10 Palevsky Acute Renal Failure
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Transcript of 10 Palevsky Acute Renal Failure
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Acute Renal Failure
Paul M. Palevsky, M.D.Professor of Medicine
Chief, Renal Section
VA Pittsburgh Healthcare System
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Acute Renal Failure
Definition The loss of renal function (measured as GFR)
over hours to days Expressed clinically as the retention of
nitrogenous waste products in the blood
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Relationship Between GFR and Serum Creatinine in ARF
120
40
80
0
GFR(mL/min)
0 7 14 21 28
4
Days
2
0
6
Serum Creatinine(mg/dL)
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Acute Renal Failure
Definitions Azotemia - the accumulation of nitrogenous
wastes Uremia - symptomatic renal failure Oliguria - urine output < 400-500 mL/24 hours Anuria - urine output < 100 mL/24 hours
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Manifestations of ARF
Azotemia progressing to uremia Hyperkalemia Metabolic acidosis Volume overload Hyperphosphatemia Accumulation and toxicity of medications
excreted by the kidney
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Differential Diagnosis of Azotemia
Etiologies of acute elevations of BUN Acute renal failure Protein loading GI bleeding Catabolic steroids Tetracycline antibiotics
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Differential Diagnosis of Azotemia
Etiologies of acute elevations of creatinine Acute renal failure Medications that block creatinine secretion
– cimetidine– trimethoprim
Substances that interfere with creatinine assay– cefoxitin– flucytosine– acetoacetate
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AcuteTubularNecrosis
AcuteInterstitialNephritis
AcuteGN
AcuteVascular
Syndromes
IntratubularObstruction
Classification of the Etiologies of Acute Renal Failure
PrerenalARF
PostrenalARF
IntrinsicARF
AcuteRenal
Failure
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Physiologic Response to Volume Depletion
Physiologic Response to Volume Depletion
Na Reabsorption
AIIAII PG
RPF
GFR
PGCFF
Urea Reabsorption
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Prerenal Acute Renal FailurePrerenal Acute Renal Failure
Na Reabsorption
AIIAII PG
RPF
GFR
PGCFF
Urea Reabsorption
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Pathogenesis of Prerenal Azotemia
RenalVasoconstriction
DecreasedGFR
Angiotensin II
Adrenergic nerves
Vasopressin
+
+
+
Nitric oxide
Prostaglandins-
-
VolumeDepletion
CongestiveHeart Failure Liver
Failure
Sepsis
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Prerenal Acute Renal Failure
Volume Depletion Decreased effective blood volume
congestive heart failure cirrhosis nephrotic syndrome sepsis
Renal vasoconstriction hepatorenal syndrome hypercalcemia nonsteroidal anti-inflammatory drugs
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Prerenal Acute Renal Failure:Clinical Presentation
History volume loss (e.g., diarrhea, acute blood loss) heart disease liver disease evidence of infection diuretic use thirst orthostatic symptoms
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Prerenal Acute Renal Failure:Clinical Presentation
Physical Examination Blood pressure and pulse Orthostatic changes in blood pressure Skin turgor Dryness of mucous membranes and axillae Neck veins Cardiopulmonary exam Peripheral edema
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Prerenal Acute Renal Failure: Clinical Presentation
BUN:Creatinine ratio > 20:1
Urine indices Oliguria
– usually < 500 mL/24 hours; but may be non-oliguric Elevated urine concentration
– UOsm > 700 mmol/L– specific gravity > 1.020
Evidence of high renal sodium avidity– UNa < 20 mmol/L
– FENa < 0.01
Inactive urine sediment
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Fractional Excretion of SodiumFractional Excretion of Sodium
FEFENa Na = = Filtered SodiumFiltered Sodium
Excreted SodiumExcreted Sodium
FEFENa Na = = PPNaNa x GFR x GFR
UUNaNa x V x V
FEFENa Na = = UUCrCr / P / PCrCr
UUNaNa / P / PNaNa
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Fractional Excretion of SodiumFractional Excretion of Sodium
Etiologies of a fractional excretion of sodium < 0.01 normal renal function prerenal azotemia hepatorenal syndrome early obstructive uropathy contrast nephropathy rhabdomyolysis acute glomerulonephritis
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Treatment of Prerenal Acute Renal Failure
Correction of volume deficits Discontinuation of antagonizing
medications NSAIDs/COX-2 inhibitors Diuretics
Optimization of cardiac function
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Postrenal Acute Renal Failure
Urinary tract obstruction level of obstruction
– upper tract (ureters)
– lower tract (bladder outlet or urethra)
degree of obstruction– partial
– complete
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Postrenal Acute Renal Failure
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Postrenal Acute Renal Failure
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Postrenal Acute Renal Failure
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Pathophysiology of Renal Failure in Obstructive Uropathy
Early Increased intratubular pressure Initial increase followed by decrease in renal
plasma flow Late
Normal intratubular pressure Marked decrease in renal plasma flow
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Etiologies of Postrenal Acute Renal Failure
Upper tract obstruction Intrinsic
– nephrolithiasis– papillary necrosis– blood clot– transitional cell cancer
Extrinsic– retroperitoneal or pelvic
malignancy– retroperitoneal fibrosis– endometriosis– abdominal aortic aneurysm
Lower tract obstruction– benign prostatic
hypertrophy
– prostate cancer
– transitional cell cancer
– urethral stricture
– bladder stones
– blood clot
– neurogenic bladder
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Postrenal Acute Renal Failure:Clinical Presentation
History Symptoms of bladder outlet obstruction
– urinary frequency
– urgency
– intermittency
– hesitancy
– nocturia
– incomplete voiding
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Postrenal Acute Renal Failure:Clinical Presentation
History Changes in urine volume
– anuria
– polyuria
– fluctuating urine volume
Flank pain Hematuria History of pelvic malignancy
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Postrenal Acute Renal Failure:Clinical Presentation
Physical Examination Suprapubic mass Prostatic enlargement Pelvic masses Adenopathy
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Postrenal Acute Renal Failure:Clinical Evaluation
Diagnostic studies BUN: Creatinine ratio > 20:1 Unremarkable urine sediment Variable urine chemistries
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Postrenal Acute Renal Failure:Clinical Evaluation
Diagnostic studies Post-void residual bladder volume
– > 100 mL consistent with voiding dysfunction
Radiologic studies– Ultrasound
– CT scan
– Nuclear medicine
– Retrograde pyelography
– Antegrade nephrostograms
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Renal Ultrasound - Hydronephrosis
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Treatment of Postrenal Acute Renal Failure
Relief of obstruction Lower tract obstruction
– bladder catheter
Upper tract obstruction– ureteral stents
– percutaneous nephrostomies
Recovery of renal function dependent upon duration of obstruction
Risk of post-obstructive diuresis
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Intrinsic Acute Renal Failure
Acute tubular necrosis (ATN) Acute interstitial nephritis (AIN) Acute glomerulonephritis (AGN) Acute vascular syndromes Intratubular obstruction
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Acute Tubular Necrosis
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Acute Tubular Necrosis
Ischemic– prolonged prerenal
azotemia
– hypotension
– hypovolemic shock
– cardiopulmonary arrest
– cardiopulmonary bypass
Sepsis
Nephrotoxic drug-induced
– radiocontrast agents
– aminoglycosides
– amphotericin B
– cisplatinum
– acetaminophen pigment nephropathy
– hemoglobin
– myoglobin
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Pathophysiology of ATN:Tubular Epithelial Cell Injury and Repair
Loss of polarityLoss of polarityNormal EpitheliumNormal Epithelium
Migration , Dedifferentiation of Viable CellsMigration , Dedifferentiation of Viable Cells
Differentiation & Differentiation & Reestablishment Reestablishment of polarityof polarity
Sloughing of viable and dead cells Sloughing of viable and dead cells with luminal obstructionwith luminal obstruction
Ischemia/ Ischemia/ ReperfusionReperfusion
ApoptosiApoptosiss
Necrosis
Cell deathCell death
Adhesion moleculesNa+/K+-ATPase
ProliferationProliferation
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Pathophysiology of Acute Tubular Necrosis
Mechanisms of decreased renal function Vasoconstriction Tubular obstruction by sloughed debris Backleak of glomerular filtrate across denuded
tubular basement membrane
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Phases of Ischemic ATN
Prerenal
Initiation
Extension
Maintenance Recovery
GFR
Time
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Pathophysiology of ATN
Ischemia
Endothelial Injury
Capillary Obstruction&
Continued Ischemia
Inflammation
Tubular Injury
Disruption of Cytoskeleton
Loss of Cell Polarity
Desquamation of Cells
Tubular Obstruction&
Backleak
Apoptosis&
Necrosis
Activation of VasoconstrictorsImpaired Vasodilation
Increased Leukocyte Adhesion
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Acute Tubular Necrosis: Clinical Presentation
History Acute illness Exposure to nephrotoxins Episodes of hypotension
Physical examination Hemodynamic status Volume status Features of associated illness
Laboratory data BUN:Creatinine ratio < 10:1 Evidence of toxin exposure
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Acute Tubular Necrosis: Clinical Presentation
Urine indices Urine volume
– may be oliguric or non-oliguric Isosthenuric urine concentration
– UOsm 300 mmol/L– specific gravity 1.010
Evidence of renal sodium wasting– UNa > 40 mmol/L
– FENa > 0.02
Urine sediment– tubular epithelial cells– granular casts
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Acute Tubular Necrosis: Clinical Presentation
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Acute Tubular Necrosis:Treatment
Supportive therapy No specific pharmacologic treatments Acute dialysis for:
volume overload metabolic acidosis hyperkalemia uremic syndrome
– pericarditis– encephalopathy
azotemia
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Prognosis ofAcute Tubular Necrosis
Mortality dependent upon comorbid conditions overall mortality ~ 50%
Recovery of renal function seen in ~ 90% of patients who survive - although not necessarily back to prior baseline renal function
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Mortality in Acute Tubular Necrosis
Chertow et al: Arch Int Med 1995; 155:1505-1511
0%
20%
40%
60%
80%
100%
0 1 2 3 4
Number of Failed Non-Respiratory Organ Systems
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Effect of Contrast Nephropathy on Mortality
0%
10%
20%
30%
40%
50%
Mor
tali
tyNo ARF ARF
Mortality
APACHE IIScore
No ARF ARF
0-3 4% 17%
4-7 5% 40%
8-11 28% 52%
>12 33% 62%
Levy et al: JAMA 1996; 275:1489-1494
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Acute Interstitial Nephritis
Acute renal failure due to lymphocytic infiltration of the interstitium
Classic triad of fever rash eosinophilia
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Acute Interstitial Nephritis
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Acute Interstitial Nephritis
Drug-induced penicillins cephalosporins sulfonamides rifampin phenytoin furosemide NSAIDs
Malignancy Idiopathic
Infection-related bacterial viral rickettsial tuberculosis
Systemic diseases SLE sarcoidosis Sjögren’s syndrome tubulointerstitial nephritis
and uveitis
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Acute Interstitial Nephritis:Clinical Presentation
History preceding illness or drug exposure
Physical examination fever rash
Laboratory Findings eosinophilia
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Acute Interstitial Nephritis:Clinical Presentation
Urine findings non-nephrotic protinuria hematuria pyuria WBC casts eosinophiluria
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Acute Interstitial Nephritis:Clinical Presentation
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Acute Interstitial Nephritis:Clinical Presentation
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Acute Interstitial Nephritis:Treatment
Discontinue offending drug Treat underlying infection Treat systemic illness Glucocorticoid therapy may be used in patients
who fail to respond to more conservative therapy
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Acute Glomerulonephritis
Nephritic presentation proteinuria
– may be in nephrotic range (> 3 g/day)
hematuria RBC casts
Diagnosis usually requires renal biopsy
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Acute Glomerulonephritis
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Acute Glomerulonephritis
Etiologies poststreptococcal glomerulonephritis postinfectious glomerulonephritis endocarditis-associated glomerulonephritis systemic vasculitis thrombotic microangiopathy
– hemolytic-uremic syndrome– thrombotic thrombocytopenic purpura
rapidly progressive glomerulonephritis
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Acute Vascular Syndromes
Renal artery thromboembolism Renal artery dissection Renal vein thrombosis
Atheroembolic disease
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Atheroembolic Disease
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Intratubular Obstruction
Intratubular crystal deposition tumor lysis syndrome
– acute urate nephropathy
ethylene glycol toxicity – calcium oxylate deposition
Intratubular protein deposition multiple myeloma
– -Bence-Jones protein deposition
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Differential Diagnosis of Acute Renal Failure
Prerenal ARF Postrenal ARF Intrinsic ARF
acute tubular necrosis acute interstitial nephritis acute glomerulonephritis acute vascular syndromes intratubular obstruction
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Acute Renal Failure: Diagnostic EvaluationAcute Renal Failure: Diagnostic Evaluation
Evaluate for prerenal causes clinical exam
– blood pressure– orthostasis
central venous pressures and cardiac output intake/output record urine sediment urine sodium
– UNa < 20 mmol/L
therapeutic trial of volume replacement
– skin turgor– mucosal membrane hydration
– FENa < 0.01
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Acute Renal Failure:Diagnostic Evaluation
Evaluate for postrenal causes bladder catheterization renal ultrasound
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Acute Renal Failure:Diagnostic EvaluationAcute Renal Failure:
Diagnostic Evaluation
Evaluation for intrinsic ARF clinical history
– medications– hypotension
physical exam urinalysis
– crystals– paraproteins
– radiocontrast agents– sepsis
– cells– casts
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Diagnostic Evaluation of ARF
Form of ARF BUN:Cr UNa (mEq/L) FENa Urine Sediment
Prerenal >20:1 <20 < 1% Normal
Postrenal >20:1 >20 variable Normal or RBC’s
Intrinsic
ATN <10:1 >40 > 2% Muddy brown casts; tubular epithelial cells
AIN <20:1 >20 >1% WBC’s WBC casts, RBC’s, eosinophils
AGN variable <40 <1% RBC’s, RBC casts
Vascular variable >20 variable Normal or RBC’s
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Acute Renal Failure: Management
Prerenal ARF volume repletion inotropic support discontinue diuretics
Postrenal ARF bladder catheterization percutaneous nephrostomy or ureteral stents fluid management during post-obstructive
diuresis
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Acute Renal Failure: Management
Intrinsic ARF General supportive care
– fluid management
– diuretics
– bicarbonate supplementation
– potassium
– phosphate
– drug dosing
– nutrition
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Acute Renal Failure: ManagementAcute Renal Failure: Management
Indications for dialysis volume overload metabolic acidosis hyperkalemia uremic syndrome
– pericarditis– encephalopathy
azotemia