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Acute Kidney Injury
新光急診 張志華醫師
Acute Kidney Injury
Definition - Acute Kidney Injury Network (AKIN)
1. Rapid time course (less than 48 hours)
2. Reduction of kidney function
• Absolute increase in SCr of ≥ 0.3 mg/dl
• Percentage increase in SCr of ≥ 50%
3. Reduction in urine output, defined as < 0.5 ml/kg/hr for more than 6 hours
Acute Kidney Injury
Definitions
Anuria: No urine outputOliguria: Urine output <400-500 mL/dAzotemia: Increased Cr, BUN
• May be prerenal, renal, postrenal• May not have any clinical findings
Chronic Renal Insufficiency:• Deterioration over months to years• GFR 20-50%of normal
ESRD: GFR <5%of normal
AKI: Signs and Symptoms
• Hyperkalemia
• Nausea/Vomiting
• HTN
• Pulmonary edema
• Ascites
• Asterixis
• Encephalopathy
Causes of AKI
• 45%: ATN (ischemia, nephrotoxins)• 21%: Prerenal (CHF, volume depletion, sepsis)• 10%: Urinary obstruction• 4%: Glomerulonephritis or vasculitis• 2%: AIN• 1%: Atheroemboli
Non -ICU ICU
AKI: Focused History• Nausea? Vomiting? Diarrhea?
• Hx of heart disease, liver disease, previous renal disease, kidney stones, BPH?
• Any recent illnesses?
• Any edema, change in urination?
• Any new medications?
• Any recent radiology studies?
• Rashes?
Physical Exam
• Volume Status - Mucosa, orthostatics• Cardiovascular - JVD• Pulmonary - Rales• Rash - Allergic interstitial nephritis• Flank knocking tenderness• Large prostate, distended urinary bladder• Extremities - Skin turgor, edema
Workup for AKI
• Blood tests
• Urine– Urine electrolytes and Urine Cr to calculate FeNa
– Urine eosinophils
– Urine sediment: casts, cells, protein
– Uosm
• Kidney U/S - r/o hydronephrosis
Fraction excretion of sodium
FeNa = (UNa x PCr) / (PNa x UCr) x 100
FENaFeNa <1%
• Prerenal• Urine Na < 20 mEq/L• Functioning tubules reabsorb lots of filtered Na
FeNa >3% • Renal / postrenal• Urine Na > 40 mEq/L
FeNa 1~3%• Urine Na = 20~40 mEq/L • Mixed
FENaand Lasix...
• Loop diuretics in past 24-48 hr • Natriuresis raises UNa and FeNa• FeNa may >1% even if pt is prerenal• Still helpful if FeNa <1%
• Can use fractional excretion of urea instead• FeUrea = (Urea x PCr) / (BUN x UCr) x 100
• If FeUrea< 35%� prerenal
A 22yo male with adhesion ileus who has been vomiting nonstop for 2 days. BUN=45, Cr=2.2.
A. ATN
B. Glomerulonephritis
C. Dehydration
D. AIN from NSAIDs
Prerenal AKI
• Hyaline casts can be seen in normal pts– NOT an abnormal finding
• UA in prerenal AKI is normal• Reversible• Prevent ATN with volume replacement
– Fluid boluses or continuous IVF– Monitor urine output
Prerenal causes• Intravascular volume depletion
– Hemorrhage, vomiting, diarrhea, third spacing, diuretics
• Reduced Cardiac output
– Cardiogenic shock, CHF, tamponade, huge PE....
• Systemic vasodilation
– Sepsis, anaphylaxis, antihypertensive drugs
• Renal vasoconstriction
– Hepatorenal syndrome
Intrinsic AKI
1. Tubular (ATN)
2. Interstitial (AIN)
3. Glomerular (Glomerulonephritis)
4. Vascular
57 yoman, oliguria and rapidly increasing BUN and Cr
A. ATNB. Acute glomerulonephritisC. Acute interstitial nephritisD. Nephrotic Syndrome
ATN
• Muddy brown granular casts (last slide)
• Renal tubular epithelial cell casts (below)
ATN
Broad casts (form in dilated, damaged tubules)
Contrast-induced ATN
• Dilute urine: failure to concentrate urine
• Many granular casts, occasional renal tubular cell casts
• No RBC casts or WBC casts
• No eosinophils
ATN Causes1. Hypotension
• Relative low BP• May occur immediately after low BP episode or up
to 7 days later2. Post-op ischemia
• Post-aortic clamping, post-CABG3. Crystal precipitation4. Myoglobinuria (rhabdomyolysis)5. Contrast Dye
• AKI usually 1-2 days after test6. Aminoglycosides (10-26%)
ATN - What to do?
• Remove any offending agent– IVF
– Try Lasix if euvolemic pt is not peeing
– Dialysis
• Most pts return to baseline Cr in 7-21 days
ATN Prerenal
Cr increases 0.3~0.5/day increases < 0.3 /day
U Na, FeNa
UNa >40
FeNa >3%
UNa <20
FeNa <1%
UA Epithelial cells, granular casts
Normal, hyaline casts
Response to volume
Poor Cr improve Good Cr improve
BUN/Cr 10~15:1 > 20:1
缺血型急性腎損傷之病理生理機轉與相關臨床表現缺血型急性腎損傷之病理生理機轉與相關臨床表現缺血型急性腎損傷之病理生理機轉與相關臨床表現缺血型急性腎損傷之病理生理機轉與相關臨床表現
56yo woman with previously normal renal function now has BUN 24, Cr 1.8
Cells in the cast have nuclei (unlike RBC casts)
Pathognomonic for Acute Interstitial Nephritis
WBC Casts
Acute Interstitial Nephritis
70%Drug hypersensitivity• Antibiotics: PCNs (Methicillin), Cephalosporins, Cipro• Sulfa drugs, NSAIDs, Allopurinol...
15% Infection• Strep, Legionella, CMV, other bact/viruses
8% Idiopathic
6% Autoimmune diseases • Sarcoid, Tubulointerstitial nephritis / Uveitis)
AIN from Drugs
Renal damage is NOT dose-dependentMay take wks after initial exposure to drug
• Up to 18 m to get AIN from NSAIDSBut only 3-5 d to develop AIN after second exposure
S/S:• Fever (27%)• Serum Eosinophilia(23%)• Maculopapular rash (15%)
AIN from Drugs
UA:• Bland sediment or WBCs, RBCs• Non-nephrotic proteinuria• WBC Castsare pathognomonic• Urine eosinophils
Hint: can also see urine eosinophils in RPGN, renal atheroembolism
AIN Management
• Remove offending agent
• Most patients recover full kidney function in 1 year
• Poor prognostic factors– ARF > 3 weeks
– Advanced age at onset
You evaluate a 32yo woman with HTN, oliguria, and rapidly increasing Cr, BUN
A. ATNB. Acute glomerulonephritisC. Acute interstitial nephritisD. Nephrotic Syndrome
Acute Glomerulonephritis
• RBC casts: cells have no nuclei• Casts in urine: think INTRINSIC renal dz• If she has Lupus with recent viral
prodrome, think Rapidly Progressive Glomerulonephritis
• If she had a sorethroat 10 days ago, think Postinfectious ProliferativeGlomerulonephritis
What are these?
Glomerular Disease
• Hematuria(dysmorphic RBCs)
• RBC casts• Lipiduria
(increased glomerular permeability)• Proteinuria(may be in nephrotic range)• Fever, rash, arthralgias, pulmonary sx• Elevated ESR, low complement levels
Type 1: Anti-GBM dz
Type 2: Immune complex• IgA nephropathy• Postinfectious glomerulonephritis• Lupus nephritis• Mixed cryoglobulinemia
Type 3: Pauci-immune• Necrotizing glomerulonephritis (often ANCA-
positive, assoc. with vasculitis)
Rapidly Progressive Glomerulonephritis
Can present with viral-like prodrome• Myalgias, arthralgias, back pain, fever, malaise
Kidney biopsy : • Extensive cellular crescents with or w/o immune
complexes
Can develop ESRD in days to weeks
Treat with glucocorticoids & cyclophosphamide
Rapidly Progressive Glomerulonephritis
• Hematuria, HTN, edema, proteinuria• Usually after strep infection of upper respiratory tract or
skin • 8-14 day latent period• Can also occur in subacute bacterial endocarditis, visceral abscesses,
osteomyelitis, bacterial sepsis
• Positive antistreptolysin O titer (90% URI and 50% skin)• Treatment is supportive
– Screen family members with throat culture and treat with antibiotics if necessary
Postinfectious ProliferativeGlomerulonephritis
A 19yo woman with Breast Cancer s/p chemo has weakness, fever, rash. WBC = 15.4, Hct 24, Plt 15K, Cr 2.9. UA = 3+ prot, 3+blood, 20 RBC.
A. Nephrotic Synd
B. Systemic Vasculitis
C. Acute Glomerulonephritis
D. Hemolytic-Uremic Synd
E. Rhabdomyolysis
TTP
• Order blood smear to r/o TTP
• TTP associated with malignancy, chemo
• TTP may mimic Glomerulonephritis on UA (RBCs, WBCs)
• Thrombocytopenia, anemia not consistent with nephrotic or nephritic syndrome
Microvascular AKI
• TTP / HUS
• HELLP syndrome
• Platelets form thrombi and deposit in kidneys � Glomerular capillary occlusion or thrombosis
• Plasma exchange, steroids, Vincristine, IVIG, splenectomy....
MacrovascularAKI
• Aortic Aneurysm• Renal artery dissection or thrombosis• Renal vein thrombus• Atheroembolic disease
– New onset or accelerated HTN?– Abdominal bruits, reduced femoral pulses?– Vascular disease? – Embolic source?
A. Renal Artery StenosisB. Contrast-Induced NephropathyC. Abdominal Aortic AneurysmD. Cholesterol Atheroemboli
68yo male with baseline Cr 1.2 had negative cardiac cath 4 days ago, now Cr 1.8 and blanching rash
His toes look like this
Renal Atheroembolic Disease
• 1% of Cardiac caths• Aatheromatous debris scraped from the aortic
wall will embolize– Retinal – Cerebral– Skin (Livedo Reticularis, Purple toes)– Renal (ARF)– Gut (Mesenteric ischemia)
Renal Atheroembolic Disease
• Unlike in Contrast-Induced Nephropathy, Cr will NOT improve with IVF
• Diagnosis of exclusion:• will NOT show up on MRI or Renal
U/S; WILL show up on renal biopsy• Tx: supportive
Post-Renal AKI
Post-Renal AKI
• Urethral obstruction: prostate, urethral stricture• Bladder calculi or neoplasms• Bilateral ureteral obstruction (neoplasm, calculi)• Pelvic or retroperitoneal neoplams• Retroperitoneal fibrosis
HD or not?
• A 35yo woman with previously normal renal function now with BUN 74, Cr 6.9
• When would you call the Renal fellow to dialyze this p’t?
Indications for acute dialysis
AEIOU• Acidosis (metabolic)
• Electrolytes - hyperkalemia
• Ingestions / Ischemia
• Overload (fluid)
• Uremia – encephalopathy, seizures
55 Y female has acute pleuriticpain and desats to 92% RA. Should r/oPE but her Cr is 1.4. What’s next?
A. Send her for Stat CT with IV contrast
B. Send her for Stat CT without IV contrast
C. Just give her heparin
D. Begin IV hydration
E. Get a VQ scan instead
Contrast-Induced Nephrotoxicity
• Cr increases 25% or > 0.5 post-procedure
• Contrast causes renal vasoconstriction �renal hypoxia
• Iodine itself may be renally toxic
• If Cr >1.4, use pre-procedure prophylaxis
Pre-Procedure Prophylaxis
1. IVF ( 0.9NS)• 1-1.5 mg/kg/hour• 12 hours prior to procedure • 6-12 hours after procedure
Pre-Procedure Prophylaxis
2. N-acetylcysteine• Free radical scavenger; prevents oxidative
tissue damage• 600 mg po BID x 4 doses
(2 before procedure, 2 after)
Pre-Procedure Prophylaxis
3. Bicarbonate• Reduce renal medullary damage• 1 L D5W + 150 mEq HCO3
(500cc D5W + 5 Amp Jusomin)• 3 mL/kg/h x 1 hr preprocedure• 1 mL/kg/h x 6 hr postprocedure
Jusomin = 16.7 mEq/20ml
Pre-Procedure Prophylaxis
4. Other measures• Possibly helpful - Fenoldopam, Dopamine• Not helpful - Diuretics, Mannitol
Thank you