaHypoxemia Rapid fluid and Rapid fluid and

electrolyte shiftselectrolyte shifts Complex equipmentComplex equipment Specialized personnelSpecialized personnel Difficult in small infantsDifficult in small infants


Continuous HemofiltrationContinuous Hemofiltration

Easy to use in PICUEasy to use in PICU Rapid electrolyte Rapid electrolyte

correctioncorrection Excellent solute Excellent solute

clearancesclearances Rapid acid/base correction Rapid 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 access Bedside vascular access

routineroutine

Systemic Systemic anticoagulation (except anticoagulation (except citrate)citrate)

Frequent filter clottingFrequent filter clotting Vascular access in Vascular access in

infantsinfants


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 abnormalitiesSevere electrolyte abnormalities Drug overdose with a filterable toxinDrug overdose with a filterable toxin AnasarcaAnasarca RhabdomyolysisRhabdomyolysis

06 Paden Acute Renal Failure

Health & Medicine

Transcript of 06 Paden Acute Renal Failure