kuliah 2 acute renal failure usage

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Acute Renal FailureAcute Renal Failure

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GAGAL GINJAL AKUT(GGA)GAGAL GINJAL AKUT(GGA)

Penurunan tiba-tiba faal ginjal pd individu dg Penurunan tiba-tiba faal ginjal pd individu dg ginjal sehat sebelumnya,dg atu tanpa oliguria ginjal sehat sebelumnya,dg atu tanpa oliguria dan berakibat azotemia progresif,disertai dan berakibat azotemia progresif,disertai kenaikan ureum dan kreatinin darah.kenaikan ureum dan kreatinin darah.Bila kita berhadapan dg GGA,hrs kita pikirka Bila kita berhadapan dg GGA,hrs kita pikirka apakah GGA pre atau GGA post renal,yg apakah GGA pre atau GGA post renal,yg keduanya potensial dpt reversibel,sedang GGA keduanya potensial dpt reversibel,sedang GGA renal sbgn besar berupa nekrosis tubuler renal sbgn besar berupa nekrosis tubuler akut(NTA),sbg kelanjutan GGA pre renal yg akut(NTA),sbg kelanjutan GGA pre renal yg terlambat atau kurang baik penangannya. terlambat atau kurang baik penangannya.

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Acute renal failureAcute renal failure is a syndrome is a syndrome defined by a sudden loss of renal defined by a sudden loss of renal

function over several hours to function over several hours to several days.several days.

Mayo Clin Proc. 2001;76:67-74

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Acute Renal FailureAcute Renal FailureAcute Renal FailureAcute Renal Failure– Prerenal azotemia/ureum>Prerenal azotemia/ureum>

An abnormally high level of An abnormally high level of nitrogen-type/ureum nitrogen-type/ureum wastes/pmbungn in the wastes/pmbungn in the bloodstream. It is caused by bloodstream. It is caused by conditions that reduce blood conditions that reduce blood flow to the kidneys.flow to the kidneys.

– Postrenal azotemiaPostrenal azotemiaAn obstruction of some kind An obstruction of some kind (i.e., bladder cancer, uric acid (i.e., bladder cancer, uric acid crystals, urethral stricture etc)crystals, urethral stricture etc)

– Intrinsic Renal DiseaseIntrinsic Renal DiseaseUsually glomerular diseaseUsually glomerular diseaseUsually leads to End Stage Usually leads to End Stage Renal DiseaseRenal Disease

Intertwin jalin mnjlin

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Pre-renal = 55%Pre-renal = 55%

Renal parenchymal (intrinsic)= 40%Renal parenchymal (intrinsic)= 40%

Post-renal = 5-15%Post-renal = 5-15%

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Azotemia: elevated blood urea nitrogen not from an intrinsic renal diseaseOliguria: urine output less than 500cc/24hr.Nonoliguria: urine output greater than 500cc/24hr.Anuria: urine output less than 50cc/24hr.

99Rid mbrshkan

1010

EpidemiologyEpidemiology

InpatientInpatient

– 2-5% all 2-5% all hospitalizationshospitalizations

– 4-15% post 4-15% post cardiopulmonary cardiopulmonary bypassbypass

– ≤≤20% all ICU patients20% all ICU patients

OutpatientsOutpatients– cases/million/yearcases/million/year

140-209 general 140-209 general populationpopulation17 adults < 50 yr17 adults < 50 yr949 adults 80-89 yr949 adults 80-89 yr

BMJ 306(6876):481-483, 1993Mayo Clin Proc. 2001;76:67-74

1111

Etiology of ARF among OutpatientsEtiology of ARF among Outpatients

Prerenal (70%)

Intrarenal (11%)

Obstruction(17%)

idiopathic(2%)

AJKD 17:191-198, 1991

1212

Etiology of ARF among InpatientsEtiology of ARF among Inpatients

ATN (45%)

Prerenal (21%)

ARF on CKD (13%)

Obstruction (10%)

GN/vasc (4%)

AIN (2%)

Atheroemboli (1%)

KI 50:811-818, 1996

1313

Etiology of ARFEtiology of ARF

0

10

20

30

40

50

60

70

80

Prerenal Intrarenal Obstruct Idiopath

OutpatientInpatient

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Natural History of ARFNatural History of ARF

48% ICU pts require dialysis48% ICU pts require dialysis58% inpt mortality among patients who 58% inpt mortality among patients who develop ARF in the ICUdevelop ARF in the ICU

3636 % mortality among all inpts with ARF% mortality among all inpts with ARF20% of survivors received dialysis20% of survivors received dialysis

Crit Care Med 24(2);192-198, 1996

JASN 9(4):692-698, 1998

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Mortality of ARFMortality of ARF

““Despite technical progress in the Despite technical progress in the management of acute renal failure over management of acute renal failure over the last 50 years, mortality rates seem to the last 50 years, mortality rates seem to have remained unchanged at around have remained unchanged at around 50%.”50%.”

Am J Med (2005)118:827-832.

1616

Predictors of Dialysis in ARFPredictors of Dialysis in ARF

Oliguria:Oliguria:– <400cc/24hr 85% will require dialysis<400cc/24hr 85% will require dialysis– >400cc/24hr 30-40% will require dialysis>400cc/24hr 30-40% will require dialysis

Mechanical ventilationMechanical ventilationAcute myocardial infarctionAcute myocardial infarctionArrhythmiaArrhythmiaHypoalbuminemiaHypoalbuminemiaICU stayICU stayMulti-system organ failureMulti-system organ failure

JASN 9(4):692-698, 1998 Arch IM 160:1309-1313, 2000

1717

The Pathophysiology of ARFThe Pathophysiology of ARF

Acute renal failure

Prerenal Postrenal FactitiousIntrarenal

Vascular InterstitialTubularGlomerular

Ischemia

Pigments

Toxins

JASN 1998;9(4):710-718 Facti gol lan

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A. Symptoms A. Symptoms 1.1.Polyuria, Oliguria or Anuria hematuria Polyuria, Oliguria or Anuria hematuria 2.2.Dysuria Dysuria 3.3.Uremia Uremia

a.a.Definition: symptomatic azotemia Definition: symptomatic azotemia b.b.Acidosis (± tachypnea) Acidosis (± tachypnea) c.c.Mental Status changes Mental Status changes d.d.Hypervolemia / Hypertension Hypervolemia / Hypertension e.e.Hyperkalemia Hyperkalemia

1919

RPGNRPGN (Rapidly Progressive (Rapidly Progressive Glomerulonephritis) is a syndrome Glomerulonephritis) is a syndrome defined by the rapid loss of renal defined by the rapid loss of renal

function over days to weeks due to function over days to weeks due to acute glomerulonephritis.acute glomerulonephritis.

2020

Acute Renal failure

Acute renal failure is an abrupt renal impairment, presenting in a fall of GFR within hours or days.

The result is a severe imbalance of fluid and electrolyte homeostasis accompanied by accumulation of nitrogenous/protein waste.

Occurs in response to a variety of insultshaemodynamicimmunologicaltoxicobstructive

Causes of acute renal failure

Insltmrugkan

2121

Renal failureDifferentiation between acute and chronic renal failure

AcuteAcute ChronicChronic

HistoryHistory Short Short (days-week)(days-week)

Long Long (month-(month-years)years)

Haemoglobin Haemoglobin concentrationconcentration NormalNormal LowLow

Renal sizeRenal size NormalNormal ReducedReducedRenal Renal osteodystrophyosteodystrophy AbsentAbsent PresentPresent

Peripheral Peripheral neuropathyneuropathy AbsentAbsent PresentPresent

Serum Creatinine Serum Creatinine concentrationconcentration

Acute Acute reversible reversible increaseincrease

Chronic Chronic irreversible irreversible

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B. Etiologies B. Etiologies 1.1. Location of Lesion Location of Lesion a.a. Prerenal - ~70% of cases Prerenal - ~70% of cases b.b. Intrinsic - ~25% of cases Intrinsic - ~25% of cases c.c. Post-renal (obstructive) - <5% of casesPost-renal (obstructive) - <5% of cases

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Acute Renal failure

Differentiation between Pre-renal, renal and post-renal causes

Causes of acute renal failure

PrerenalPrerenal RenalRenal postrenalpostrenalHypovolaemiaHypovolaemiaDecreased active Decreased active blood volumeblood volumeDecreased Decreased cardiac outputcardiac outputRenovascular Renovascular obstructionobstruction

Acute tubular necrosisAcute tubular necrosisInterstinal nephritisInterstinal nephritisGlomerular disease Glomerular disease (acute (acute glomerulonephritis)glomerulonephritis)Small vessel dieaseSmall vessel dieaseIntrarenal Intrarenal vasoconstriction (in vasoconstriction (in sepsis)sepsis)Tubular obstructionTubular obstruction

Bilateral ureteric Bilateral ureteric obstructionobstructionUnilateral Unilateral ureteric ureteric obstructionobstructionBladder outflow Bladder outflow obstructionobstruction

Often result of renal ischaemia death of tubular cellsor direct toxic injury by endogenous chemicals such as myoglobin (from muscle rhabdomyolysis)Integrity of tubule is destroyed

obstructions, back-leakage

2424

1.1. Pre-renal azotemia Pre-renal azotemia

Decreased effective arterial volumeDecreased effective arterial volume- CHF,,Cirrhosis,,Nephrotic syndrome,,SepsisCHF,,Cirrhosis,,Nephrotic syndrome,,Sepsis- Renal Artery Stenosis (atherosclerosis, Renal Artery Stenosis (atherosclerosis,

fibromuscular dysplasia) fibromuscular dysplasia) - Cardiopulmonary bypass (>3 hours)Cardiopulmonary bypass (>3 hours)

Intravascular volume depletionIntravascular volume depletion– GI loss…Vomiting..diarrhea…etcGI loss…Vomiting..diarrhea…etc– Renal loss diuretc..osmotic diuresis..etcRenal loss diuretc..osmotic diuresis..etc– Cutaneous loss hyperthermia..burnsCutaneous loss hyperthermia..burns– HemorrhageHemorrhage– Third space pancreatitis..severe Third space pancreatitis..severe

hypoalbuminemia..cappillary leakhypoalbuminemia..cappillary leak

2525

II.Parenchymal Damage II.Parenchymal Damage • Nephritis (inflammation): glomerular vs. Nephritis (inflammation): glomerular vs.

interstitial interstitial • Tubular Injury: most common cause of ARF Tubular Injury: most common cause of ARF

Nephrotic Syndrome (total protein losses) Nephrotic Syndrome (total protein losses)

III. Obstruction of Outflow (~5%) Urinary Tract III. Obstruction of Outflow (~5%) Urinary Tract Infection (UTI) with Pyelonephritis Infection (UTI) with Pyelonephritis

a.a. Urinary Calculus disease (renal stones) Urinary Calculus disease (renal stones) b.b. Crystal Deposition Crystal Deposition c.c. Bladder tumors with extensive invasion Bladder tumors with extensive invasion d.d. Prostatic Enlargement: BPH vs. Carcinoma Prostatic Enlargement: BPH vs. Carcinoma e.e. Unilateral obstruction with only one Unilateral obstruction with only one

functioning kidney functioning kidney

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1.1. Drug Induced Drug Induced a.a. ACE Inhibitors ACE Inhibitors b.b. Radiocontrast Dye Interstitial Nephritis Radiocontrast Dye Interstitial Nephritis

- sulfonamides, NSAIDS, other - sulfonamides, NSAIDS, other antibiotics antibiotics

c.c. Amphotericin Amphotericin d.d. Cis-Platinum Cis-Platinum e.e. Aminoglycosides Aminoglycosides f.f. Non-steroidal anti-inflammatory drugs Non-steroidal anti-inflammatory drugs

(NSAIDs) (NSAIDs)

2727

C. Initial Evaluation C. Initial Evaluation 1.1. Consider possible etiologies and direct Consider possible etiologies and direct

evaluation evaluation 2.2. Medications should always be suspected Medications should always be suspected

2828

Pathology SummaryPathology Summary1.1. Glomerular Involvement Glomerular Involvement a.a. Diffuse: all glomeruli in a section are diseased Diffuse: all glomeruli in a section are diseased b.b. Focal: some glomeruli in a section are diseased Focal: some glomeruli in a section are diseased c.c. Segmental: parts of individual glomerulus Segmental: parts of individual glomerulus

affectedaffected 2.Focal Glomerulonephritis: 2.Focal Glomerulonephritis: a.a. Some glomeruli are dead( necrosis, collapse, Some glomeruli are dead( necrosis, collapse,

sclerosis sclerosis b.Acute or chronic inflamation is often seen b.Acute or chronic inflamation is often seen

2929

4.4. Focal and Segmental Glomerulosclerosis: Focal and Segmental Glomerulosclerosis: portions of many glomeruli are destroyed portions of many glomeruli are destroyed

5.5. Minimal Change Glomerulonephritis Minimal Change Glomerulonephritis a.a. Glomeruli appear okay, but function is poor Glomeruli appear okay, but function is poor b.b. Electron microscopic evidence of basement Electron microscopic evidence of basement

membrane disease membrane disease c.c. Response to glucocorticoids is usually very Response to glucocorticoids is usually very

goodgood 6.6. IgA Deposition IgA Deposition a.IgA nephropathy a.IgA nephropathy b.Deposition of IgA immune complexes b.Deposition of IgA immune complexes

3030

7.7. Proliferative Glomerulonephritis Proliferative Glomerulonephritis a.a. Increase in mesangeal cell number Increase in mesangeal cell number b.b. Usually follows insults (eg. Post-Usually follows insults (eg. Post-

Streptococcal) Streptococcal) c.c. May be seen in collagen vascular disease, May be seen in collagen vascular disease,

SLESLE

3131

8.8.Tubular Necrosis Tubular Necrosis a.a.Tubular cells die and slough off basement Tubular cells die and slough off basement

membrane membrane b.b.The dead tubular cells form casts which The dead tubular cells form casts which

can occlude lumen can occlude lumen c.c.Glomular basement membrane may also Glomular basement membrane may also

be damaged be damaged

3232Uptodate Online 11.2, Rose BD, 2003 mddykruh

3333

Stepwise Diagnostic Approach to Stepwise Diagnostic Approach to Acute Renal FailureAcute Renal Failure

Step 1Step 1– HistoryHistory– Record reviewRecord review– Physical examinationPhysical examination

Volume status assessmentVolume status assessment– Bladder evaluationBladder evaluation– UrinalysisUrinalysis

JASN 9(4):710-718, 1998

3434

Sanjad S, www.baylorcme.org

3535


Step 2Step 2– Urinary indicesUrinary indices– Renal/urinary imagingRenal/urinary imaging– Additional volume status measuresAdditional volume status measures– Renal vascular statusRenal vascular status– Blood and urine lab testsBlood and urine lab tests

3636


Step 3Step 3– Consider therapeutic trialsConsider therapeutic trials

Hemodynamic supportHemodynamic support

Step 4Step 4– Consider renal biopsyConsider renal biopsy– Consider empiric therapyConsider empiric therapy

3737

Treatment of ARFTreatment of ARF

Eliminate the toxic insultEliminate the toxic insultHemodynamic supportHemodynamic supportRespiratory supportRespiratory supportFluid managementFluid managementElectrolyte managementElectrolyte managementMedication dose adjustmentMedication dose adjustmentDialysisDialysis

3838

E. Management E. Management

Renal Diet Renal Diet a.a. Low phosphate, potassium, sodium, and Low phosphate, potassium, sodium, and

protein protein b.b. High calcium and vitamin D High calcium and vitamin D c.c. Various multivitamin formulas available for Various multivitamin formulas available for

renal patients, renal patients, d.d. Low protein diet may slow progression slightly Low protein diet may slow progression slightly

in chronic renal disease in chronic renal disease e.e. Phosphate and Calcium Phosphate and Calcium

3939

Acute Renal Failure Acute Renal Failure ManagementManagement

Make/think about the diagnosisMake/think about the diagnosisTreat life threatening conditionsTreat life threatening conditionsIdentify the cause if possibleIdentify the cause if possible– HypovolemiaHypovolemia– Toxic agents (drugs, myoglobin)Toxic agents (drugs, myoglobin)– ObstructionObstructionTreat reversible elementsTreat reversible elements– HydrateHydrate– Remove drugRemove drug– Relieve obstructionRelieve obstruction

4040

ARF: Life Threatening ARF: Life Threatening ConditionsConditions

HyperkalemiaHyperkalemiaVolume overloadVolume overloadVascular accessVascular access

4141

Hyperkalemia SymptomsHyperkalemia SymptomsWeaknessWeaknessLethargyLethargyMuscle crampsMuscle crampsParesthesiasParesthesiasHypoactive DTRsHypoactive DTRsDysrhythmiasDysrhythmias

4242

Hyperkalemia & EKGHyperkalemia & EKGK > 5.5 -6K > 5.5 -6Tall, peaked T’sTall, peaked T’sWide QRSWide QRSProlong PRProlong PRDiminished PDiminished PProlonged QTProlonged QTQRS-T merge – sine QRS-T merge – sine wavewave

4545

Prevention of ARFPrevention of ARFDiminish risk of nosocomial infectionDiminish risk of nosocomial infection– conservative use of IV cathetersconservative use of IV catheters– judicious use of antibioticsjudicious use of antibiotics– hand-washinghand-washingPrevention of nephrotoxicityPrevention of nephrotoxicity– avoid/reduce nephrotoxinsavoid/reduce nephrotoxins

– N-acetylcysteine, sodium bicarbonateN-acetylcysteine, sodium bicarbonate– correct hypokalemia, hypomagnesemiacorrect hypokalemia, hypomagnesemia– correct/treat other systemic diseasescorrect/treat other systemic diseasesPharmacologyPharmacology– avoid overlapping nephrotoxinsavoid overlapping nephrotoxins– follow drug levels closelyfollow drug levels closelyAttention to fluid statusAttention to fluid status JASN 9(4):710-718, 1998

4646

1.1. Acidosis Acidosis Renal tublar acidosis (RTA) is common in Renal tublar acidosis (RTA) is common in early renal failure early renal failure Oral bicitra (citrate replaces bicarbonate) Oral bicitra (citrate replaces bicarbonate) may be used may be used Bicitra is contraindicated in edematous Bicitra is contraindicated in edematous states due to high sodium content states due to high sodium content

2.2. Hyperuricemia Hyperuricemia Check uric acid levels Check uric acid levels Uric acid deposition in renal tubules may Uric acid deposition in renal tubules may worsen progression of renal failure worsen progression of renal failure Allopurinol may be given (100-200mg po Allopurinol may be given (100-200mg po qd) to attempt normalization of uric acidqd) to attempt normalization of uric acid

4747

3.3. Hypertension Hypertension a.a. ACE inhibitors generally contraindicated in ACE inhibitors generally contraindicated in

moderate to severe renal failure moderate to severe renal failure b.b. Calcium blockers such as nifedipine Calcium blockers such as nifedipine c.c. Labetolol is also very effective but patient Labetolol is also very effective but patient

should have LV EF>50% and no should have LV EF>50% and no bronchospasm bronchospasm

d.d. Consider Hydralazine for afterload reduction Consider Hydralazine for afterload reduction

e. Diuretic improve hypertension/ volume e. Diuretic improve hypertension/ volume overload overload

4848

5.5. Protein Load Protein Load

a.a. Reducing protein load is thought to reduce Reducing protein load is thought to reduce azotemia azotemia

b.b. Appears to slow progression of CRFAppears to slow progression of CRFc.c. Patients with moderate renal disease - some Patients with moderate renal disease - some

decrease in progression on low protein diet decrease in progression on low protein diet d.d. Patients with severe renal disease show no Patients with severe renal disease show no

benefit on low protein diet benefit on low protein diet

6.6. Hospital inpatients with ARF ~50% mortality Hospital inpatients with ARF ~50% mortality raterate

4949

8. Dialysis Indications8. Dialysis Indications1.1. Serum abnormalities unresponsive to medical Serum abnormalities unresponsive to medical

therapy therapy a.a. Severe Acidosis Severe Acidosis b.b. Severe Hyperkalemia Severe Hyperkalemia

IIII Uremia Uremia a.a. Mental status changes (usually delirium) Mental status changes (usually delirium) b.b. Nausea and vomiting Nausea and vomiting c.c. Pericarditis (pericardial friction rub) Pericarditis (pericardial friction rub)

5050

IIIIII Volume Overload Volume Overload • Hemofiltration or hemodialysis can be used Hemofiltration or hemodialysis can be used

to allow recovery of kidney after ARF to allow recovery of kidney after ARF a.a. Average duration of need for these Average duration of need for these

therapies was 9 days in ARF therapies was 9 days in ARF b.b. After this time, kidneys regain function and After this time, kidneys regain function and

increase urine output increase urine output c.c. Native kidneys may continue with minimal Native kidneys may continue with minimal

function for 6-12 months of hemodialysis function for 6-12 months of hemodialysis d.d. After that, native kidneys usually shut down After that, native kidneys usually shut down

permanentlypermanently

5151

Kidney Transplantation Kidney Transplantation

Excellent (and improving) results with Excellent (and improving) results with cadaveric grafts.cadaveric grafts.

1.1. New kidney usually placed in New kidney usually placed in extraperitoneally in the pelvis extraperitoneally in the pelvis

2.2. Cyclosporin ,Prednisone, immunosuppression Cyclosporin ,Prednisone, immunosuppression

THE END

5252

TERIMA TERIMA KASIHKASIH

kuliah 2 acute renal failure usage

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