13 Evaluation And Management Of Acute Renal Failure

Evaluation and Management of Evaluation and Management of Acute Renal FailureAcute Renal Failure

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調節水份調節酸鹼調節電解質尿液的形成內分泌器官– Vitamin D, erythropoi

etin, RAS

Anuria:Anuria: urine < 100ml/day urine < 100ml/dayOliguria:Oliguria: urine <400-500 mL/d urine <400-500 mL/dAzotemia:Azotemia: Increase Cr, BUN Increase Cr, BUN• May be prerenal, renal, postrenalMay be prerenal, renal, postrenal• Does not require any clinical findingsDoes not require any clinical findingsChronic Kidney Disease: Chronic Kidney Disease: graduated loss of renal function, Natigraduated loss of renal function, Nati

onal kidney fundation: stage 1~5onal kidney fundation: stage 1~5ESRD ESRD = = Loss of kidney function >3 monthsLoss of kidney function >3 months

Blood Urea Nitrogen (BUN)Blood Urea Nitrogen (BUN)

• Catabolism of aminoacids generates NHCatabolism of aminoacids generates NH33

NHNH22

2 NH2 NH33 + CO + CO2 =2 = C = 0 + H C = 0 + H22OO NHNH22

• Urea Mol wt : 60; BUN Mol wt. : 28Urea Mol wt : 60; BUN Mol wt. : 28• Normal BUN 10-20 mg/dlNormal BUN 10-20 mg/dl• After filtration › 50% is reabsorbed by the tubuleAfter filtration › 50% is reabsorbed by the tubule• BUN level is related to: Renal function, protein intake, BUN level is related to: Renal function, protein intake,

liver function, GI bleeding, steroid, hyper catabolic staliver function, GI bleeding, steroid, hyper catabolic statestes

CreatinineCreatinine

• Formed at a constant rate by dehydration of muscle creatinFormed at a constant rate by dehydration of muscle creatinee

• Normally 1–2% of muscle creatine is broken into creatinineNormally 1–2% of muscle creatine is broken into creatinine• Mol. Wt. 113Mol. Wt. 113• Creatinine is freely filtered by the glomerulii and is not reabCreatinine is freely filtered by the glomerulii and is not reab

sorbed sorbed 10–15% is secreted into proximal tubule10–15% is secreted into proximal tubule

GFR Estimation by Plasma CreatinineGFR Estimation by Plasma Creatinine

Cockcroft and Gault Formula*Cockcroft and Gault Formula*Calculated creatinine clearanceCalculated creatinine clearance = = (140–age) x wt (kg)(140–age) x wt (kg)72 X serum creatinine(mg/dl)72 X serum creatinine(mg/dl)

For females, subtract 15% (or multiply by 0.85); for parFor females, subtract 15% (or multiply by 0.85); for paraplegics multiply by 0.8, for quadriplegics, multiply baplegics multiply by 0.8, for quadriplegics, multiply by 0.6y 0.6

*Applicable only when patient is in a steady state, not *Applicable only when patient is in a steady state, not edematous and not obeseedematous and not obese

Factors that affect serum creatinine concentrationFactors that affect serum creatinine concentration FactorFactor Effect on serEffect on ser

um creatininum creatininee

Mechanism (comment)Mechanism (comment)

Kidney Disease Kidney Disease IncreaseIncrease Decreased GFR(increase is blunted by increaseDecreased GFR(increase is blunted by increased tubular secretion of creatinine and by reduced tubular secretion of creatinine and by reduced creatinine generation)d creatinine generation)

Reduced Reduced muscle mass muscle mass

DecreaseDecrease Reduced creatinine generation (common in chilReduced creatinine generation (common in children, women, and older and malnourished patiedren, women, and older and malnourished patients) nts)

Ingestion of Ingestion of cooked meat cooked meat

Increase Increase Transient increase in creatinine generation (incTransient increase in creatinine generation (increase may be blunted by transient increase in Grease may be blunted by transient increase in GFR) FR)

Use of cimetidinUse of cimetidine, trimethoprime, trimethoprim

Increase Increase Inhibition of tubular creatinine secretion Inhibition of tubular creatinine secretion

Ketoacidosis Ketoacidosis IncreaseIncrease Positive interference with picric acid assay for Positive interference with picric acid assay for creatinine creatinine

Acute Renal FailureAcute Renal Failure

Definition:Definition:• Rapid (hours to weeks) decline in glomerular filtRapid (hours to weeks) decline in glomerular filt

ration rate and retention of waste productsration rate and retention of waste products• It is a clinical syndrome cause by many renal or It is a clinical syndrome cause by many renal or

extrarenal diseasesextrarenal diseases• Lack a uniform definition Lack a uniform definition

– Cr > 1.5x, urine output <0.5ml/kg/hrCr > 1.5x, urine output <0.5ml/kg/hr– Cr increase Cr increase ≥ 1.0 mg/dl/2d≥ 1.0 mg/dl/2d

The Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group

The facts you need to know about ARFThe facts you need to know about ARF

• Acute renal failure may reversible and should look Acute renal failure may reversible and should look for the causes to managementfor the causes to management

• Incidence:Incidence: - 2-5% of hospitalized patients(55% iatrogenic)- 2-5% of hospitalized patients(55% iatrogenic) - 7-23% of ICU patients- 7-23% of ICU patients - 20-60% require dialysis; of those who survive - 20-60% require dialysis; of those who survive

initial dialysis, <25% require long-term dialysisinitial dialysis, <25% require long-term dialysis

The facts you need to know about ARFThe facts you need to know about ARF

Motality: Motality: – Liano(1996) reported mortality rate of 60% for patient with ATN, 3Liano(1996) reported mortality rate of 60% for patient with ATN, 3

5% for acute on chronic renal failure, 27% for obstructive ARF an5% for acute on chronic renal failure, 27% for obstructive ARF and 26% for renal disorder other than ATN. d 26% for renal disorder other than ATN.

– Knaus(1986)50% for combination of acute renal and respiratory fKnaus(1986)50% for combination of acute renal and respiratory failure towards 100% with 5 system failureailure towards 100% with 5 system failure

– In community-acquired ARF with mostly prerenal and postrenal caIn community-acquired ARF with mostly prerenal and postrenal causes and the prognosis is better.uses and the prognosis is better.

– Rates not significantly decreased over past 50 years despite advaRates not significantly decreased over past 50 years despite advances in dialysis and critical care (increased patient age and co monces in dialysis and critical care (increased patient age and co morbid illnesses)rbid illnesses)

Symptoms and Signs of Renal FailureSymptoms and Signs of Renal Failure

• Retention of nitrogenous waste productsRetention of nitrogenous waste products– Nausea, vomiting, diarrhea, hiccup, foul taste, dry crusteNausea, vomiting, diarrhea, hiccup, foul taste, dry cruste

d mouth, itching, d mouth, itching, – Drowsiness, clouding of consciousness, neuropathy, perDrowsiness, clouding of consciousness, neuropathy, per

icarditis, GI bleeding, icarditis, GI bleeding, – ComaComa

• Retention of salt and waterRetention of salt and water– Pulmonary edema, peripheral edema, ascites, pleural effPulmonary edema, peripheral edema, ascites, pleural eff

usionusion

Symptoms and Signs of Renal FailureSymptoms and Signs of Renal Failure

• Retention of potassiumRetention of potassium– Weakness, lassitude, paralysis, EKG changes with tentiWeakness, lassitude, paralysis, EKG changes with tenti

ng T waves, widening of QRS complex, increased PR intng T waves, widening of QRS complex, increased PR interval, sine wave pattern, cardiac arrest, VTerval, sine wave pattern, cardiac arrest, VT

• Retention of acidRetention of acid– Kussmaul respiration, hyperreflexia, hypotension Kussmaul respiration, hyperreflexia, hypotension

A: Cr, BUNB: H, P, KC: NaCl

Classification of ARFClassification of ARF

Acute Renal Failure

Pre-renal Intrinsic Post-renal

Glomerular Interstitial VascularTubular

Pre-renal ARFPre-renal ARF

• Accounts for 60-70% of cases of ARFAccounts for 60-70% of cases of ARF• Represents physiologic response to mild-moderate Represents physiologic response to mild-moderate

renal hypoperfusionrenal hypoperfusion• Renal parenchymal tissue is not damagedRenal parenchymal tissue is not damaged

therefore rapidly reversible upon restoration of RBF therefore rapidly reversible upon restoration of RBF and glomerular filtration pressureand glomerular filtration pressure

• Elderly and those with pre-existing renal disease at Elderly and those with pre-existing renal disease at increased riskincreased risk


I. HypovolemiaI. Hypovolemia• A. Hemorrhage, burns, dehydrationA. Hemorrhage, burns, dehydration• B. GI fluid loss: vomiting, surgical drainage, diarrheaB. GI fluid loss: vomiting, surgical drainage, diarrhea• C. Renal fluid loss: diuretics, osmotic diuresis (e.g., diabetes mellitus), hypoC. Renal fluid loss: diuretics, osmotic diuresis (e.g., diabetes mellitus), hypo

adrenalismadrenalism• D. Sequestration in extravascular space: pancreatitis, peritonitis, trauma, buD. Sequestration in extravascular space: pancreatitis, peritonitis, trauma, bu

rns, severe hypoalbuminemiarns, severe hypoalbuminemiaII. Low cardiac outputII. Low cardiac output• A. Diseases of myocardium, valves, and pericardium; arrhythmias; tamponaA. Diseases of myocardium, valves, and pericardium; arrhythmias; tampona

dede• B. Other: pulmonary hypertension, massive pulmonary embolus, positive prB. Other: pulmonary hypertension, massive pulmonary embolus, positive pr

essure mechanical ventilationessure mechanical ventilation


III. Altered renal systemic vascular resistance ratioIII. Altered renal systemic vascular resistance ratio• A. Systemic vasodilatation: sepsis, antihypertensives, afterload reducA. Systemic vasodilatation: sepsis, antihypertensives, afterload reduc

ers, anesthesia, anaphylaxisers, anesthesia, anaphylaxis• B. Renal vasoconstriction: hypercalcemia, norepinephrine, epinephrinB. Renal vasoconstriction: hypercalcemia, norepinephrine, epinephrin

e, cyclosporine, tacrolimus, amphotericin Be, cyclosporine, tacrolimus, amphotericin B• C. Cirrhosis with ascites (hepatorenal syndrome)C. Cirrhosis with ascites (hepatorenal syndrome)IV. Renal hypoperfusion with impairment of renal autoregulatory responsIV. Renal hypoperfusion with impairment of renal autoregulatory respons

eses• Cyclooxygenase inhibitors, ACEICyclooxygenase inhibitors, ACEIV. Hyperviscosity syndrome (rare)V. Hyperviscosity syndrome (rare)• Multiple myeloma, macroglobulinemia, polycythemiaMultiple myeloma, macroglobulinemia, polycythemia

Intrinsic Renal CausesIntrinsic Renal Causes

• Accounts for 25-40% of cases of ARFAccounts for 25-40% of cases of ARF• Types:Types:

– Acute glomerulonephritis <5%Acute glomerulonephritis <5%– Interstitial nephritis 10%Interstitial nephritis 10%– Intrarenal vascular disease <5%Intrarenal vascular disease <5%– ATN 85%ATN 85%

I. Renovascular obstruction (bilateral or unilateral in the setting of one fuI. Renovascular obstruction (bilateral or unilateral in the setting of one functioning kidney)nctioning kidney)

• A. Renal artery obstruction: atherosclerotic plaque, thrombosis, emboA. Renal artery obstruction: atherosclerotic plaque, thrombosis, embolism, dissecting aneurysm, vasculitislism, dissecting aneurysm, vasculitis

• B. Renal vein obstruction: thrombosis, compressionB. Renal vein obstruction: thrombosis, compressionII. Disease of glomeruli or renal microvasculatureII. Disease of glomeruli or renal microvasculature• A. Glomerulonephritis and vasculitisA. Glomerulonephritis and vasculitis• B. Hemolytic uremic syndrome, thrombotic thrombocytopenic purpura,B. Hemolytic uremic syndrome, thrombotic thrombocytopenic purpura,

disseminated intravascular coagulation, toxemia of pregnancy, accel disseminated intravascular coagulation, toxemia of pregnancy, accelerated hypertension, radiation nephritis, systemic lupus erythematosuerated hypertension, radiation nephritis, systemic lupus erythematosus, sclerodermas, scleroderma



III. Acute tubular necrosisIII. Acute tubular necrosis• A. Ischemia(60%): as for prerenal ARF (hypovolemia, low cardiac outA. Ischemia(60%): as for prerenal ARF (hypovolemia, low cardiac out

put, renal vasoconstriction, systemic vasodilatation), obstetric complicput, renal vasoconstriction, systemic vasodilatation), obstetric complications (abruptio placentae, postpartum hemorrhage)ations (abruptio placentae, postpartum hemorrhage)

• B. Toxins(40%)B. Toxins(40%) 1. Exogenous: radiocontrast, cyclosporine, antibiotics (e.g., aminogly1. Exogenous: radiocontrast, cyclosporine, antibiotics (e.g., aminogly

cosides), chemotherapy (e.g., cisplatin), organic solvents (e.g., ethylecosides), chemotherapy (e.g., cisplatin), organic solvents (e.g., ethylene glycol), acetaminophen, illegal abortifacientsne glycol), acetaminophen, illegal abortifacients

2. Endogenous: rhabdomyolysis, hemolysis, uric acid, oxalate, plasm2. Endogenous: rhabdomyolysis, hemolysis, uric acid, oxalate, plasma cell dyscrasia (e.g., myeloma)a cell dyscrasia (e.g., myeloma)


IV. Interstitial nephritisIV. Interstitial nephritis• A. Allergic: antibiotics (e.g., A. Allergic: antibiotics (e.g., -lactams, sulfonamides, trimethoprim, rifa-lactams, sulfonamides, trimethoprim, rifa

mpicin), nonsteroidal anti-inflammatory agents, diuretics, captoprilmpicin), nonsteroidal anti-inflammatory agents, diuretics, captopril• B. Infection: bacterial (e.g., acute pyelonephritis, leptospirosis), viral B. Infection: bacterial (e.g., acute pyelonephritis, leptospirosis), viral

(e.g., cytomegalovirus), fungal (e.g., candidiasis)(e.g., cytomegalovirus), fungal (e.g., candidiasis)• C. Infiltration: lymphoma, leukemia, sarcoidosisC. Infiltration: lymphoma, leukemia, sarcoidosis• D. IdiopathicD. IdiopathicV. Intratubular deposition and obstructionV. Intratubular deposition and obstruction• Myeloma proteins, uric acid, oxalate, acyclovir, methotrexate, sulphoMyeloma proteins, uric acid, oxalate, acyclovir, methotrexate, sulpho

namidesnamidesVI. Renal allograft rejectionVI. Renal allograft rejection

Post-renal Causes of ARFPost-renal Causes of ARF

• Account for 5% of cases of ARFAccount for 5% of cases of ARF• ARF occurs when both urinary outflow tracts are ARF occurs when both urinary outflow tracts are

obstructed or when one tract is obstructed in a obstructed or when one tract is obstructed in a patient with a single functional kidneypatient with a single functional kidney

Post-renal Causes of ARFPost-renal Causes of ARF

I. UretericI. Ureteric• Calculi, blood clot, sloughed papillae, cancer, external comCalculi, blood clot, sloughed papillae, cancer, external com

pression (e.g., retroperitoneal fibrosis)pression (e.g., retroperitoneal fibrosis)II. Bladder neckII. Bladder neck• Neurogenic bladder, prostatic hypertrophy, calculi, cancer, Neurogenic bladder, prostatic hypertrophy, calculi, cancer,

blood clotblood clotIII. UrethraIII. Urethra• Stricture, congenital valve, phimosisStricture, congenital valve, phimosis

InvestigationsInvestigations

ARF: Focused HistoryARF: Focused History• Nausea? Vomiting? Diarrhea?Nausea? Vomiting? Diarrhea?• Hx of heart disease, liver disease, previous renal disease, kiHx of heart disease, liver disease, previous renal disease, ki

dney stones, BPH?dney stones, BPH?• Any recent illnesses?Any recent illnesses?• Any edema, change in Any edema, change in urination?urination?• Any new medications? Any new medications? • Any recent radiology studies?Any recent radiology studies?• Rashes?Rashes?


Physical Examination: Physical Examination: • Infection sign ? Blood pressure, vital signInfection sign ? Blood pressure, vital sign• Volume Status Volume Status

– Mucus membranes, orthostatics, skin turgor, EdemaMucus membranes, orthostatics, skin turgor, Edema• CardiovascularCardiovascular

– JVD, rubsJVD, rubs• PulmonaryPulmonary

– Decreased breath soundsDecreased breath sounds– RalesRales

• Abd and back: bladder distension, masses, ascites, CVA tendernesAbd and back: bladder distension, masses, ascites, CVA tenderness, large prostate s, large prostate

• Rash (Allergic interstitial nephritis)Rash (Allergic interstitial nephritis)


• BloodBlood– CBC-DCCBC-DC– Electrolyte, Ca, Mg, PElectrolyte, Ca, Mg, P– Urea, CreatinineUrea, Creatinine– Others: LDH, Alb, CRP…Others: LDH, Alb, CRP…

• UrineUrine– Urine sodium, CrUrine sodium, Cr– Urine osmolalityUrine osmolality– UrinalysisUrinalysis

• Renal echoRenal echo

FeNa = FeNa = (urine Na x plasma Cr)(urine Na x plasma Cr) (plasma Na x urine Cr) (plasma Na x urine Cr)FeNa <1%FeNa <1% 1. PRERENAL1. PRERENAL• Urine Na < 20. Functioning tubules reabsorb lots of filtered Na Urine Na < 20. Functioning tubules reabsorb lots of filtered Na 2. ATN (unusual)2. ATN (unusual)• Postischemic dz: most of UOP comes from few normal nephrons, Postischemic dz: most of UOP comes from few normal nephrons,

which handle Na appropriatelywhich handle Na appropriately• ATN + chronic prerenal dz (cirrhosis, CHF)ATN + chronic prerenal dz (cirrhosis, CHF)3. Glomerular or vascular injury3. Glomerular or vascular injury• Despite glomerular or vascular injury, pt may still have well-preservDespite glomerular or vascular injury, pt may still have well-preserv

ed tubular function and be able to concentrate Naed tubular function and be able to concentrate Na

More FeNaMore FeNa

FeNa 1%-2% FeNa 1%-2% 1.1. Prerenal-sometimesPrerenal-sometimes2.2. ATN-sometimesATN-sometimes3.3. AIN-higher FeNa due to tubular damageAIN-higher FeNa due to tubular damage

FeNa >2%FeNa >2%1.1. ATN Damaged tubules can't reabsorb NaATN Damaged tubules can't reabsorb Na

Calculating FeNa after pt has gotten Lasix.Calculating FeNa after pt has gotten Lasix.1. Fractional Excretion of Lithium (endogenous) (<7% in prerenal )1. Fractional Excretion of Lithium (endogenous) (<7% in prerenal )2. Fractional Excretion of Uric Acid (<7% in prerenal )2. Fractional Excretion of Uric Acid (<7% in prerenal )

IIs the renal failure really acute?

Factors suggesting chronicityFactors suggesting chronicity Duration of symptoms for monthsDuration of symptoms for months Absence of acute illness in the face of very high urea and crAbsence of acute illness in the face of very high urea and cr

eatinineeatinine Anaemia of chronic disordersAnaemia of chronic disorders Bone disease (renal Bone disease (renal osteodystrophy) Sexual dysfunctionSexual dysfunction Skin disorders, pruritusSkin disorders, pruritus Neurological complicationsNeurological complications Small kidneys on renal imagingSmall kidneys on renal imaging

Management Management

• PreventionPrevention• Etiology treatment Etiology treatment • Prevention additional injuryPrevention additional injury• Treatment of complicationTreatment of complication• Conservative measurement Conservative measurement • Renal replacement therapyRenal replacement therapy

PreventionPrevention

• Identification of high-risk patients for pharmacologic agents-Identification of high-risk patients for pharmacologic agents-induced nephrotoxicityinduced nephrotoxicity– iodinated radiocontrast medium, NSAIDs iodinated radiocontrast medium, NSAIDs

• Aggressive surveillance for nephrotoxin-induced renal dysfuAggressive surveillance for nephrotoxin-induced renal dysfunction nction – cisplatin, amphotericin B, aminoglycosidecisplatin, amphotericin B, aminoglycoside

• Use of volume expansion in selected clinical settingsUse of volume expansion in selected clinical settings– Hyperpigmenturia: hemoglobinuria, myoglobinuriaHyperpigmenturia: hemoglobinuria, myoglobinuria– Crystaluria: uric acid, acyclovir, methotrexate, sulfonamidesCrystaluria: uric acid, acyclovir, methotrexate, sulfonamides

• Minimalization of catheters use to avoid nosocomial sepsis Minimalization of catheters use to avoid nosocomial sepsis

Etiology TreatmentEtiology Treatment

• Correct postrenal factorCorrect postrenal factor• Correct prerenal factorCorrect prerenal factor• Treat underlying sepsisTreat underlying sepsis• Stop nephrotoxic drugsStop nephrotoxic drugs

Conservative MeasurementConservative Measurement

• Fluid balanceFluid balance– Careful monitoring of I/O and body weightCareful monitoring of I/O and body weight

• Fluid restrictionFluid restriction– (usually less than 1 L/day in oliguric ARF)(usually less than 1 L/day in oliguric ARF)– Total intake < urine output +extrarenal lossesTotal intake < urine output +extrarenal losses

• Electrolytes and acid -base balanceElectrolytes and acid -base balance– hyperkalemiahyperkalemia– hyponatremiahyponatremia– Keep serum bicarbonate >15Keep serum bicarbonate >15– hyperphosphatemiahyperphosphatemia– Treat hypocalcemia only if symptomaticTreat hypocalcemia only if symptomatic

Guide of Volume ExpansionGuide of Volume Expansion

• CVP 8-14 cm HCVP 8-14 cm H22O (5-2 rule)O (5-2 rule)

• PAWP 12-16 mmHg (7-3 rule)PAWP 12-16 mmHg (7-3 rule)• Urine output 0.5-1.0ml/kg/hourUrine output 0.5-1.0ml/kg/hour• Weighing the patient dailyWeighing the patient daily• Insensible water loss from the skin and respiratory Insensible water loss from the skin and respiratory

tract (500 ml/day)tract (500 ml/day)

Dietary modificationDietary modification

• total caloric intake– 35~ 50 kcal/kg/daytotal caloric intake– 35~ 50 kcal/kg/day to avoid catabolism to avoid catabolism Salt restriction– 2~4 g/daySalt restriction– 2~4 g/day Potassium intake– 40 meq/dayPotassium intake– 40 meq/day Phosphorus intake– 800 mg/dayPhosphorus intake– 800 mg/day

• Uremia-nutritionUremia-nutrition– Restriction protein is not necessary in ARF, maintain caloric Restriction protein is not necessary in ARF, maintain caloric

intakeintake– Carbohydrate ≥ 100gm/day to minimize ketosis and protein Carbohydrate ≥ 100gm/day to minimize ketosis and protein

catabolismcatabolism• DrugDrug

– Review all medication, Stop magnesium-containing Review all medication, Stop magnesium-containing medicationmedication

– Adjusted dosage for renal failure, Readjust with improvement Adjusted dosage for renal failure, Readjust with improvement of GFR of GFR

Conservative MeasurementConservative Measurement

Absolute indicationAbsolute indication

• CCr CCr 5 ml/min or serum Cr 5 ml/min or serum Cr 10.0 mg/dl 10.0 mg/dl

Relative indicationRelative indication

• CCr CCr 10 ml/min or serum Cr 10 ml/min or serum Cr 8.0 mg/dl 8.0 mg/dl

• With accompanied symptoms or signsWith accompanied symptoms or signs

== CHF/Pulmonary edema CHF/Pulmonary edema == Uremic pericarditis Uremic pericarditis== Bleeding tendency Bleeding tendency == Neurologic symptoms Neurologic symptoms== Drug-resistant hyper-K Drug-resistant hyper-K == Drug-resistant metabolic acidosis Drug-resistant metabolic acidosis == Drug-resistant nausea/vomiting Drug-resistant nausea/vomiting== Others Others

Indication of DialysisIndication of Dialysis

Take Home PointsTake Home Points

• Features of the history and physical examination in Features of the history and physical examination in addition to relevant lab and radiologic investigations addition to relevant lab and radiologic investigations help to determine the most likely cause(s) of ARF in help to determine the most likely cause(s) of ARF in a given patienta given patient

Take Home PointsTake Home Points

• Management of a patient with ARF involves:Management of a patient with ARF involves:– Treating potentially life-threatening complicationsTreating potentially life-threatening complications– Reversing pre-renal and post-renal causesReversing pre-renal and post-renal causes– Minimizing further hemodynamic and toxic insults to the Minimizing further hemodynamic and toxic insults to the

kidneykidney– Admission and appropriate consultationAdmission and appropriate consultation– Lack of evidence for converting oliguric to non-oliguric Lack of evidence for converting oliguric to non-oliguric

ARFARF

13 Evaluation And Management Of Acute Renal Failure

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Transcript of 13 Evaluation And Management Of Acute Renal Failure