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Intrinsic Renal Failure (exam2) Flashcards

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1
Q

Intrinsic causes of Renal Failure are up to what percentage

A

50%

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2
Q

The sites of damage for Intrinsic Renal Failure

A

Glomeruli, the interstitium, and or tubules

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3
Q

Most common cause of Intrinsic Renal Failure

A

Acute Tubular Necrosis (ATN)

-disease is secondary to ischemia or nephrotoxins

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4
Q

Nephrotic / Nephritic

A

Nephrotic think lots of protein loss. With Nephritic think lots of blood loss. So with nephritic think more of an inflammation process

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5
Q

ATN the BUN:Cr ratio is usually what

A

<20:1

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6
Q

what is ATN

A

Acute tubular necrosis

  • Acute damage to tubule epithelium of nephron
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7
Q

What percentage of Intrinsic AKI is from ATN

A

85% of cases

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8
Q

Two main causes of ATN

A

Ischemia & Nephrotoxin Exposure

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9
Q

GFR is increased or decreased in Ischemic Tubular injury

A

Decreased

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10
Q

How does Pre-Renal evolve into Intrinsic AKI

A

Because of Decreased or inadequate renal blood flow leading to hypoxic kidney cells and death of cells

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11
Q

Third leading cause of inpt Toxic tubular injuy comes from?

A

Radiologic contrast dye

Iatrogenic - happened by medical providers

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12
Q

Endogenous causes of toxic Tubular injury

A

Heme-containing proteins (myoglobin, hemoglobin)

heme- containing proteins, bence jones proteins, gout… etc.

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13
Q

Clinical presentation of ATN

A

Generally nonspecific signs and symptoms of Acute Renal Failure

They can include

  • Anorexia
  • Nausea/Vomiting
  • Delirium
  • weakness/fatigue
  • HTN
  • Coma/ seizures.
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14
Q

Diagnostic evaluation of ATN

A
  • Elevated BUN and Creatinine, Decreased GFT
  • usually BUN:Cr rat.- <20:1
  • Muddy brown sediment visible granular casts in Microscopic evaluation of Urinalysis
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15
Q

What electrolyte imbalances are often present with pts suffering from ATN

A

Hyperkalemia and Hyperphosphatemia

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16
Q

Urinary output of ATN

A

Variable

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17
Q

Renal absorption of sodium is often _______ . with ATN

A

impaired
- this results in and increased FEna - greater than or equal to 2%

increased sodium in urine

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18
Q

Tx of ATN

A

Remove the offending agent (if applicable)

Avoid volume overloading

Diuretics (if fluid overload)

Dialysis- may be included if life-threatening electrolyte abnormality.

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19
Q

Average maintenance phase of ATN is

A

1-3 wks

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20
Q

True or false - A nephrologists must be involved in all cases with ATN

A

True

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21
Q

What is Acute interstitial Nephritis

A

An inflammatory disorder of renal interstitium

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22
Q

What is the cause of Acute Iterstitial Nephritis in over 70% of cases

A

Drugs

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23
Q

Most common drugs that cause Acute Interstitial Nephritis

A

Penicillins, Cephalosporins, Sulfonamides, NSAID’s, PPIs, Rifampin, Phenytoin, and Allopurinol

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24
Q

Clinical presentations of Acute interstitial Nephritis

A

classic picture is that of a previously healthy pt developing suden renal dysfunction after starting a new medication (sometimes starting the new drug can cause a delay

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25
Common Clinical presentation of Acute Interstitial Nephritsi
Fever- (80$) Transient maculopapular rash(25-50%) Flank pain d/t renal capsule distension Myalgias and Arthralgias
26
Acute Interstitial Nephritis Diagnostic EValuation
Elevated BUN and Creatinine Decreased GFR hematuria is common Modest proteinuria WBC's present in urine in >95% of cases WBC casts CBC shows eosinophilia
27
True or false- renal imaging is helpful for Acute Interstitial Nephritis
False- not helpful
28
Renal Biopsy is or is not required for a definitirve diagnosis of Acute interstitial nephritis
Is =)
29
Treatment of Acute Interstitial Nephritis
Discontinue offending medication Supportive care 1/3 pts require temporary dialysis Corticosteroids
30
Most pts recover from acute interstitial Nephritis within?
a few weeks to months
31
Glomerulonephritis (GN) is comprised of what process
An inflammatory process involving primarily the glomerulus
32
what other structures can be effected by Glomerulonephritis
Renal vasculature interstitium tubular epithelium
33
Glomerulonephritis is relatively an uncommon cause of AKI corresponding to what percentage?
about 5%
34
What damage can occur due to Glomerular inflammation
Damage to the glomerular basement membrane or capillary endothelium
35
What is often the causation of the inflammatory process of Glomerulonephritis
Antigen-antibody complex formation and deposition
36
Where do complexes or antibodies become trapped to cause the inflammation during the filtration with GN
the glomerulus
37
what increases the risk / poorer prognosis with GN
The more glomeruli that are involved
38
Infection-related GN
Sequela of group A beta-hemolytic Strep or Staph Aureus infection
39
Clinical presentation of infection-related GN
Tea colored urine Edema (common around mouth) Oliguria HTN
40
What titer may be elevated for weeks in Infection-related GN
Antistreptolysin O (ASO)
41
Most kids will recover spontaneously, or will not recover from Infection-related GN
recover spontaneously
42
What percentage of Adults never fully recover from Infection-Related GN
30-70% of affected adults
43
What is the other name for IgA Nephropathy
Berger's Disease
44
Pathophys of IgA Nephropathy
Deposition of IgA immune complexes in the glomeruli, causing structural damage
45
What is the initial presentation of IgA Nephropathy
episode of hematuria
46
Hallmark of Burger's Disase
2-6 days of Hematuria
47
Confirmation of IgA Nephropathy
Renal Biopsy - IgA deposition on immunohistology
48
Tx of Burger's
Teat the HTN with ACE or ARB
49
What percentage of Burger's disease suffering pts will have recurrent episodes
50% -typically this leads to progressive, chronic loss of renal function and CKD
50
What is HSP
Henoch-Schonlein Purpura
51
Hsp is not only kidney disease but...
An acute systemic immune-mediated small vessel vasculitis
52
What is the population that HSP effects mostly
Children less than 10 years of age
53
Clinical presentation and course of Henoch-Schonlein Purpura
Children present with hematuria, and large purple purpura on lower extremities Arthralgias, abd pain, and proteinuria Generally self-limited resolving in 94% of pts within 4 weeks
54
Membranoproliferative GN is due to
deposition of immune-complex and or complement factors
55
What are the effects of Membranoproliferative GN
Mesangial cell proliferation and capillary wall remodeling
56
Common population of Membranoproliferative GN
Children and young adults
57
Clinical presentation of Membranoproliferative GN
Most commonly presents as nephrotic syndrome May present with recurrent gross hematuria
58
Diagnosis of Membranoproliferative GN requires what
Renal Biopsy
59
TX of Membranoproliferative GN
Corticosteroids and cyclophosphamide
60
if pts develop antibodies against the glomerular basement membrane (GBM) they have what disease
Anti-GBM Antibody Disease
61
because of tissue similarity in capillaries in the lung Anti-GBM antibodies may also do what
affect the Lungs and cause Hemorrhage
62
The anti-GBM antibody disease GN has also been known as what
Goodpasture's syndrome
63
Pts with Anti-GBM antibody disease GN can present how
with glomerulonephritis alone or with glomerulonephritis and hemoptysis together
64
Diagnosis of anti-GBM GN
Made with anti-GBM antibodies testing
65
TX for Anti-GBM GN
Plasma exchange, chemotherapy drugs, steroids
66
Lupus Nephritis GN is secondary to what disease
Systemic Lupus Erythematosus (SLE)
67
what percentage of Lupus pts suffer from Lupus Nephritis GN
about 50%
68
What is the pathogenisis of Lupus Nephritis
Antinuclear antibodies (ANA) form immune complexes and cause inflammation and glomerular damage
69
Diagnostic Criteria of Lupus Nephritis
Lupus, plus one or more of the following Persistent proteinuria Cellular casts RBCs and or WBCs consistently in urine
70
Indication of Renal biopsy is appropriate in all Lupus pts with evidence of nephritis
True
71
Tx of Lupus Nephritis depends on the severity of the disease but can include
High-dose corticosteroids which often are used to treat the autoimmune condition. ACE or ARB should be started as well
72
Rapidly Progressing GN's Clinical presentation
can be any of the glomerular conditions: not specific disease process.
73
What is the range that loss of renal function occurs in Rapidly Progressing GN
Days to weeks
74
Pts might have presentation of what in Rapidly progressing GN
Edema Proteinuria Hypertension RBC casts
75
What is Characteristic of RPGN
Crescent Formations on Renal Biopsy
76
RPGN is represented by what percentage of GN
roughly 20 percent
77
what is the Diagnostic Evaluation for a Glomerulonephritis (GN)
- Serum Creatinine can rise over days to months - UA showing hematuria and proteinuria - UA microscopy will show cellular elements, such as RBCs, RBC casts and occasional WBCs
78
What are characteristic of GN
RBCs and RBC casts
79
Treatment of GN
Depends on underlying condition causing glomerulonephritis the treatment may consist of - High dose steroids - Cytotoxic Agents like cyclophosphamide - Plamsa Exchange (Goodpasture's )
80
True or False - Although complex Glomerulonephritis does not need a Nephrologist involved with every pt case immediately
False- because of the complexity Nephrologists should be involved immediately. PC PA's should not attempt to manage these cases on their own .

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