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GU: Clin Med IIA > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

Group of dx that all result in ￬ GFR and subsequent ￪ BUN and/or serum Cr, often with ￬ urine volume

A

AKI

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

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2
Q

AKI Criterias

A
  1. KDIGO - Most recent, most preferred
  2. RIFLE Criteria - Risk, Injury, Failure, Loss, ESRD
  3. AKIN (Acute Kidney Injury Network) Criteria
  4. All correlate with prognosis in AKI patients
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3
Q

Increase by 1.5-1.9x baseline w/n 7 d OR increase by >0.3 mg/dL w/n 48 hrs
<0.5 mL/kg/h x 6-12 hrs
what is this KDIGO stage?

A

1

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4
Q

increase by 2-2.9x baseline
<0.5 mL/kg/h for >12 hrs
what is this KDIGO stage?

A

2

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5
Q

increase by >3x baseline, >4mg/cK, OR pts <18 y/o with decrease in estimated GFR to <35 mL/min/1.72m2
<0.3 mL/kg/h for >24 hrs OR anuria for >12 hrs
what is this KDIGO stage?

A

3

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6
Q

normal urine output amount

A

800-2000 mL/day

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7
Q

< 50 mL/24 hrs of urine output is considered what?

A

anuria
Ominous finding!
Acute obstruction, cortical necrosis, aortic dissection, etc.

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8
Q

< 400 mL/24 hrs of urine output is considered what?

A

Oliguria
Poor prognostic sign in AKI
Higher mortality and poorer recovery than non-oliguric AKI

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9
Q

excessive urine (2500 - 3000 mL/day +) is considered what?

A

Polyuria

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10
Q

￪ nitrogenous wastes in the blood
is called what?

A

Azotemia

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11
Q

nonspecific sx caused by elevated nitrogenous waste (esp urea) in the blood is called what?
what are the sx?

A

Uremia
General - weakness, fatigue
Neuro - tremors, seizures, encephalopathy, confusion, coma
Skin - itching, dryness
CV - pericardial effusion, pericarditis, HTN
GI - anorexia, N/V
Other - shallow breaths/tachypnea, metabolic acidosis

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12
Q

risk factors for AKI

A
  1. renal problems
    - History of CKD or AKI
    - Single functioning kidney
  2. meds
    - ACEIs or ARBs
    - Antimicrobials - Aminoglycosides, Amphotericin B, PCNs, Vancomycin
    - Immunosuppressants - Cyclosporine, Methotrexate
    - Diuretics
    - Iodinated contrast agents
    - NSAIDs
    - PPIs
  3. hypoperfusion
    - Hypovolemia - Trauma, hemorrhage, GI loss
    - Sepsis
  4. Comorbidities
    - HF, Liver disease, DM, BPH
    - Infection (renal or systemic)
    - Cancer
    - >65 y/o
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13
Q

what can determine the risk of developing mod-severe AKI in next 12 hrs in critically ill patients

A

NephroCheck - emerging technology

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14
Q

MCC of AKI (40-80%)
Caused by renal hypoperfusion

A

Prerenal azotemia

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15
Q

major categories of AKI

A
  1. Prerenal azotemia
  2. Intrinsic kidney injury
  3. Postrenal obstruction
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16
Q

Up to 50% of all cases of AKI
Direct injury to 1+ renal structures

A

Intrinsic kidney injury

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17
Q

LCC of AKI (5-10%)
Caused by obstruction of urinary flow

A

Postrenal obstruction

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18
Q

causes of Prerenal Azotemia

A

Inadequate renal perfusion
1. Hypovolemia - dehydration, hemorrhage, GI loss, diuresis, pancreatitis, burns, peritonitis, etc.
2. Decreased CO - decompensated HF, cardiogenic shock, PE, pericardial tamponade, arrhythmias, liver failure (hepatorenal syndrome)
3. Changed vascular resistance
- ￬ - sepsis, anaphylaxis, anesthesia
- ￪ - EPI, high-dose dopamine, RAS
- Meds interfering renal vascular autoregulation - NSAIDs, iodinated contrast, ACEIs/ARBs

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19
Q

￬ GFR and ￪ BUN/Cr with BUN:Cr ratio > 20:1 is usually seen in what category of AKI

A

Prerenal Azotemia

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20
Q

for prerenal azotemia, If oliguric, there should be a ____ fractional excretion of sodium (FENa+) in the urine

A

low - <1%
Kidney can still reabsorb sodium
Often have normal urine osmolality

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21
Q

what would the urinary sediment look like with prerenal azotemia

A

usually normal
may see hyaline casts - Formed from Tamm-Horsfall mucoprotein secreted by tubule

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22
Q

s/s of prerenal azotemia

A
  1. Uremia is possible (depending on stage)
  2. Signs of cause - vary, may include:
    - Dehydration and/or hypovolemia
    - Arrhythmias, cardiomegaly
    - Sepsis
  3. Nonspecific diffuse abdominal pain and ileus
  4. May see decreased urine output
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23
Q

tx for prerenal azotemia

A
  1. resolve underlying cause
    - Maintain euvolemia
    - Correct abnormal electrolytes
    - Avoid nephrotoxic drugs
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24
Q

Obstruction of urinary outflow can affect the kidneys how?

A

Postrenal Obstruction

  1. Affecting both kidneys or a single functioning kidney
  2. Affecting one kidney and the second kidney cannot compensate

Elevated intraluminal pressure → damaged renal parenchyma

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25
Q

causes of postrenal obstruction

A

Obstruction of urethra, bladder, ureters, or renal pelvises
1. In men - BPH MCC
2. Devices - Obstructed Foley catheter
3. Meds - anticholinergic
4. Other causes - cancer, retroperitoneal fibrosis, neurogenic bladder
- Rare - blood clots, stones or strictures of the urethra or bilateral ureters, bilateral papillary necrosis

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26
Q

s/s of Postrenal Obstruction

A
  1. Anuria or polyuria possible
  2. May have lower abdominal pain
  3. May see large prostate, distended bladder, pelvic/abdominal mass
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27
Q

what can be helpful to look for hydroureter and obstruction

A

Bladder catheterization and/or abdominopelvic US

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28
Q

lab findings of postrenal obustrction

A
  1. ￬ GFR and ￪ BUN/Cr with BUN:Cr > 20:1 usually
  2. Urine sodium - varies
  3. Urine osmolality - 400 mosm/kg or less
  4. Urine sediment - often normal; may see RBCs, WBCs, crystals
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29
Q

intrinsic kidney injury is usually caused by ?

A

direct damage
infections, sepsis, nephrotoxins, ischemia

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30
Q

possible sites of intrinsic kidney injury?

A

tubules, glomeruli, interstitium, vasculature

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31
Q

in many causes, what is a precursor cause of tubular injury?

A

prerenal azotemia

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32
Q

3 types of intrinsic kidney injury

A
  1. acute tubular necrosis (MC)
  2. acute glomerulonephritis
  3. acute interstitial nephritis
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33
Q

AKI due to tubular damage

A

acute tubular necrosis (ATN)
85% of intrinsic AKI

34
Q

3 causes of ATN

A
  1. ischemia - inadequate GFR and blood flow
    - prolonged hypotension or hypoxemia
  2. nephrotoxins - endo- or exogenous
    - EXO MC
  3. sepsis - both hypoperfusion and direct injury
35
Q

what are the exogenous nephrotoxins that cause ATN (6)

A
  1. aminoglycosides: up to 30% of pt
    - 5-7 days of tx
    - Can remain in renal tissues up to 1 month
    - Trough levels are most useful to predict toxicity
  2. amphotericin B - >2-3g
  3. other antimicrobials
    - abx - vanc, sulfonamides, cephalos, tetracycline
    - Antivirals - acyclovir, foscarnet
  4. radiographic contrast media
    - Pre-existing DM and kidney dysfunction poses greatest risk (15-50%)
  5. chemo/immunosuppressant - MTX, cyclosporine, cisplatin
  6. environmental toxins
    - Heavy metals
    - Ethylene glycol
    - Insecticides/herbicides
36
Q

what aminoglycoside is least nephrotoxic

A

Streptomycin

37
Q

what may reduce the risk of exogenous nephrotoxin from radiographic contrast media?

A

3 mL/kg/hr IV 0.9% NS over 4-6 hrs before and after contrast

38
Q

due to rhabdomyolysis, muscle necrosis causing ATN

A

Myoglobinuria

39
Q

what can cause myoglobinuria that eventually leads to endogenous nephrotoxins

A
  1. Directly damaging to tubules; can also cause tubule obstruction
    - Crush injury, muscle necrosis from prolonged unconsciousness
40
Q

ATN from directly damaging to tubules can lead to a CK of ?

A

> 20,000-50,000 IU/L

41
Q

what can happen to the urine with Myoglobinuria - ATN

A
  1. false (+) dipstick for hemoglobin
  2. appears dark brown, but has no RBCs on microscopy
42
Q

tx for ATN - Myoglobinuria

A
  1. rehydration
    - Hypocalcemia may occur but usually self-corrects with rehydration
    — No calcium replacement needed unless severe or symptomatic
    - Hyperkalemia, hyperphosphatemia, hyperuricemia may also occur
43
Q

what endogenous nephrotoxin is seen in transfusion reactions and hemolytic anemia

A

Hemoglobinuria

44
Q

tx for Hemoglobinuria ATN

A

Reversal of underlying disorder, hydration

45
Q

which endogenous nephrotoxin is seen in rapid cell turnover and lysis

A

hyperurcemia

46
Q

usual cause of hyperuricemia

A

chemo for germ cell neoplasms, leukemia, lymphoma

47
Q

Intratubular deposition of ___ causes hyperuricemia ATN?

A

uric acid crystals
Serum uric acid often > 15-20 mg/dL
Medications to lower uric acid level can help

48
Q

what endogenous nephrotoxin is directly toxic, obstructs tubules that causes ATN
Seen in association with multiple myeloma

A

Bence Jones Protein

49
Q

s/s ATN

A

Signs of underlying cause
May see arrhythmias, abdominal pain, uremia
Oliguric or nonoliguric

50
Q

labs for ATN

A
  1. Hyperkalemia and hyperphosphatemia MC
  2. ￬ GFR and ￪ BUN/Cr with BUN:Cr < 20:1 usually
  3. Urine Na elevated
  4. Urinary sediment - pigmented granular casts or “muddy brown” casts, renal tubular cells, epithelial cell casts
51
Q

tx for ATN

A

remove cause, avoid complications
1. Avoid volume overload and hyperkalemia
- Volume overload - loop diuretics or dialysis (if persistent/severe)
— Diuretics not shown to improve recovery or reduce risk of death
- No improvement in outcomes with diuretics in oliguric AKI
2. Dietary changes
- Protein restriction - to prevent metabolic acidosis
- ￪ or ￬ dietary phosphate, calcium, magnesium

52
Q

MCC of acute glomerulonephritis

A

nephritic

53
Q

almost all acute glomerulonephritis involves the development of ?

A

inflammatory glomerular lesions
crescent lesions = severe breaks in glomerular walls

54
Q

pt comes in with HTN, edema, and urine containing protein, RBCs, WBCs, and RBC casts
what is most likely the diagnosis?

A

acute glomerulonephritis

55
Q

what are the types of acute glomerulonephritis

A
  1. Immune Complex Deposition
  2. Anti-GBM-associated acute glomerulonephritis
  3. C3 Glomerulopathy
  4. Monoclonal Ig-Mediated Glomerulonephritis
  5. Pauci-Immune Glomerulonephritis
56
Q

when antigen excess over antibody production occurs
what type of acute glomerulonephritis?

A

Immune Complex Deposition

57
Q

what lodge in glomerular basement membrane (GBM) that causes immune complex deposition?

A

antigen-antibody complexes
Complement activation to resolve complexes → destruction of GBM

58
Q

MCC of Immune Complex Deposition

A

1. post-infectious - endocarditis and strep
2. autoimmune disease - lupus
3. IgA nephropathy (Berger disease)
4. membranoproliferative (MPGN)
5. cryoglobulinemic glomerulonephritis (HCV)

59
Q

Autoantibodies against glomerular basement membrane (GBM)
May be confined to kidney or involve lungs as well
what type of acute glomerulonephritis

A

anti-GBM-associated acute glomerulonephritis
Can cause pulmonary hemorrhage

60
Q

what type of acute glomerulonephritis is renal + pulmonary involvement

A

Goodpasture’s Syndrome - Anti-GBM-associated acute glomerulonephritis

61
Q

deposition in the glomerulus, +/- Ig deposition
Minimal role played by immunoglobulins, unlike other GN
Caused by abnormalities in the alternative complement pathway
what type of acute glomerulonephritis?

A

C3 Glomerulopathy
(C3 deposition)

62
Q

what lab can help identify C3 glomerulopathy

A

Low serum C3 levels
normal C3 DOES NOT r/o

63
Q

deposited in GBM and/or tubular basement membrane
No excess amounts of antigen as seen in immune complex GN
Associated with monoclonal gammopathies
what type of acute glomerulonephritis?

A

Monoclonal Ig-Mediated Glomerulonephritis

64
Q

what can help identify Monoclonal Ig-Mediated Glomerulonephritis, and what other tests?

A
  1. Serum Protein Electrophoresis (SPEP)
  2. immunofixation and free light chain analysis
65
Q

small-vessel vasculitis associated with ANCAs
Can see manifestations in other areas of the body
Tissue injury secondary to cell-mediated immune processes
what type of acute glomerulonephritis?

A

Pauci-Immune Glomerulonephritis

66
Q

Other Causes of pauci-immune glomerulonephritis besides cell-mediated immune processes

A

HTN emergencies, thrombotic microangiopathies (HUS, TTP)

67
Q

pt comes in with severe HTN and swelling of his scrotum, what is the most likely diagnosis?

A

Acute Glomerulonephritis
Often have HTN and edema
Edema seen first in body parts with low tissue tension - Scrotal edema, periorbital edema

68
Q

potential labs to get and their results of glomerulonephritis

A
  1. Serum Cr rises over days - months
    - BUN:Cr ratio not reliable kidney fxn marker, but can help assess volume status
  2. Urinalysis - hematuria, moderate proteinuria
  3. Urine sediment - RBCs, WBCs, RBC casts
  4. Complement levels - low levels may help
    - C3 and C4 low in immune complex GN
    - C3 alone low in C3 glomerulonephropathy
  5. ASO titers - help evaluate for recent strep infection
  6. anti-GBM antibodies
  7. SPEP
  8. P-ANCA and C-ANCA levels
  9. Other general autoimmune labs - CRP, ESR, ANA
69
Q

tx for acute glomerulonephritis

A
  1. underlying disease process!
    - High-dose corticosteroids
    - Cytotoxic agents may be used
    - Plasma exchange - Goodpasture disease, pauci-immune glomerulonephritis
70
Q

Interstitial inflammatory response
Edema and possible tubular damage
Cell-mediated immune reactions predominate
what type of intrinsic AKI?

A

Acute Interstitial Nephritis

71
Q

causes of acute interstitial nephritis

A
  1. meds (MC)
    - Antimicrobials - PCNs (β-lactams), cephalosporins, rifampin, sulfonamides, HIV drugs
    - Others - diuretics, NSAIDs, rifampin, anticonvulsants, allopurinol, PPIs, H2 blockers
  2. Infections -
    - Bacterial - strep, staph, diphtheria, legionella, rickettsia (RMSF)
    - Viral - CMV, EBV
    - Fungal - histoplasmosis
  3. Immunologic - SLE, Sjogren’s, sarcoidosis, etc.
    - MCC glomerulonephritis
  4. Others - allergic reaction, collagen vascular disease
72
Q

fever, rash, arthralgia is the classic triad for what intrinsic AKI?

A

Acute Interstitial Nephritis

73
Q

labs of Acute Interstitial Nephritis

A
  1. CBC - eosinophilia
  2. Urine sediment - WBCs (95%), RBCs, eosinophiluria, WBC casts
    - < proteinuria unless NSAID-related
  3. Renal biopsy - inflammatory cells within renal interstitium
74
Q

tx for Acute Interstitial Nephritis

A
  1. removal of cause, supportive care
    - IV or oral corticosteroids if renal injury
    persists
    - Urgent dialysis may be necessary in up to ⅓ of all pts
75
Q

Serum BUN:Cr - > 20:1
Concentration of Na - < 20
Fractional Excretion of Na - < 1%
Osmolality (mosm/kg) - > 500
Urine Sediment - Benign or hyaline casts
what type of AKI?

A

Prerenal Azotemia

76
Q

serum BUN: Cr > 20:1
Na concentration Varies
fractional excretion of Na Varies
osmolality - < 400
urine sediment - Benign or RBC, WBC, crystals
what type of AKI?

A

Postrenal Azotemia

77
Q

BUN:Cr < 20:1
Na concentration > 20
fractional excretion of Na > 1% (if oliguric)
osmolality 250-300
urine sediment - Granular (muddy brown) casts, renal tubular casts
what type of AKI

A

ATN - intrinsic kidney injury

78
Q

BUN:Cr > 20:1
[Na] < 20
fractional excretion of Na < 1%
osmolality Varies
urine sediment - RBC, WBC, RBC casts
what type of AKI

A

Acute Glomerulonephritis
Intrinsic Kidney Injury

79
Q

BUN:Cr < 20:1
[Na] Varies
fractional excretion of Na < 1%
osmolality Varies
urine sediment - RBC, WBC, WBC casts, eosinophiluria
what type of AKI

A

Acute Interstitial Nephritis
Intrinsic Kidney Injury

80
Q

other diagnostic tools for AKI

A
  1. Abdominal/Pelvic US
    - Most AKI - normal-sized kidneys
    - Acute interstitial nephritis - Enlarged kidneys
    - Hx of CKD - normal, or may see small or polycystic kidneys
    - Postrenal AKI - May see dilated urine collecting system proximal to point of obstruction
  2. Urethral Cath - r/o urethral obstruction
  3. Bladder Scan - r/o urethral obstruction
  4. Kidney Biopsy
    - Primarily when prerenal, postrenal, and ischemic/nephrotoxic AKI etiologies have been ruled out
    - Can help dx glomerulonephritis, vasculitis, interstitial nephritis, etc.

GU: Clin Med IIA (13 decks)

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