SM 195a - AKI: Pre, Post, and Intrinsic Flashcards
What diagnostic studies could help you diagnose post-renal AKI?
- Post-void residual bladder volume reveals lower tract obstruction
- Renal ultrasound reveals upper tract obstruction
- Non-contrast CT
- BUN/Serum Cr ratio
- >20:1 implies enhanced urea reabsorption
- Also elevated in prerenal AKI
How are electrolyte derangements in post-renal AKI resolved?
They resolve on their own after post-obstructive duresis
(Diuresis naturally occurs after obstruction is relieved; will stop when the patient achieves electrolyte and volume homeostasis)
What infections are associated with acute interstitial nephritis (AIN)?
HIV, sepsis, legionella
The presence of eosinophils, WBCs, and WBC casts in the urine would increase your suspicion for which cause of AKI?
What would you expect from urine Na+?
Acute Interstitial Nephritis (AIN)
Urine Na+ >30 mEq/L
(This implies that the tubules are not working to reabsorb Na+)
What laboratory results would be consistent with pre-renal AKI?
- Urin Na:
- FENa:
- BUN/SCr:
- Sediment:
- Urin Na: < 20 mmol/L
- Implies increased Na+ reabsorption
- FENa: <1%
- BUN/SCr: >20
- Implies increased reabsorption of urea
- Sediment: bland
- Implies no intrinsic kidney injury
These numbers are consistent with physiological responses to decreased perfusion to the kidney
What are the ischemic causes of ATN?
- Pre-renal
- Pre-renal AKI that persists can cause ATN
(an intrinsic AKI)
- Pre-renal AKI that persists can cause ATN
- Sepsis
As blood pressure falls, what adaptations occur in the kidney in order to maintain blood flow into the glomerulus?
As mean arterial pressure falls, when does this mechanism begin to fail??
Autoregulation
- Afferent arteriole dilates
- Due to prostaglandins
- Efferent arteriole constricts
- Due to RAAs activation -> ANG II secretion
Autoregulation begins to fail when mean arterial BP falls below 80 mmHg
What are the broad categories of causes of intrinsic AKI?
- Glomerular
- Acute glomerular nephritis (AGN)
- Tubular
- Acute tubular necrosis (ATN)
- Interstitial
- Acute interstitial nephritis (AIN)
- Vascular
What is the effect of decreased effective blood volume + NSAIDS on GFR?
Decreased EBV + NSAIDS -> Decreased GFR
NSAIDS inhibit the vasodilatory prostaglandins that normally cause vasodilation of the afferent artriole when EBV drops (autoregulation)
Inability to dilate the efferent arteriole -> decreased GFR
What is the most common cause of AKI in hospitalized patients?
- Pre renal
- Intrinsic
- Post renal
b. Intrinsic
Usually tubular etiology (ex: acute tubular necrosis)
What is Acute Interstitial Nephritis (AIN)?
Interstitial etiology of intrinsic AKI
Most often associated with drugs/medications, also think of infection, cancer, or autoimmune
What lab results would be consistent with interstitial AKI?
- Blood, WBCs in the urine
- Eosinophils in the urine
- WBC casts
Use of nephrotoxic drugs and/or recent infection increase suspicion for acute interstitial nephritis (AIN) as a cause of AKI
All of the following physical or laboratory findings would be suggestive of pre-renal AKI except:
A. Orthostatic hypotension
B. Urine sodium of 75
C. BUN/Cr ratio of 30
D. Urine Osmolality of 500
B. Urine sodium of 75
Usually urine Na+ is low (<20) in pre-renal AKI
Most signs of pre-renal AKI are consistent with low EBV
What are the major interstitial causes of intrinsic AKI?
- Acute Interstitial Nephritis
- Usually drug-induced, abx a common culprit
- Infiltration
- Lymphoma, sarcoidosis
- Some herbs
- Aristolochic acid
How does obstruction distal to the kidney lead to post-renal AKI?
- Obstruction distal to the kidney
- -> Increased hydrostatic pressure in the renal pelvis
- -> Decreased GFR
Can also cause…
- Derangements in urinary concentrating ability
- Na+ imbalance
- Acute -> Na+ reabsorption
- Chronic -> Na+ wasting
- Defects in K+ and H+ secretion
List 3 risk factors for developing AKI
Hypvolemia
Older age
Underlying chronic kidney disease
AKI due to hypo-perfusion to the kidney is classified as _____________
AKI due to hypo-perfusion to the kidney is classified as pre-renal AKI
What is the effect of prostaglandins on GFR?
Explain
Prostaglandins -> Incresae in GFR
Dilate the afferent arteriole to increase perfusion to the glomerulus
The presence of muddy brown casts in the urine would increase your suspicion for which cause of AKI?
What woudl you expect from urine Na+?
Muddy brown casts = Acute Tubular Necrosis (ATN)
Urine Na+ > 30 mEq/L
(This implies that the tubules are not working to reabsorb Na+)
Name 2 diagnostic tests/maneuvers to rule out post-renal problems as the cause of AKI
Renal ultrasound
Foley catheter placement
What features of a patient’s history and PE are consistent with pre-renal AKI?
-
History - Anything that causes decreased effective blood volume
- Vomiting, diarrhea
- Hemorrhage
- Overdiuresis
- Burns
- Fevers
- Pancreatitis, Heart failure, liver disease
-
Physical exam - Any signs of volume depletion
- Decrease in SBP ≥20 mm Hg or DBP ≥10 mmHg whn going from sitting to standing
- Poor skin turgor
- Dry buccal mucosa
- Congestive HF
- Edema
- Signs of liver disease
What features of a patient’s history and PE are consistent with intrinsic AKI?
- History
- Recent infection
- Hemoptysis, sinusitis, pharyngitis, other infection
- Muscle trauma w/rhabdomyolysis
- Red urine
- Use of nephrotoxic medications
- IV contrast
- Recent infection
- Physical exam
- Edema
- Signs of recent infection
- Rash
- Muscle tenderness
What is the effect of decreased effective blood volume on GFR?
Decreased blood volume -> GFR remains normal
(Up to a point, and then GFR decreases)
- Vasodilatory prostaglandins -> afferent arteriole dilation
- Local angiotensin II -> efferent arteriole constriction
Describe the proper management of a patient with post-renal AKI
Rapid diagnosis and relief of obstruction are necessary to preserve kidney function
- Relief of obstruction
- Percutaneous nephrostomy tube placement
- Bladder catheter placement
Expect post-obstructive diuresis; resolves on its own when the patient returns to electrolyte and volume homeostasis
What features of a patient’s history and physical exam would be consistent with post-renal AKI?
-
History
- Decreased urinary stream
- Nocturia
- Frequency
- Dribbling
- Flank pain
- Anuria
-
Physical exam
- Distended bladder
- Enlarged prostate
- Abdominal or pelvic masses
Describe the pathophysioogy of hepatorenal syndrome
Healthy kidneys, diseased liver
- Splanchnic artirial vasodilation
- -> Compensatory vasconstriction in other systems
- -> Impaired Na+ and H2O handling
- -> Ascites, edema
- -> Further decrease in effective blood volume
PE findings are consistent with prerenal AKI that is unresponsive to volume repletion
The US Renal Data System suggests that ESRD accounts for nearly _____% of all Medicare expenditures.
The US Renal Data System suggests that ESRD accounts for nearly 7% of all Medicare expenditures.
What is the effect of Angiotensin II on GFR?
Explain
Angiotensin II -> increased GFR
Causes constriction of the efferent arteriole to increase hydrostatic pressure in the glomerulus
(Note: Decreased volume and solute delivery to the macula densa
-> Renin secretion -> Increased RAAs activity ->
increased Angiotensin II production)
If a patient has AKI, are they more likely to have hyperkalemia or hypokalemia?
Hyperkalemia
The kidneys are not doing a good job secreting K+
Acute tubular necrosis may be ________ or
________ in etiology
Acute tubular necrosis may be ischemic or
nephrotoxic in etiology
What causes of intra-tubular obstruction can cause ATN?
- Myeloma
- -> Proteins aggregate and block tubules
- Tumor lysis syndrome
- -> Uric acid crystalization
- Drugs: Acyclovir, methotrexate
The presence of RBCs and RBC casts in the urine would increase your suspicion for which cause of AKI?
What would you expect from urine Na+?
RBCs, RBC casts = Glomeruloneprhitis
Urine Na+ < 20 mEq/L
(This implies that the tubules are working to properly reabsorb Na+)
What is hepatorenal syndrome?
Basically, pre-renal AKI caused by liver failure
- A consequence of renal vasoconstriction in the setting of normal kidneys and andvanced liver disese
- Pre-renal AKI unresponsive to volume repletion
- Oliguria, bland urine sediment, UNa <10
What causes post-renal AKI?
Obstruction anywhere in the urinary tract (distal to the kidney) that causes AKI
- Ureters
- Must be bilateral to cause AKI if there are 2 functional kidneys
- Tumors, calculi, clots, fibrosis, lymphadenopathy
- Bladder neck
- Tumors, calculi, clots, prostate enlargement, neurogenic
- Urethra
- Strictures, tumors, obstructed catheters
Would a patient with post-renal AKI more likely be hyperkalemic or hypokalemic?
Hyperkalemic
Impaired K+ excretion
(Chronic: Decreased Na+ reabsorption ->
Decreased K+ secretion)
What factors are released when glomerular filtration is reduced?
Renin -> RAAs -> Angiotensin II
Prostaglandins
Aldosterone
ADH
What is the prognosis for a patient with post-renal AKI for <1 week?
What about >12 weeks?
< 1 week = likely to have a near complete recovery
> 12 weeks = almost no recovery possible
Would a patient with post-renal AKI more likely have metabolic acidosis or alkylosis?
Acidosis
Impaired H+ secretion
What is the most common cause of intrinsic AKI in hospitalized patients?
Tubular problems (Acute Tubular Necrosis) -> AKI
Usually caused by ischemia, toxins, or pigments
What nephrotoxins cause ATN?
- Exogenous
- Aminoglycosides
- IV contrast dye
- Some herbs
- Endogenous
- Myoglobinuria
- Muscle trauma, crush injury, malignant hyperthermia, drug-induced
- Hemoglobinuria
- Mechanical destruction of RBCs,
- Transfustion reaction
- Heat stroke
- Burns
- Venoms
- Myoglobinuria
Aldosterone and ADH are secreted in response to
________ glomerular filtration.
What is the effect?
Aldosterone and ADH are secreted in response to
decreased glomerular filtration.
Aldosterone -> increased Na+ reabsorption
ADH -> increased H2O reabsorption
The result is concentrated urine with low Na+ content
(conservation of sodium and water to increase blood volume)
What do you look for in a urine sediment if you suspect intrinsic AKI?
- Renal epithelial cells
- Muddy brown casts
- => Tubular problem (Acute Tubular Necrosis)
- RBC casts
- => Glomerular problem (glomerular nephritis)
- WBC casts
- => Inflammation (Acute Interstitial Nephritis)
What is normal for serum creatinine?
Adult Male: 0.6 - 1.2 mg/dL
Adult Female: 0.5 - 1.1 mg/dL
What drugs are associated with acute interstitial nephritis (AIN)?
- Penicillins
- Rifampin
- Cephalosporins
- Allopurinol
- NSAIDs
What are the most common vascular etiologies of AKI?
- Vascular obstruction/occlusion
- Thrombosis or embolism of the renal artery or vein
- Must be bilateral to cause AKI
- Vasculitis
In what scenarios would you have a increased FENa in pre-renal AKI?
If the patient is taking duretics
(Usually FENa <1% in pre-renal AKI becuase the tubules are able to appropriately reabsorb Na+)
How is AKI diagnosed?
ONE of the following
- Increase in serum creatinine
- Increase of 0.3 mg/dL above baseline in 48h
- Increase in serum creatinine of 1.5x baseline in 7 days
- Decrease in urine output
- <0.5 mL/kg/hr for 6 hours
Does post-renal AKI cause sodium reabsorption or sodium wasting?
- Acute -> Na+ reabsorption
- Chronic -> Na+ wasting
What is the effect of decreased effective blood volume + ACEI or ARB on GFR?
Decreased GFR
Angiotensin II normally causes constriction of the efferent arteriole as a part of autoregulation of GFR
ACEI or ARB -> Decreased RAAs -> Decreased Angiotensin II -> efferent arteriole does not constrict
The result is low GFR
What are the most common causes of pre-renal AKI?
- Hypovolemia – most common
- Hypotension
- Pharmacologic
- Large-vessel compromise
s post-renal AKI more common in the inpatient or outpatient setting?
Outpatient
If a patient has AKI, are they more likely to have metabolic acidosis or alkylosis?
Acidois
(W/ urine that is not acidified/does not contain NH4+, which implies that the kidneys are not properly secreting H+)
Which of the following would be appropriate for the management of a patient with pre-renal AKI?
- Start iv fluids, eg normal saline
- Stop ACE Inhibitor (Lisinopril)
- Stop ibuprofen
- Check for post-void residual urine; place catheter into the bladder
- All of the above
e. All of the above
Goal = increase EBV, increase perfusion to the kidney
AKI complicates ____% of all hospital admissions and _____% of critical care admissions
AKI complicates 5-7%** of all hospital admissions and **65% of critical care admissions
Pre-renal AKI is the most common cause of AKI in the _________ setting
Pre-renal AKI is the most common cause of AKI in the outpatient setting
