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CVPR > CVPR Week 8: AKI > Flashcards

CVPR Week 8: AKI Flashcards

1
Q

Objectives

A
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2
Q

Identify

A
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3
Q

Excretion =

A

Excretion = filtration - reabsorption + secretion

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4
Q

What happens at 1, 2, 3 and 4?

A
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5
Q

Textbook definition of AKI

A

an acute sustained decrease in renal function

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6
Q

What is the practical or research definition of AKI?

A

AKI is a serum creatinine increase > 0.3 mg/dL within 48 hours

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7
Q

What is the cutoff for AKI and why is it used?

A
  • the cutoff is 0.3 mg/dL within 48 hours because
  • 1.0 mg/dL (would be normal) / 1.3 mg/dL (increase in serum Cr) = .76 which is 24% decrease in renal function
  • Studies have shown that a Cr rise > 0.3 mg/dL is associated with adverse outcomes in hospitalized patients
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8
Q

Adverse outcomes within hospitalized patients for a > 0.3 mg/dL rise in Cr

A
  • Higher risk of progression to CKD and ESKD
  • Higher risk of cardiovascular mortality
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9
Q

AKI hose?

A
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10
Q

What is the force behind filtration?

A

Filtration is “powered” by cardiac contraction proved by BP

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11
Q

What is the typical glomerular hydrostatic pressure?

A

~55 mmHg inside the glomerulus

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12
Q

What is the oncotic pressure of the arteriole vs the glomerulus

A

~30 mmHg pulling ultrafiltrate back into the glomeruli

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13
Q

What is the glomerular capsule hydrostatic pressure?

A

~15 mmHg pushing water back into the glomerular capillaries

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14
Q

What is a typical net filtration pressure?

A

so 55mmHg (hydrostatic into the capsule) - (30 mmHg (oncotic pressure back into the capillary from the capsule) + 15 mmHg (glomerular capsule hydrostatic pressure) = 10 mmHg (net filtration pressure out of the capillaries)

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15
Q

Describe how the kidney performs filtration

A
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16
Q

What is GFR?

A

The glomerular filtration rate which is how much plasma is being filtered by the kidneys in one minute

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17
Q

If the normal GFR is cut in half how does this represent a change in kidney function

A

a 50% decrease in GFR is akin to a 50% decrease in normal kidney function

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18
Q

At what GFR is dialysis needed?

A

< 10 mL/min

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19
Q

When is GFR valid?

A

GFR only applies in a steady state CKD ok but not in AKI

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20
Q

Calculate the amount of plasma filtered per day if the average person has

4 L of plasma

and assume GFR = 100 mL/min

A
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21
Q

How many times is plasma cleaned in a dialysis session?

A
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22
Q

CKD-EPI equations

A
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23
Q

Types of AKI etiologies

A
  • Prerenal AKI
  • Intrarenal AKI
  • Postrenal AKI
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24
Q

What is the most common type of outpatient AKI?

A
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25
Q

What is the most common type of hospital-acquired AKI?

A
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26
Q

Case #1

A
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27
Q

What does stenosis do to renal blood flow?

A
  • stenosis decreases renal blood flow and therefore glomerular capillary hydrostatic pressure
  • also, patients with RAS usually have increased Renin -> high angiotensin II which normally helps to maintain filtration pressure in the face of reduced afferent blood flow by promoting efferent vasoconstriction
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28
Q

Are ACEi and ARB renoprotective?

A

yes they work by reducing efferent vasoconstriction (over the long term, reducing net filtration pressure does offer renoprotection to the glomerulus)

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29
Q

Does GFR change after starting an ACEi/ARB?

A

Yes the net filtration pressure is reduced and this offers renoprotection

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30
Q

Describe a typical prerenal AKI scenario

A
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31
Q

Prerenal AKI pathology

A
  • Renal blood flow autoregulation is overwhelmed by hypovolemia
  • In hypovolemia, renal blood flow is reduced and kidneys will try to maintain constant glomerular pressure of 55 mmHg
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32
Q

Kidney mechanisms of autoregulation in hypovolemia

A

In hypovolemia, renal blood flow is reduced and kidneys will try to maintain constant glomerular pressure of 55 mmHg by 2 processes

  • Efferent arteriole vasoconstriction
  • Afferent arteriole vasodilation
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33
Q

How does afferent renal vasodilation occur/?

A
  • myogenic reflex
  • tubuloglomerular feedback
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34
Q

What is the myogenic reflex

A

less blood flowing into afferent arteriole -> less arteriolar stretching -> arteriole reflexively vasodilate -> allowing more blood flow into the glomerulus

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35
Q

What is tubuloglomerular feedback?

A

Hypovolemia -> less afferent blood flow -> increased NaCl reabsorption at PCT to retain volume -> less NaCl delivery to the DCT -> sensed by receptors at macula densa lining DCT -> releases NO and prostaglandin -> promote afferent vasodilation -> allowing more blood flow into the glomerulus

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36
Q

Describe efferent vasoconstriction by RAAS activation

A
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37
Q

Prerenal AKI =

A

reduced glomerular hydrostatic pressure through hypovolemic shock

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38
Q

Causes of hypovolemic shock

A
  • hemorrhage
  • plasma loss through burns
  • diuresis
  • diabetes insipidus
  • Decreased body fluids
  • GI-loss through (Nausea, Vomiting, Diarrhea)
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39
Q

What is the best way to diagnose prerenal AKI?

A

good Hx pointing to hypovolemia

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40
Q

Tests to help diagnose prerenal AKI

A
  1. BUN/Cr ratio
  2. Fractional excretion of sodium (FENa)
  3. Fractional excretion of urea (FEurea) if on diuretics that increases renal sodium excretion

The rationale for these tests is based on the fact that the kidneys want to retain more volume in prerenal AKI by absorbing more sodium and urea (meaning lower sodium and urea concentrations in urine)

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41
Q

BUN:Cr ratio in prerenal AKI

A

BUN:Cr ratio > 20

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42
Q

Can BUN:Cr be higher than 20 without a prerenal AKI?

A
  • Lower Cr production from malnutrition
  • Higher BUN production from steroid use or GI bleed
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43
Q

Can you have a BUN:Cr ratio < 10 and still have a prerenal AKI?

A

Yes, when lower BUN production from low protein intake

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44
Q

What is a normal BUN:Cr ratio?

A

Ratio is normally < 10

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45
Q
A
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46
Q

FENa AKA

A

Fractional excretion of Na+

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47
Q

What does a FENa < 1% mean?

A

Prerenal AKI

  • Means < 1% of filtered Na+ is excreted while >99% is reabsorbed to increase volume
  • Also seen Na+ avid states like CHF/cirrhosis where effective circulating volume is low so the RAAS activated to retain Na+
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48
Q

Situations where a FENa < 1% but isn’t an AKI

A
  • Hepatorenal syndrome (Na+ avid state)
  • Acute tubular necrosis in the setting of cirrhosis or heart failure (Na+ avid state)
  • Contrast nephropathy -> ATN (contrast -> afferent vasoconstriction -> RAAS -> aldosterone causes kidney to retain more sodium)
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49
Q

FENa =

A

UNa x PCr x 100%

PNa x UCr `

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50
Q

FEurea AKA

A

Fractional excretion of urea

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51
Q

FEurea =

A

Urine urea x Plasma urea x 100%

Plasma urea x urine Cr

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52
Q

FENa on diuretics

A
  • patients on diuretics may have an increased Na+ excretion so FENa becomes less reliable unless it is still <1%
  • FEurea may replace FENa for patients on diuretics
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53
Q

FEurea on diuretics

A
  • Urea excretion is not affected by diuretic use
  • Urea excretion is reduced in prerenal AKI to retain volume
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54
Q

FEurea levels to indicate an AKI?

A

FEurea <35% -> indicates prerenal AKI with > 90% specificity

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55
Q

Not really sure

A
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56
Q

Tx of AKI

A
  • Hold diuretics
  • BP medications to minimize renal hypoperfusion
  • Replete volume with IVF patients who are hypovolemic
  • Discontinue medications that disable the protective mechanisms of afferent vasodilation (NSAIDs) or efferent vasoconstrictions *ACEi, ARBs)
  • Try to maintain MAP (mean arterial pressure) > 65 mmHg to ensure adequate renal perfusion
  • Dialysis is almost never needed in prerenal AKI even when potassium is very elevated
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57
Q

Dialysis in AKI

A

Dialysis is almost never needed in prerenal AKI even when potassium is very elevated

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58
Q

Where does an ATN tubular injury occur?

A
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59
Q

Where does atheroembolic renal disease occur?

A
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60
Q

Where does glomerulonephritis with injury to glomeruli occur?

A
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61
Q

Where does AIN interstitial injury occur?

A
62
Q

Describe the features of a typical case of Acute Tubular Sclerosis

A
63
Q

ATN AKA

A

Acute tubular necrosis

64
Q

Identify

A
65
Q

Histological features of ATN

A
66
Q

Classes of etiologies of ATN

A
  • Ischemic injury
  • Exogenous nephrotoxic injury
  • Endogenous nephrotoxic injury
67
Q

ATN ischemic injury causes

A

Shock

  • Septic
  • Cardiogenic
  • Hemorrhagic
68
Q

ATN exogenous nephrotoxic injury causes

A
69
Q

ATN endogenous neprhotoxic injury causes

A
70
Q

Why are the proximal tubules so vulnerable to ischemic/toxic injury?

A
  • Kidney receives 25% of Cardiac output so it is more vulnerable to hypotension
  • Outer medulla (location of proximal tubules) is at watershed area and chronically hypoxic at baseline but has high O2 use due to lots of Na+/Cl- ATPase (70% of NaCl reabsorbed at PCT)
  • Drug/toxins become more concentrated in tubular fluid as water is reabsorbed
71
Q

What area of the kidney has the lowest blood supply

A
72
Q

Oliguria in ATN

A
  • 70% of all ATN cases will have oliguria
  • why are the kidneys not doing enough filtration to make urine
  • Glomeruli (site of filtration) are actually intact in ATN. It is the proximal tubules that are damaged in ATN
73
Q

What is Oliguria?

A

50 mL/day < UOP < 500 mL/day

74
Q

What is anuria?

A

UOP < 50mL/day

75
Q

What is the injured site in ATN?

A
  • The proximal tubules are damaged
  • the glomeruli is intact
76
Q

Why is oliguria common in ATN?

A

Oliguria is a protective mechanism to prevent further tubular loss into the urine through tubuloglomerular feedback

77
Q

How is oliguria protective in ATN?

A
  • 99% of the daily filtered plasma is reabsorbed by healthy tubules and retunred to systemic circulation
  • If ATN, of glomeruli keep filtering while injure proximal tubules are not reabsorbing at 99% capacity than a person can become severely volume depleted if filtraton is not scaled back or stopped all together
78
Q

What is the mechanism of oliguria in ATN?

A

tubuloglomerular feedback

79
Q

When was IV fluid invented?

A

during the 1832 cholera epidemic

80
Q

IV and tubuloglomerular feedback

A
81
Q

Describe the mechanism of tubuloglomerular feedback

7 steps

A
82
Q

ATN clinical course phases

3 listed

A
  • Induction and expansion phase
  • maintenance phase
  • Recovery phase
83
Q

Clinical course of ATN: Induction and expansion phase

A

Cr steadily rises and UOP drops

84
Q

Clinical course of ATN: Maintenance phase

A
  • Cr rise is stabilized, with bery low or no UOP
  • Dialysis may be needed for volume control or hyperkalemia during this phase
  • A flat Cr maybe a sign the kidneys are about to get better
85
Q

Tx of ATN

A
  • No specific treatment/supportive care only
86
Q

Tx of ATN if hypotensive

A

give IVF to keep MAP > 65 mmHg to ensure renal perfusion

87
Q

Loop diuretics in ATN

A

Loop diuretics do not make ATN better (theoretically Lasix reduces O2 consumption at the renal tubules by blocking Na/K/Cl channels)

88
Q

Dialysis for ATN

A

Dialysis may sometimes be required for refractory hypervolemia or electrolyte derangements

89
Q

The worst predictor of mortality in ATN

A

Fluid gain > 10% of baseline body weight is the worst predictor of mortality in ATN

90
Q

AEIOU in Tx of?

A

ATN

91
Q

AEIOU

A
  • Acidosis (refractory pH < 7.1)
  • Electrolyte (refractory hyperkalemia > 6.5, hypercalcemia > 13 with oliguria)
  • Intoxication (ethylene glycol, lithium toxicity)
  • Overload of volume (unable to maintain O2 sat)
  • Uremia
92
Q

Uremia is a ________, not high ________ level

A

Uremia is a clinical syndrome, not a high BUN level

93
Q

Uremia is a clinical syndrome, not high BUN level

A
  • CNS (fatigue, confusion, myoclonic jerks, hiccups)
  • GI (nausea, vomiting, anorexia)
  • CVS (pericardial effusion)
94
Q

AIN AKA

A

Acute interstitial nephritis

95
Q

Describe a typical case of acute interstitial nephritis

A
96
Q

AIN histological features

A
97
Q

Identify

A
98
Q

Common etiologies of AIN

A
  • Medications account for 70% of AIN
  • Infections account for 10%
  • the other 20% consist of rare causes
99
Q

Medications that cause AIN

A
  • Penicillins (nafcillin)
  • Quinolones (cipro)
  • Bactrim
  • PPIs (due to widespread use)
  • Loop diuretics
100
Q

Infections that cause AIN

A
  • CMV
  • Legionella
  • HIV
  • EBV (mononucleosis
101
Q

Rare causes of AIN

A
  • Autoimmune disorders like lupus, Sjogren’s
  • TINU syndrome
  • Hypercalcemia (recent case at UNMH, pt has sarcoidosis in lungs but renal biopsy shows no granulomatous lesions, just interstitial infiltrate, takes no meds)
102
Q

AIN delayed type III hypersensitivity reaction

A
  • 3-4 days response in which performed IgG+drug antigen forms immune complex getting trapped on kidneys and causing inflammatory interstitial injury in the kidneys
  • Glomeruli are spared so urine has no protein or hematuria
  • Almost always reversible when offending agents stopped
103
Q

Clinical features of AIN

A
  • Asymptomatic in most cases
  • Constitutional symptoms (fever, chills, malaise, etc.)
  • Bilateral flank tenderness due to renal inflammation
  • Traditional triad: fever, rash, eosinophilia seen only in 10% of cases
104
Q

Urine eosinophils for AIN

A

neither sensitive nor specific

105
Q

AIN Dx

A

mostly a clinical diagnosis based on Hx of recent new drug exposure, unexplained Cr rise, and findings of WBC or WBC cast in urine

106
Q

Tx of AIN

A
  • Discontinuing suspected offending agent should lead to improvement of renal function within 3-7 days in most cases
  • If Cr does not improve in 3-7 days or worsens, consider renal biopsy or empiric trial of steroid at 1 mg/kg for one month with fast taper
  • Complete recovery may take up to 6 weeks
107
Q

Describe a typical case of rapidly progressing glomerulonephritis

A
108
Q

Case 4 question

A
109
Q

In anti-GBM disease?

A

The autoantibodies turn against type IV collagens in the glomeruli and lung tissues

110
Q

What is pulmonary renal syndrome

A
  • hemoptysis
  • with renal failure and/or hematuria
111
Q

Pulmonary renal syndrome DDx

A
  • ANCA vasculitis (microscopic polyangitis and Wegener’s -> now called granulomatosis with polyangitis)
  • Anti-GBM disease (AKA goodpasture disease)
  • Lupus nephritis
112
Q

ANCA vasculitis

A

ANCA vasculitis is due either to anti-MPO (myeloperoxidase) or anti-PR3 (proteinase), which are antigens only expressed in immature neutrophils confined to bone marrows and may be associated with cocaine abuse

113
Q

Scleroderma

A

Centromere and anti-SCL 70 antibodies are associated with scleroderma, which can cause scleroderma renal crisis (sudden and dramatic increase in BP)

114
Q

RPGN immunofluorescence

A
115
Q

RPGN syndromes

A
116
Q

RPGN pathophysiology

A
117
Q

RPGN AKA

A

Rapidly progressing glomerulonephritis

118
Q

RPGN types?

A
  • Nephrotic syndrome
  • Nephritic syndrome
119
Q

Nephrotic syndrome etiology

A

Due to noninflammatory causes (autoantibody) that direct against podocytes foot processes

120
Q

Nephritic syndrome etiology

A

Due to inflammatory causes (immune-complexes) that damages glomerular capillaries

121
Q

Nephrotic syndrome proteinuria

A

massive proteinuria > 3 g /day

122
Q

Nephritic syndrome proteinuria

A

Subnephrotic proteinuria < 3 g / day

123
Q

Nephrotic syndrome hematuria

A

Usually no hematuria

124
Q

Nephrotic syndrome edema

A

massive edema

125
Q

Nephritic syndrome edema

A

mild edema

126
Q

Nephrotic syndrome examples

A
  • Membranous nephropathy (autoantibodies to phospholipase A2 receptors on podocytes)
  • Minimal changed disease
127
Q

Nephritic syndrome examples

A
  • Lupus nephritis
  • ANCA vasculitis
128
Q

Tests to order in suspected glomerulonephritis

A
129
Q

Describe how to work up suspected glomerular diseases

A
130
Q

Tx of Glomerulonephritis

A
131
Q

Indications for immunosuppression in Tx of glomerulonephritis

A
  • nephrotic proteinuria > 3.5 g
  • Crescents on biopsy
  • Rapid decline in renal function
  • examples lupus nephritis, ANCA vasculitis
132
Q

Tx regimen for glomerulonephritis

A

sometimes all is needed is just an ACEi or ARB such as mild IgA nephropathy or membranous nephropathy

  • Usually 6 cycles of alternating monthly cyclophosphamide and steroid for induction therapy
  • Followed by 12-24 months of azathioprine for maintenance therapy to prevent relapse
133
Q

Describe a typical case of postrenal AKI

A
134
Q

Case 5 question

A
135
Q

Tx of bladder outlet obstruction

A
  • immediate relief through placing Foley catheter
  • urethral sphincter smooth muscle contraction is activated by alpha receptors so alpha blockers like terazosin or tamsulosin
  • Many medications used by the elderly especially anticholinergics like oxybutynion and donepzil will promote bladder detrusor muscle relaxation and make urine obstruction worse
136
Q

Pathogenesis of postobstructive nephropathy

A
  • obstruction increases intratubular hydrostatic pressure -> leads to increased capsular hydrostatic pressure, a force that opposes the force of filtration
  • thus net filtration pressure is reduced in obstruction
137
Q

Sites of obstruction in postrenal AKI

A
138
Q

Ureter obstruction etiologies

A
139
Q

Bladder obstruction etiologies

A
140
Q

Urethra obstruction etiologies

A
141
Q

Agents that cause bladder detrusor muscle relaxation

A
  • Anesthetics
  • Anticholinergics (oxybutinyn and tolterodine)
  • Tricyclics (amitriptyline, nortryptiline)
  • Antihistamines
  • Antiparkinson medications
  • antipsychotics like Haldo
  • Muscle relaxants like baclofen
142
Q

Agents that cause urethral sphincter contraction

A
  • alpha-1 agonist (pseudoephedrine)
  • Alpha-1 blockers like flomax works by relaxing urethral sphincter and prostate smooth muscles
143
Q

Clinical manifestation of postrenal AKI

A
144
Q

Normal or high UOP?

A

does not rule out urine obstruction

145
Q

Dx of postrenal AKI

A
146
Q

Postrenal AKI ultrasound

A
147
Q

Tx of postrenal AKI

A
148
Q

Is renal failure from urine obstruction reversible?

A
149
Q

Postobstructive diuresis

A
150
Q

How to manage postobstructive polyuria

A

CVPR (93 decks)

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