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Clin med A 2 > AKI part 1 > Flashcards

AKI part 1 Flashcards

1
Q

AKI results in sudden decrease in what kidney functions

A

deceased ability to manage:
* fluid
* electrolytes
* acid base balance
* excretion of waste products (decreased excretion of urea and creatinine)

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2
Q

what labs result from AKI

A

deceased GFR
increased BUN and/or serum Cr
deceased Urine volume

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3
Q

what should you keep in mind when observing AKI

A

that by the time serum Cr rises, GFR usually has already fallen significantly!

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4
Q

What is the criteria for diagnosing AKI

A

KDIGO - Most recent, most preferred
RIFLE Criteria - Risk, Injury, Failure, Loss, ESRD
AKIN (Acute Kidney Injury Network) Criteria
All correlate with prognosis in AKI patients

dont think we need this

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5
Q

what is the KDIGO staging criteria for AKI

A

she said not testable so basically skip this

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6
Q

what is considered anuria and what does anuria indicate

A

<50mL/24 hrs
* Ominous finding!
* indicates Acute obstruction, cortical necrosis, aortic dissection, etc.

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7
Q

what is considered oliguria. what is oliguria indicative of

A

<400mL/24 hrs of urine output
* indicated poor prognosis in AKI
* Higher mortality and poorer recovery than non-oliguric AKI

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8
Q

what is considered polyuria

A

excessive urine (2500 - 3000 mL/day +)

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9
Q

what is azotemia

A

increased nitrogenous wastes in the blood

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10
Q

what is uremia and what are the symptoms

A

nonspecific symptoms caused by elevated nitrogenous waste (especially urea) in the blood

symptoms could include:
General - weakness, fatigue
Neuro - tremors, seizures, encephalopathy, confusion, coma
Skin - itching, dryness
Cardiovascular - pericardial effusion, pericarditis, HTN
GI - anorexia, nausea, vomiting
Other - shallow breaths/tachypnea, metabolic acidosis

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11
Q

risk factors for AKI

A

does not expect us to know but says that by the end of class this may be intuitive to us

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12
Q

Know the difference between prerenal, intrarenal and post renal (pic)

A
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13
Q

what are the three categories of AKI

A

prerenal azotemia
intrinsic kidney injury
postrenal obstruction

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14
Q

what is the MCC of AKI

A

prerenal azotemia

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15
Q

what is the least common cause of AKI

A

postrenal obstruction

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16
Q

what is prerenal azotemia

A

caused by inadequate renal perfusion due to:
* hypovolemia
* decreased cardiac output
* changed vascular resistance

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17
Q

what lab findings are present with prerenal azotemia

A
  • decreased GFR and increased BUN:Cr ratio (>20:1 usually)
  • if oliguric there should be low fractional excretion of sodium (FENa+) in the urine - <1%
  • normal Urinary sediment - may see hyaline casts
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18
Q

what are the signs and symptoms associated with prerenal azotemia

A
  • uremia
  • signs of cause (dehydration, sepsis, cardiomegaly ect)
  • diffuse abdominal pain and ileus
  • decreased urine output
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19
Q

what are the hyaline casts in urinary sediment caused by in prerenal azotemia

A

formed from Tamm-Horsfall mucoprotein secreted by the tubule

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20
Q

what is the treatment for prerenal azotemia

A

resolve underlying cause!

usually by:
* maintaining euvolemia
* correcting electrolytes
* avoid nephrotoxic drugs. (NSAIDS, ACEi, ARBs ect)

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21
Q

what is postrenal obstruction

A

obstruction of urinary outflow that is affecting one or both kidneys

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22
Q

what is the pathophysiology of postrenal obstruction

A

the obstruction causes elevated intraluminal pressure which leads to damaged renal parenchyma

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23
Q

what areas are common in postrenal obstruction

A

obstruction of urethra, bladder, ureters, or renal pelvises

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24
Q

what are common causes of postrenal obstruction

A
  • benign prostatic hyperplasia (MCC in men)
  • devices (foley cath)
  • medications (anticholinergics)
  • cancer
  • retroperitoneal fibrosis
  • neurogenic bladder

other rare causes can include:
* blood clots
* stones
* benign papillary necrosis

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25
Q

what are signs and symptoms of postrenal obstruction

A
  • anuria or polyuria
  • lower abdominal pain
  • large prostate, distended bladder, pelvic/abdominal mass
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26
Q

what is used to look for hydroureter and obstruction

A

bladder catheterization
or
abdominopelvic US

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27
Q

what are lab findings in postrenal obstruction

A
  • decreased GFR
  • increased BUN:Cr (>20:1)
  • urine sodium (varies)
  • urine osmolality of 400 or less
  • normal urine sediment (may see RBCs, WBCs or crystals)
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28
Q

What are intrinsic kidney injuries

A

direct damage to the kidney as a result of:
infections
sepsis
nephrotoxins
ischemia

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29
Q

what are the most common sites of instrinsic kidney injury

A
  • tubules
  • glomeruli
  • interstitium
  • vasculature
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30
Q

what can prerenal azotemia progress to

A

tubular injury (intrinsic kidney injury)

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31
Q

what are the major forms of intrinsic kidney injury

A
  • acute tubular necrosis
  • acute glomerulonephritis
  • acute interstitial nephritis
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32
Q

what is the most common intrinsic AKI

A

acute tubular necrosis (ATN)

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33
Q

what are the 3 major causes of ATN

A

ischemia (prerenal turning into intrinsic problem)
nephrotoxins
sepsis

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34
Q

what are the MC antimicrobial exogenous nephrotoxins?

A
  • Aminoglycosides - up to 30% of patients at therapeutic levels (typically begins 5-7 days after tx started)
  • Amphotericin B - nephrotoxic after 2-3 grams
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35
Q

what is the least nephrotoxic aminoglycoside?

A

streptomycin

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36
Q

what other antimicrobials are known to be exogenous nephrotoxins

A

ABX - vanc, sulfonamides, cephs, tetracycline
Antivirals - acyclovir, foscarnet

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37
Q

what non-antimicrobial things are known to be nephrotoxic

A
  • Radiographic contrast
  • chemo/immunosuppressant - MTX, cyclosporine, cisplatin
  • environmental toxins (heavy metals, ethylene glycol, insecticides/herbicides)
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38
Q

what is the endogenous nephrotoxins

A

Myoglobinuria
hemoglobinuria
hyperuricemia
Bence Jones Protein

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39
Q

what is myoglobinuria a result of

A

rhabdomyolysis and muscle necrosis

40
Q

How is myoglobinuria nephrotoxic

A

it is directly damaging to tubules and can cause tubule obstruction.

41
Q

what lab values often indicates presence of myoglobinuria

A
  • CK>20,000-50,000 IU/L
  • false + hemoglobin in urine dipstick
  • urine will appear dark brown but no RBCs are present on microscopy
42
Q

what is the mainstay of treatment for myoglobinuria

A

rehydration.

43
Q

what are possible complications of myoglobinuria

A
  • hypocalcemia (usually resolves on its own)
  • hyperkalemia
  • hyperphosphatemia
  • hyperuricemia
44
Q

when is hemoglobinuria seen

A
  • transfusion reaction
  • hemolytic anemia
45
Q

when is hyperuriciemia common

A
  • rapid cell turnover and lysis such as during chemo
46
Q

what lab value is seen with hyperuricemia

A
  • serum uric acid of >15-20mg/dL

intratubular deposition of uric acid crystals may also be seen

47
Q

how do you treat hyperuricemia

A

medications to lower uric acid may help

48
Q

how is Bence Jones Protein harmful

A

it is directly toxic to the kidneys and obstructs the tubules.

49
Q

when is Bence Jones Protein seen

A

Multiple myeloma

50
Q

what are signs and symptoms of ATN

A
  • signs of underlying cause
  • arrhythmias
  • abdominal pain
  • uremia
  • oliguria or nonoliguria (wow thats just great)
51
Q

what are labs associated with ATN

A
  • hyperkalemia and hyperphosphatemia
  • decreased GFR, increased BUN:Cr (<20:1)
  • elevated urine sodium
  • urinary sediment shows pigmented granular casts or “muddy brown” casts, renal tubular cells and epithelial cell casts
52
Q

what is the treatment for ATN

A
  • remove the cause and avoid complications
  • avoid volume overload and hyperkalemia
  • diet changes
53
Q

what should be done if a patient is at risk of volume overload with ATN

A

start loop diuretics or dialysis

54
Q

what dietary changes should be done in ATN

A
  • protein restriction to prevent metabolic acidosis
  • increase or decrease dietary phosphate, calcium and magnesium accordingly
55
Q

what is the prognosis for ATN

A

20-50% mortality rate
70% mortality rate in ICU
may never fully return to baseline renal function

56
Q

what suggests better long-term outcome for ATN

A

nonoliguric ATN

57
Q

what is acute glomerulonephritis

A

intrinsic glomerular AKI mostly involving inflammation of the glomerulus

58
Q

what are the two types of intrinsic glomerular AKI

A

nephritic - involving inflammation
nephrotic - minimal inflammation but with proteinuria present

59
Q

acute glomerular AKI (acute glomerularnephritis) is accountable for what percent of intrinsic AKI cases?

A

5%

60
Q

what is developed in almost all acute glomerulonephritis cases

A
  • inflammatory glomerular lesions
  • crescent lesions (severe breaks in glomerular walls)
61
Q

what is the classic presentation of acute glomerulonephritis

A

HTN
edema
urine containing protein, WBCs, RBCs and RBC casts.

62
Q

what are the different types of acute glomerulonephritis

A

immune complex deposition
Anti-GBM-associated
C3 Glomerulopathy
Monoclonal Ig-Mediated
Pauci-Immune glomerulonephritis

63
Q

what is immune complex deposition type acute glomerulonephritis

A

when antigen excess over antibody production occurs and antigen-antibody complexes get lodged in glomerular basement membrane.

64
Q

what are the causes of immune complex deposition

A
  • IgA nephropathy (Berger disease)
  • Post-infectious (especially seen with endocarditis and streptococcus)
  • Autoimmune disease (especially lupus)
  • Membranoproliferative (MPGN)
  • Cryoglobulinemic glomerulonephritis (HCV)
65
Q

what is Anti-GBM-associated acute glomerulonephritis

A

autoantibodies against glomerular basement membrane (GBM). This can be confined to the kidney or involve lungs as well

66
Q

what is Goodpastures syndrome

A

Anti-GBM-associated acute glomerulonephritis with pulmonary involvement

67
Q

what is C3 Glomerulopathy

A

C3 deposition in the glomerulus, +/- Ig deposition

68
Q

what causes C3 glomerulopathy

A

abnormalities in the alternative complement pathway

69
Q

what are labs that can indicate C3 Glomerulopathy

A

Low serum C3 levels can help identify, but normal C3 does not rule out

70
Q

What is monoclonal Ig-Mediated Glomerulonephritis

A

Monoclonal Ig deposited in GBM and/or tubular basement membrane.

no excess antigens as seen in immune complex GN

(so many antibodies floating around in blood stream that they just get stuck and cause destruction. )

71
Q

what labs can help identify monoclonal Ig-Mediated glomerulonephritis

A
  • Serum protein electrophoresis

can also use:
immunofixation
free light chain analysis

72
Q

what is Pauci-Immune Glomerulonephritis

A

small-vessel vasculitis associated with Antineutrophil cytoplasmic antibodies (ANCAs)

73
Q

what is the pathophysiology of pauci-immune glomerulonephritis

A
  • No immune complexes or direct Ig or complement deposition or binding
  • Tissue injury secondary to cell-mediated immune processes
  • Can see manifestations in other areas of the body (lungs, skin, upper airway)

pathophysiology probs isnt the right word here. Im doing my best lol

74
Q

what are other known causes of acute glomerulonephritis

A
  • hypertensive emergencies
  • thrombotic microangiopathies
75
Q

what are signs and symptoms of acute glomerulonephritis

A

HTN and edema.

edema usually begins with in body parts with low tissue tension such as scrotal edema or periorbital edema

(Edema caused because 1. na is being reabsorbed because kidneys sense damage. 2. protein is being lost in the urine. protein is responsible for keeping water in the vessels/cells and so without protein, water is moved out of the vessels and into the tissues) said in class

76
Q

what are lab findings in acute glomerulonephritis

A

Serum Cr (high)
Urinalysis - hematuria, moderate proteinuria
Urine sediment - RBCs, WBCs, RBC casts
complement levels - C3/C4 low in Gn, only C3 low in C# glomerulonephropathy
ASO titers - evaluate for recent strep infection
ANti-GBM antibodies
SPEP
P-ANCA and C-ANCA levels
Other general autoimmune labs - CRP, ESR, ANA

(in class - “ if you ask professor jensen which should I order first? just be like me and order all of them at once as soon as you are suspicious” )

77
Q

how do you treat acute glomerulonephritis

A
  • treat underlying disease
  • high dose corticosteroids
  • cytotoxic agents
  • plasma exchange for goodpasture disease and pauci-immune glomerulonephritis
78
Q

what is acute interstitial nephritis

A

interstitial inflammatory response causing inflammation of the area surrounding the tubules of the nephron (the interstitium)

79
Q

what percent of intrinsic AKI does acute interstitial nephritis account for

A

10-15%

80
Q

what are the causes of acute interstitial nephritis

A
  • medications (70%)
  • infections
  • immunologic
  • other
81
Q

what medications are known to cause acute interstitial nephritis

A

antimicrobials such as:
PCN, cephs, rifampin, sulfonamides, HIV drugs

Other meds: diuretics, NSAIDS, anticonvulsants, allopurinol, PPIs, H2 blockers

82
Q

what infections are potential causes of acute interstitial nephritis

A

bacterial - strep, staph, diptheria, legionella, rickettsia
viral - CMV, EBV
fungal - histoplasmosis

83
Q

what immunologic diseases could potentially cause acute interstitial nephritis

A

SLE
Sjogrens
Sarcoidosis

84
Q

what are the “other” causes of acute interstitial nephritis

A

allergic reaction
collagen vascular disease

85
Q

what are the signs and symptoms of acute interstitial nephritis

A

the classic triad:
* fever
* rash
* arthralgia

it says all three only present in 10% of patients which is so dumb, like why is it called the “classic triad” then

86
Q

what lab values are found in acute interstitial nephritis

A
  • eosinophilia
  • urine sediment with WBCs, RBCs, WBC casts, eosinophiluria.

minimal proteinuria unless it is NSAID related

87
Q

what labs/studies are ordered for Acute interstitial nephritis

A

CBC
Urine sediment
Renal biopsy

88
Q

what would a renal biopsy of acute interstitial nephritis show

A

inflammatory cells within renal interstitium

89
Q

what is the treatment for acute interstitial nephritis

A

removal of cause and supportive care

90
Q

If you remove the cause of acute interstitial nephritis and your patient is still suffering from renal injury what could you do

A

start oral or IV corticosteroids
urgent dialysis may be necessary in 1/3 of patients

91
Q

what is the prognosis of acute interstitial nephritis

A

recover over weeks to months
may have slightly better outcomes than other AKI causes

92
Q

How does a Abdominal/Pelvic US present in most AKI

A

normal-sized kidneys

93
Q

How does a Abdominal/Pelvic US present in acute interstitial nephritis

A

enlarged kidneys

94
Q

How does a Abdominal/Pelvic US present in patients with hx of CKD

A

normal, may have polycystic kidneys

95
Q

How does a Abdominal/Pelvic US present in postrenal AKI

A

may see dilated urine collecting system proximal to point of obstruction

96
Q

what diagnostic studies are used to rule out urethral obstruction when evaluating an AKI

A

urethral catheter
bladder scan

97
Q

when is a kidney biopsy used in AKI diagnosis

A
  • Primarily when prerenal, postrenal, and ischemic/nephrotoxic AKI etiologies have been ruled out
  • Can help dx glomerulonephritis, vasculitis, interstitial nephritis, etc.

Clin med A 2 (30 decks)

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