2. LearningObjectives
• Define acute kidney injury (AKI) and understand
terminology
• Understand the etiology/categories anddiagnostic
approach to AKI
• Prerenal
• Intrinsic renal
• Postrenal
• General approach to the patient with AKI
• Treatment and prevention ofAKI
.
3. Defined by:
• Abrupt lossof kidney function
• Retentionofurea and other
nitrogenous wasteproducts
• Dysregulation of extracellular
volume andelectrolytes
Acute KidneyInjury(AKI)
4. TermsYouShouldKnow
Creatinine:
• Breakdown product of creatine
phosphate in muscle
• Filtered by the kidney and usedto
estimate kidneyfunction/filtration
• Inversely proportional to function:
the higher the creatinine, the lower the
filtration
Anuria:< 100 mL urine output/24 h
Blood urea nitrogen(BUN):
• Urea nitrogen formed fromprotein
catabolism by theliver
• Filtered by the kidney and used as an
additional measure of kidneyfunction
• High BUN generally reflectslower
filtration
• Caveat: BUN canincrease
independently ofkidneyfunction
• Steroids, tetracycline antibiotics,or
reabsorptionof blood in GI tract
Oliguria: < 500 mL urine output/24 h
5. In critically ill patients withAKI:
• Mortality rate of 40 60% ina
60-day interval
• Hospital stay prolonged
Acute KidneyInjury (AKI)Is BAD!
7. Staging System for Acute KidneyInjury
Stage 3
Failure
Stage 2
Injury
Stage 1
Risk
↑ Creatinine dLor
1.5 2 times frombaseline
↑ Creatinine 2 3 times
frombaseline
↑ Creatinine 3 4times
from baselineor
> 4 mg/dLwith acute
increase dL
< 0.5 mL/kg/h for > 12 h
<0.3 mL/kg/h for 24 h
or anuriafor 12 h
Serumcreatininecriteria
< 0.5 mL/kg/h for > 6 h
Urine outputcriteria
48 hours
8. Staging System for Acute KidneyInjury
48 hours
↑ Creatinine 3 4 times
from baseline or <0.3 mL/kg/h for 24 h
Stage 3 > 4 mg/dLwith acute or anuria for12 h
Failure increase dL
Stage 2 ↑ Creatinine 2 3 times
Injury from baseline
< 0.5 mL/kg/h for > 12 h
Stage 1 ↑ Creatinine dLor
Risk 1.5 2 times from baseline < 0.5 mL/kg/h for > 6 h
Serumcreatininecriteria Urine outputcriteria
The higher the stage the worse the outcome!
9. • Based on serum creatinine and urine output imperfect
biomarkers (biological markers for organ injury)
• ↑ Serum creatinine or ↓ urine output substantial
injury may have takenplace
• Diminishes ability to begin treatments aimed at
preventing the loss of renalfunction
• Development of novel biomarkers (NGAL, KIM1, NAG),
not ready
Problemswith the StagingSystem
10. ConceptualModel for AKI
Complications
Staging
Insult and
injury
Normal
Increased
risk
Damage ↓ GFR
Kidney
failure
Death
Age
Blood volume Diabetes
NSAID
Susceptibility:
Creatinine level and urineoutput
are inadequate for definingwhen
the injury occurs
12. Test case
You are asked to see a 72-year-old woman who is admitted to
the hospital from a skilled nursing facility. She has altered
mental status and her caregiver notes she has not been eating
or drinking for the past severaldays.
Physical exam:Orthostatic hypotension, tenting of her skin,
and dry mucousmembranes
Labs:Serum creatinine 2.3 mg/dL (normal 0.5 1.0 mg/dL)
BUN high at 58 mg/dL (normal 5 20 mg/dL)
She is given 2 L of normal saline and her serum creatinine
decreases to 1.3 mg/dL the followingmorning.
72-year-old Woman with Altered Mental Status
What type of acute kidney injury does she have?
13. Test case
You are asked to see a 72-year-old woman who is admitted to
the hospital from a skilled nursing facility. She has altered
mental status and her caregiver notes she has not been eating
or drinking for the past severaldays.
,tenting of her skin,
Physical exam:Orthostatic hypotension
and dry mucousmembranes
Labs:Serum creatinine 2.3 mg/dL (normal 0.5 1.0 mg/dL)
BUN high at 58 mg/dL (normal 5 20 mg/dL)
She is given 2 L of normal saline and her serum creatinine
decreases to 1.3 mg/dL the followingmorning.
72-year-old Woman with Altered Mental Status
Signs of volumedepletion
Acute kidney injury
Prerenal reversible injury
What type of acute kidney injury does she have?
Hypovolemia
14. Test case
You are asked to see a 72-year-old woman who is admitted to
the hospital from a skilled nursing facility. She has altered
mental status and her caregiver notes she has not been eating
or drinking for the past severaldays.
,tenting of her skin,
Physical exam:Orthostatic hypotension
and dry mucousmembranes
Labs:Serum creatinine 2.3 mg/dL (normal 0.5 1.0 mg/dL)
BUN high at 58 mg/dL (normal 5 20 mg/dL)
She is given 2 L of normal saline and her serum creatinine
decreases to 1.3 mg/dL the followingmorning.
72-year-old Woman with Altered Mental Status
Signs of volumedepletion
Acute kidney injury
What type of acute kidney injury does she have?
Prerenal AKI due to volumedepletion
Hypovolemia
Prerenal reversible injury
16. Two Major Causes of RenalHypoperfusion
Decreased effective arterial blood volume
• Refers to extracellular fluid(ECF)volume
in the arterial circulation
• Total ECFvolume may be increased but
arterial blood volume perceived by
baroreceptorsin the carotid sinus and
glomerular afferentarterioles islow
edematous states
• Heart failure
• Hepatic cirrhosis
• Sepsis
True volume depletion
• Loss of Na+ from the extracellular fluid
volume
• GI losses
• Hemorrhagic shock
• Renal losses
• Cutaneous losses
20. Glomerular Filtration Rate (GFR) underAutoregulatoryControl
↓ Renal perfusion
↑ Filtrationfraction
↑ Oncotic pressure
in postglomerular
capillaries
↑ Salt and water absorption
in proximal tubule
↓ Urine Na+ and
concentrated urine
Activation of
angiotensin II and
antidiuretic hormone
Normal GFRmaintained
26. • BUN: creatinine > 20:1(normal 10:1)
• Urine osmolality > 500mOsmol/kg H2O
• Urine Na+ < 10 mEq/L, urine Cl < 10 mEq/L
• Urinalysis
• High specific gravity; noprotein,
blood, or white bloodcells
• Sediment review bland no casts,
no cells
Diagnostic Workup LaboratoryEvaluation
27. FENa measures the percent of filtered
Na+ excreted in the urine and is used to
differentiate between prerenal disease
and acute tubular necrosis.
Fractional Excretion (FE)ofNa+ FENa
28. Estimated by simultaneously obtaining urine
and plasma specimens of Na+ and creatinine:
Fractional Excretion (FE) of Na+ FENa
x 100
x 100
29. • FENa < 1%in prerenal diseaseand indicates that the
patient will be responsive to volume (i.e.IV fluids)
• Best to use when patients are oliguric
Fractional Excretion (FE) of Na+ FENa
34. Test case
You are asked to see a 56-year-old man who recently
underwent coronary angiography with stent placement to his
left anterior descending artery (LAD) for acute coronary
syndrome.His serum creatinine was noted to increase 2 days
following the procedure.
Physical exam:unremarkable
Labs:serum creatinine 2.3 mg/dL (normal0.5 1.0mg/dL), was
0.9 mg/dL on the day of the angiography
BUN 28 mg/dL (normal 5 20 mg/dL)
He is given 2 L of normal saline but his creatinine is continuing
to rise.
56-year-old Man with CoronaryAngiography
What type of acute kidney injury does he have?
35. Test case
56-year-old Man with CoronaryAngiography
Radiocontrast
administration from
angiography
Tubular injury
Intrinsic renal disease
You are asked to see a 56-year-old man who recently
underwent coronary angiography with stent placement to his
left anterior descending artery (LAD) for acute coronary
syndrome.His serum creatinine was noted to increase 2 days
following the procedure.
Physical exam:unremarkable
Labs:serum creatinine 2.3 mg/dL (normal0.5 1.0mg/dL), was
0.9 mg/dL on the day of the angiography
BUN 28 mg/dL (normal 5 20 mg/dL)
He is given 2 L of normal saline but his creatinine is continuing
to rise.
What type of acute kidney injury does he have?
36. Test case
56-year-old Man with CoronaryAngiography
Radiocontrast
administration from
angiography
Tubular injury
Intrinsic renal disease
Intrinsic renal disease acute tubularnecrosis
You are asked to see a 56-year-old man who recently
underwent coronary angiography with stent placement to his
left anterior descending artery (LAD) for acute coronary
syndrome.His serum creatinine was noted to increase 2 days
following the procedure.
Physical exam:unremarkable
Labs:serum creatinine 2.3 mg/dL (normal0.5 1.0mg/dL), was
0.9 mg/dL on the day of the angiography
BUN 28 mg/dL (normal 5 20 mg/dL)
He is given 2 L of normal saline but his creatinine is continuing
to rise.
What type of acute kidney injury does he have?
44. Causes of Acute TubularNecrosis
Ischemia
• Acute drop in meanarterial
pressure
• Prolonged volume depletion
• Sepsis
Decreased
perfusion
45. Causes of Acute TubularNecrosis
Toxin
Radiocontrast media
• Iodinated contrast for CTscan
and angiography
Risk factors:
• Underlying chronic kidney
disease
• Diabetes mellitus
• Concurrent hypotension
46. Causes of Acute TubularNecrosis
Toxin
Drugs
• Aminoglycosides
• Amphotericin B
• Cisplatin
Tend to be nonoliguric > 500 mL
Urine change 24h to 24h
Heme pigments
• Rhabdomyolysis breakdown
of skeletal muscle (crushinjury)
47. Causes of Acute TubularNecrosis
Toxin
Drugs
• Aminoglycosides
• Amphotericin B
• Cisplatin
Tend to be nonoliguric > 500mL
Urine change 24h to 24h
Heme pigments
• Rhabdomyolysis breakdown
of skeletal muscle (crushinjury)
48. • Prolonged period of hypotension
in the ICU
• Ischemia
• Exposure to radiocontrast
• CT scans
• Angiograms
• Sepsis
Acute TubularNecrosis Diagnostic Workup History and Chart Review
49. Acute Tubular Necrosis Diagnostic Workup History and Chart Review
• Drugs
• Aminoglycosides bacterial
infections
• Amphotericinfor fungal
infections
• Crush injuries or found down for
prolonged time
• Rhabdomyolysis
50. • BUN: creatinine 10 15:1
• Urine Na+ and Cl > 20 meq/L
• FENa> 2%
• Urine analysis
• Isosthenuric specific gravity ~1.01
due to loss of concentratingability
• Urine osmolality < 450mOsm/kg
Acute TubularNecrosis Diagnostic Workup Laboratory Evaluation
51. Acute TubularNecrosis Diagnostic Workup Laboratory Evaluation
• May have low gradeproteinuria
• ~ < 500 mg 1g per 24 h
• Due to impaired reabsorptionof
protein at the proximaltubule
• Urine sediment
• Pigmented granular casts orfree
floating tubular epithelial cells
52. Acute TubularNecrosis DiagnosticWorkup LaboratoryEvaluation
• May have low gradeproteinuria
• ~ < 500 mg 1g per 24 h
• Due to impaired reabsorptionof
protein at the proximaltubule
• Urine sediment
• Pigmented granular casts orfree
floating tubular epithelial cells
53. Clinical Course of Acute Tubular Necrosis
21days
• Creatinineplateaus
in 7 10 days
• Excess solutes and water areexcreted
as tubule undergoes repair
• Marks the polyuricphase (days 1014)
of ATN > 3 Lof urine output per 24 h
• Recovery usually occurs between
days 14 21
Recovery phase
Initiation phase Maintenance phase
0 7 14
54. Acute TubularNecrosis Treatment/Prevention
Identify patients who are atrisk Interventions that decreaserisk
• Major surgery, shock
(vasodilatory, hemorrhagic,
cardiogenic)
• Comorbid conditions, e.g.:
chronic kidney disease,
peripheral vascular disease,
diabetes mellitus,malignancy,
heart failure,malnourished
• Optimizing volume status/maintain
hemodynamic stability
• Avoid nephrotoxins
• Contrast-induced nephrotoxicity
• Volume expand with crystalloid pre-and
post-contrast
• Minimize contrastvolume
There is no evidencethat
diureticsare helpful duringATN.
55. Test case
You are asked to see a 35-year-old woman with increase in
serum creatinine from 0.7 mg/dL to 3.2 mg/dL. She is currently
in the ICU receiving nafcillin (a penicillin) by continuous infusion
for Staph aureusendocarditis.
Physical exam:Febrile, erythematous, maculopapular rash over
her thorax andextremities
Labs:Serum creatinine is 3.2 mg/dL (normal 0.5 1.0 mg/dL).
CBC has an increased number of eosinophils on the differential.
Urine analysis shows WBCs and white blood cell casts. Urine
culture was negative.
35-year-old Woman with IncreasedSerum Creatinine
What type of acute kidney injury does she have?
56. Test case
You are asked to see a 35-year-old woman with increase in
serum creatinine from 0.7 mg/dLto 3.2 mg/dL.She is currently
in the ICU receiving nafcillin (a penicillin) by continuous infusion
for Staph aureusendocarditis.
Physical exam:Febrile, erythematous, maculopapular rash over
her thorax andextremities
Labs:Serum creatinine is 3.2 mg/dL (normal 0.5 1.0 mg/dL).
CBC has an increased number of eosinophils on the differential.
Urine analysis shows WBCsand white bloodcell casts. Urine
culture was negative.
35-year-old Woman with IncreasedSerum Creatinine
What type of acute kidney injury does she have?
Rise in serumcreatinine
Allergic or hypersensitivity
process
Allergic interstitial nephritis
Absence of bacteriuria
57. Test case
You are asked to see a 35-year-old woman with increase in
serum creatinine from 0.7 mg/dLto 3.2 mg/dL.She is currently
in the ICU receiving nafcillin (a penicillin) by continuous infusion
for Staph aureusendocarditis.
Physical exam:Febrile, erythematous, maculopapular rash over
her thorax andextremities
Labs:Serum creatinine is 3.2 mg/dL (normal 0.5 1.0 mg/dL).
CBC has an increased number of eosinophils on the differential.
Urine analysis shows WBCsand white bloodcell casts. Urine
culture was negative.
35-year-old Woman with IncreasedSerum Creatinine
Rise in serumcreatinine
Allergic or hypersensitivity
process
Allergic interstitial nephritis
Absence of bacteriuria
What type of acute kidney injury does she have?
Acute/allergic interstitial nephritis
59. Acute interstitial nephritis is aninflammatory
cell infiltration in the kidney interstitium
caused by an immune response.
Acute Interstitial Nephritis
64. Test case
You are asked to see a 47-year-old woman who has a history
of Non- lymphoma. Her tumor is high grade but very
responsive to chemotherapy. She underwent her first cycle
2 days prior and now is admitted with hyperkalemia and
decreased urine output.
Physical exam:Unremarkable
Labs:Serum creatinine is 4.2 mg/dL (normal 0.5 1.0 mg/dL). K+
is 5.9 (normal 3.5 5.2 mEq/L), phosphorus 7 (normal 2.4 4.2
mg/dL), uric acid 15 mg/dL (normal 3.0 6.5mg/dL)
Urine analysis shows uric acidcrystals.
47-year-old Woman withNon-
What type of acute kidney injury does she have?
65. Test case
You are asked to see a 47-year-old woman who has a history
of Non- lymphoma. Her tumor is high grade but very
responsive to chemotherapy. She underwent her first cycle
2 days prior and now is admitted with hyperkalemia and
decreased urine output.
Physical exam:Unremarkable
Labs:Serum creatinine is 4.2 mg/dL (normal 0.5 1.0 mg/dL). K+
is 5.9 (normal 3.5 5.2 mEq/L), phosphorus 7 (normal 2.4 4.2
mg/dL), uric acid 15 mg/dL (normal 3.0 6.5mg/dL)
Urine analysis shows uric acidcrystals.
47-year-old Woman withNon-
What type of acute kidney injury does she have?
Acute tubularobstruction
from uric acid or tumor
lysis syndrome
Oliguric
Acute tubular obstruction
66. Test case
You are asked to see a 47-year-old woman who has a history
of Non- lymphoma. Her tumor is high grade but very
responsive to chemotherapy. She underwent her first cycle
2 days prior and now is admitted with hyperkalemia and
decreased urine output.
Physical exam:Unremarkable
Labs:Serum creatinine is 4.2 mg/dL (normal 0.5 1.0 mg/dL). K+
is 5.9 (normal 3.5 5.2 mEq/L), phosphorus 7 (normal 2.4 4.2
mg/dL), uric acid 15 mg/dL (normal 3.0 6.5mg/dL)
Urine analysis shows uric acidcrystals.
47-year-old Woman withNon-
Acute tubularobstruction
from uric acid or tumor
lysis syndrome
Oliguric
Acute tubular obstruction
What type of acute kidney injury does she have?
Acute tubular obstruction due to tumor lysis syndrome
68. Acute Tubular Obstruction
Precipitation of a substance in tubules:
Occurs in settingof volume
depletion andacidic urine
• Protein
• Urate
• Calcium phosphate
• Intratubular crystal
69. Causes of Acute Tubular Obstruction
• Multiple myeloma (plasmacell
dyscrasia/malignancy)
• Overproduction of immunoglobulin light
chains are produced and filtered into the
urine
• Occurs following chemotherapy
• Large tumor burden
• Intracellular release of uricacid,
phosphate, potassium
Tumorlysissyndrome
Cast nephropathy
70. Causes of Acute Tubular Obstruction
• Bowel preparation for colonoscopy
• Acute calcium phosphate depositionin
tubules with associated interstitial
inflammation
• Highest risk in patients withunderlying
CKD
• Intravenousacyclovir
• Methotrexate
• Sulfonamide antibiotics
Medications
Phosphorus-containingenemas
71. • Known history of multiple myeloma
• Malignancy with recentchemotherapy
administration (tumor lysissyndrome)
•
oral sodium phosphorus laxative
• Medications review
• IV acyclovir, methotrexate,sulfonamides
Acute TubularObstruction Diagnostic Workup History & ChartReview
75. Acute TubularObstruction Treatment
Cast nephropathy
Chemotherapy agents
(dexamethasone,proteasomal
inhibitor-based regimen)
Tumor lysissyndrome
Isotonic fluids (saline) and uric acid
lowering agents (allopurinol or
rasburicase)
Acute phosphatenephropathy
(phosphorus containing
enemas/laxatives)
Supportive care
Medication-induced crystalline
nephropathies
Remove offending drug
76. Test case
You are asked to see a 63-year-old man who was admitted with
nausea, fatigue and lethargy. He is taking no new medications
other than clopidogrel which he started 5 weeks ago following
coronary angiography with stent placement to his left
circumflex.
Physical exam:Skin exam demonstrateslivedo reticularis (lace-
like purplish discoloration)
Labs:Serum creatinine is 3.9 mg/dL (normal 0.5 1.0 mg/dL).
CBC has an increased number of eosinophils on the differential.
Serum complement levels are low. Urine analysis is bland.
63-year-old Man with Nausea, Fatigue and Lethargy
What type of acute kidney injury does he have?
77. Test case
You are asked to see a 63-year-old man who was admitted with
nausea, fatigue and lethargy. He is taking no new medications
other than clopidogrel which he started 5 weeks ago following
coronary angiography with stent placement to his left
circumflex.
Physical exam:Skin exam demonstrateslivedo reticularis (lace-
like purplish discoloration)
Labs:Serum creatinine is 3.9 mg/dL(normal 0.5 1.0 mg/dL).
CBC has an increased number of eosinophils on the differential.
Serum complement levels are low. Urine analysis is bland.
63-year-old Man with Nausea, Fatigue and Lethargy
What type of acute kidney injury does he have?
Renal atheroembolicdisease
Microvascular ischemia
Renal atheroembolic
syndrome
Helps to distinguish
atherembolic disease from
ATN from radiocontrast
78. Test case
You are asked to see a 63-year-old man who was admitted with
nausea, fatigue and lethargy. He is taking no new medications
other than clopidogrel which he started 5 weeks ago following
coronary angiography with stent placement to his left
circumflex.
Physical exam:Skin exam demonstrateslivedo reticularis (lace-
like purplish discoloration)
Labs:Serum creatinine is 3.9 mg/dL(normal 0.5 1.0 mg/dL).
CBC has an increased number of eosinophils on the differential.
Serum complement levels are low. Urine analysis is bland.
63-year-old Man with Nausea, Fatigue and Lethargy
What type of acute kidney injury does he have?
Renal atheroembolicdisease
Renal atheroembolicdisease
Microvascular ischemia
Renal atheroembolic
syndrome
Helps to distinguish
atherembolic disease from
ATN from radiocontrast
81. Causesof Vascular Disease Renal Atheroembolic Disease
• Embolizesdistally partial or total occlusion
of multiple small arteries or glomerular
arterioles
occurs
• Serum creatinine risesubacute
between 2 8 weeks following
manipulation/procedure
• Contrast to radiocontrast exposurewhich
causes rise in creatinine within 72h
• Associated with low complement in serum,
eosinophilia,and rash (livedoreticularis)
Plaque
82. Causesof Vascular Disease Renal Atheroembolic Disease
• Embolizesdistally partial or total occlusion
of multiple small arteries or glomerular
arterioles
occurs
• Serum creatinine risesubacute
between 2 8 weeks following
manipulation/procedure
• Contrast to radiocontrast exposurewhich
causes rise in creatinine within 72h
• Associated with low complement in serum,
eosinophilia,and rash (livedoreticularis)
93. • Cholesterolemboli
• Low complements
• Peripheral eosinophilia
• Urine analysis is bland or may have
cholesterol crystals
VascularDisease Diagnostic Workup Laboratory Evaluation
95. VascularDisease Treatment
Renal atheroembolic disease
(cholesterol emboli)
• Supportive care
Vasculitis
• Immune-mediated therapy
directed at underlying cause
Thrombotic microangiopathies
• TTP plasma exchange
• Shiga-toxin HUS supportive care
• Complement mediatedTMA
eculizumab
• Drug-induced TMA remove
offending drug
96. Test case
You are asked to see a 62-year-old woman who was admitted
with nausea, fatigue, lethargy, and hemoptysis.
Physical exam:Hypertensive 160/98 mmHG Imaging:CXR
shows bilateral interstitial infiltrates Labs:Serum creatinine
is 3.6 mg/dL (normal 0.5 1.0mg/dL).
Urine analysisshows, proteinuria, dysmorphic red blood cells
and red blood cell casts.
62-year-old Woman with Nausea, Fatigue and Lethargy
What type of acute kidney injury does she have?
97. Test case
You are asked to see a 62-year-old woman who was admitted
with nausea, fatigue, lethargy, and hemoptysis.
Physical exam:Hypertensive 160/98 mmHG
Imaging:CXRshows bilateral interstitial infiltrates
Labs:Serum creatinine is 3.6 mg/dL (normal 0.5 1.0 mg/dL).
Urine analysis shows, proteinuria, dysmorphic red blood cells
and red blood cell casts.
62-year-old Woman with Nausea, Fatigue and Lethargy
What type of acute kidney injury does she have?
Nephritic process
Nephritic syndrome
Pulmonary renalsyndrome
(glomerular disease)
98. Test case
You are asked to see a 62-year-old woman who was admitted
with nausea, fatigue, lethargy, and hemoptysis.
Physical exam:Hypertensive 160/98 mmHG
Imaging:CXRshows bilateral interstitial infiltrates
Labs:Serum creatinine is 3.6 mg/dL (normal 0.5 1.0 mg/dL).
Urine analysis shows, proteinuria, dysmorphic red blood cells
and red blood cell casts.
62-year-old Woman with Nausea, Fatigue and Lethargy
What type of acute kidney injury does she have?
Nephritic syndrome, microscopicpolyangiitis
Nephritic process
Nephritic syndrome
Pulmonary renalsyndrome
(glomerular disease)
100. Rapidly Progressive Glomerulonephritis (RPGN)
Type I
Anti-glomerular basement
membrane (anti-GBM)
disease
Type III
Pauci-immune/
ANCA-associated
vasculitis/glomerulonephritis
Type II
Immune complex diseases
• Lupus nephritis
• IgAnephropathy
• Post-infectious glomerulonephritis
• Membranoproliferative glomerulonephritis
Many disease involve the glomerulibut
only RPGNspresent as acute kidney injury!
102. • Urine sedimentevaluation
• Dysmorphic red blood cells
• Red blood cell casts
• May have white blood cellcasts
• Urine Na+ <20 meq/L FENa
Renal biopsy isdefinitive.
GlomerularDisease Diagnostic Workup Laboratory Evaluation
103. • Urine sedimentevaluation
• Dysmorphic red blood cells
• Red blood cell casts
• May have white blood cellcasts
• Urine Na+ <20 meq/L FENa
Renal biopsy isdefinitive.
GlomerularDisease Diagnostic Workup Laboratory Evaluation
104. • Urine sedimentevaluation
• Dysmorphic red blood cells
• Red blood cell casts
• May have white blood cellcasts
• Urine Na+ <20 meq/L FENa
Renal biopsy isdefinitive.
GlomerularDisease Diagnostic Workup Laboratory Evaluation
.
105. Test case
You are asked to see a 66-year-old man who was admitted with
obstructive voiding symptoms (hesitancy, dribbling, double
voiding). His symptoms worsened after taking an over-the-
counter cold medicine.
Physical exam:Tender to palpation over hissuprapubic
region
Labs:Serum creatinine is 2.0 mg/dL (normal 0.5 1.0 mg/dL).
BUN is elevated to 49 mg/dL. Urine analysis is bland.
66-year-old Man withVoiding Symptoms
What type of acute kidney injury does he have?
.
106. Test case
You are asked to see a 66-year-old man who was admitted with
obstructive voiding symptoms (hesitancy, dribbling, double
voiding). His symptoms worsened after taking an over-the-
counter cold medicine.
Physical exam:Tender to palpation over hissuprapubic
region
Labs:Serum creatinine is 2.0 mg/dL (normal 0.5 1.0 mg/dL).
BUN is elevated to 49 mg/dL. Urine analysis is bland.
66-year-old Man withVoiding Symptoms
What type of acute kidney injury does he have?
Benign prostatic hyperplasia/
hypertrophy (BPH)
Acute obstruction of urine
outflow in this setting
Urinary obstruction
107. Test case
You are asked to see a 66-year-old man who was admitted with
obstructive voiding symptoms (hesitancy, dribbling, double
voiding). His symptoms worsened after taking an over-the-
counter cold medicine.
Physical exam:Tender to palpation over hissuprapubic
region
Labs:Serum creatinine is 2.0 mg/dL (normal 0.5 1.0 mg/dL).
BUN is elevated to 49 mg/dL. Urine analysis is bland.
66-year-old Man withVoiding Symptoms
What type of acute kidney injury does he have?
Post-renal, obstructive uropathy from benign
prostatic hyperplasia/hypertrophy(BPH)
Benign prostatic hyperplasia/
hypertrophy (BPH)
Acute obstruction of urine
outflow in this setting
Urinary obstruction
108. • Obstruction of the flow of urine anywhere from the
renal pelvis to theurethra
• Renal failure can be acute orsubacute
ObstructiveUropathy
.
109. Calculi
• Stone at the ureteropelvic junction in a
solitary kidney or bilateral staghorncalculi
• Can be seen in youngerand older adults
Anatomic abnormalities
(most commonly seen in children)
• Urethral valves
• Stricture
• Stenosis at the ureterovesicalor
ureteropelvic junction
Causesof ObstructiveUropathy
111. • BPH: hesitancy, dribbling, double voiding
• Stones
• Flank pain
• Gross hematuria
• History of malignancy
ObstructiveUropathy Diagnostic Workup History and Chart Review
112. • BPH: enlarged prostateon
digital rectal exam
• Stones:tenderness to
percussion at the costovertebral
angle
• Malignancy:palpation of an
abdominal/pelvic mass
ObstructiveUropathy Diagnostic Workup Physical Exam
113. • BPH:enlarged prostate on
digital rectal exam
• Stones:tenderness to
percussion at the costovertebral
angle
• Malignancy:palpation of an
abdominal/pelvic mass
ObstructiveUropathy Diagnostic Workup Physical Exam
114. • BPH: enlarged prostateon
digital rectal exam
• Stones:tenderness to
percussion at the costovertebral
angle
• Malignancy:palpation of an
abdominal/pelvic mass
ObstructiveUropathy Diagnostic Workup Physical Exam
115. Imaging
• Renal ultrasound
• Hydronephrosis
• CT of the abdomen/pelviswithout
radiocontrast
• Best for calculi and pelvic masses
Laboratory evaluation
• BUN: Creatinineratio > 20:1
• Urine sediment is bland or maycontain
crystals in the case ofcalculi/stones
ObstructiveUropathy DiagnosticWorkup
116. Imaging
• Renal ultrasound
• Hydronephrosis
• CT of the abdomen/pelviswithout
radiocontrast
• Best for calculi and pelvic masses
Laboratory evaluation
• BUN: Creatinineratio > 20:1
• Urine sediment is bland or maycontain
crystals in the case ofcalculi/stones
ObstructiveUropathy DiagnosticWorkup
117. Imaging
• Renal ultrasound
• Hydronephrosis
• CT of the abdomen/pelviswithout
radiocontrast
• Best for calculi and pelvic masses
Laboratory evaluation
• BUN: Creatinineratio > 20:1
• Urine sediment is bland or maycontain
crystals in the case ofcalculi/stones
ObstructiveUropathy DiagnosticWorkup
118. BPH
• Urinary catheter insertion
• Removal of medications that canprecipitate
obstruction (αagonists)
• Medical and surgical therapy forprostate
Stones
• Stone removal
• Ureteral stent placement
• Nephrostomy
ObstructiveUropathy Treatment
119. BPH
• Urinary catheter insertion
• Removal of medications that canprecipitate
obstruction (αagonists)
• Medical and surgical therapy forprostate
Stones
• Stone removal
• Ureteral stent placement
• Nephrostomy
ObstructiveUropathy Treatment
125. Complications from Acute Kidney Injury
Uremia Electrolyte abnormalities
• Nausea
• Vomiting
• Anorexia
• Dysgeusia
• Altered cognition
• Pericarditis
• Hyperkalemia
• Aminoglycosides,
cisplatin can cause
hypokalemia due to
polyuria/increased
urinary flow
• Metabolic acidosis
• Extracellular volume
excess
• Volume overload
(edema)
Chronickidneydisease
• Unresolved AKIor
repeated episodes of
AKI can lead to CKD
126. • Look for episodes of prolongedhypotension
• ICU septic shock
• Medicationand nephrotoxinexposure
• Radiocontrast exposure
• NSAIDs, aminoglycosides,amphoteracin,
medications that can cause intratubular
crystal precipitation (Acyclovir)
• Medications that cause AIN(penicillins)
General Approach to a Patient with AcuteKidney Injury
Take a goodhistory!
127. • Estimatevolume status(neck veins, skin turgor)
• Look for rash(exanthematousdrug rash or livedo
reticularis)
Imaging
• Ultrasoundto rule out obstruction
General Approach to a Patient with AcuteKidney Injury
Do agood physical exam!
128. • Urine Na+ and FENato distinguish between
prerenal diseaseand ATN
• Proteinuria and hematuriaonurinanalysispoints
to glomerular disease
• Crystalscan be seen with intratubularcrystal
obstructionand nephrolithiasis(stones)
General Approach to a Patient with AcuteKidney Injury
Always look at theurine!
.
129. • Sediment review
• Muddy brown casts ATN
• White blood cell casts AIN
• Dysmorphic red blood cells, redblood
cell casts, white blood cellcasts
RPGN
• Renal biopsy inselect cases
General Approach to a Patient with AcuteKidney Injury
Always look at theurine!
130. • Maintain renal arterialperfusionby
ensuring mean arterial pressure(MAP)
> 65/70 mmHG
• Avoid further nephrotoxicexposures
including
• NSAIDs, nephrotoxic medications
• Ensurerenally cleared medicationsare
function or GFR
Treatment of Acute Kidney Injury General Principles
131. Renal replacementtherapy(dialysis)
• Indicated in patients who have
complications of acutekidney
injury
• Refractoryacidemia
• Volume overload (extracellular
volume excess)
• Hyperkalemia
• Uremia
Treatment and Prevention of Acute Kidney Injury General Principles
