Acute Renal Failure Flashcards

(50 cards)

1
Q

Define azotemia

A

Excess of urea or other nitrogenous compounds in blood (aka high BUN)

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2
Q

MC causes of AKI

A
  • Prerenal (RBF, 40-80% of cases)
  • Intrinsic renal (small vessels, glomeruli, tubules)
  • Postrenal (obstruction to urine flow in ureters, bladder, urethra)
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3
Q

Pathophys of AKI

A
  • Low RBF leads to ischemia and cell death
  • Continued cell injury even after restoration of RBF
  • GFR is decreased and infiltrates leak
  • Dying cells slough off which obstruct tubules
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4
Q

Recovery from AKI is dependent upon what?

A

Restoration of normal RBF

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5
Q

Clinical presentation of prerenal failure

A
  • Hypovolemia
  • Elders w/vague mental status
  • CHF w/low renal perfusion
  • Restricted fluid access
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6
Q

Clinical presentation of intrinsic renal failure

A
  • Nephritic syndrome
  • Acute tubular necrosis
  • Pigment induced AKI
  • Allergic interstitial nephritis
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7
Q

Nephritic diseases are characterized by:

A

Active urine sediment w/glomerular hematuria (and often with proteinuria)

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8
Q

Clinical presentation of postrenal failure

A
  • Older men w/prostatic obstruction
  • Gyn surgery or abd/pelvic malignancy
  • Flank pain and hematuria
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9
Q

What is the most important thing to assess in clinical presentation of AKI?

A

Volume status!

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10
Q

Relationship of urine output and AKI?

A
  • Most causes of AKI are nonoliguric

- Normal urine output

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11
Q

Interpretation of urine electrolytes

A

May be erroneous in nonoliguric states (normal urine output)

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12
Q

What is FENa?

A
  • Marker of Na excretion in kidneys
  • Useful only in oliguria (to determine whether prerenal or intrinisic failure)
  • Less than 1% is prerenal
  • Greater than 1% is ATN
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13
Q

How is GFR measured for kidney function?

A
  • Not possible to measure directly

- Serum Cr is used as a surrogate to calculate (estimate) GFR

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14
Q

Treatment of AKI

A

-Correct volume and electrolytes
-Avoid nephrotoxic agents, adjust doses of renal excreted meds
-Salt and fluid restriction
(mainly supportive tx)

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15
Q

What are the RIFLE criteria?

A
  • Uniform, accepted definition of AKI

- Risk, Injury, Failure, Loss, ESRD

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16
Q

Iatrogenic renal injury occurs MC when?

A

When RBF is low

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17
Q

What happens once RBF is restored?

A
  • Remaining functional nephrons increase their filtration leading to hypertrophy
  • Continued hyperfiltration results in progressive glomerular sclerosis
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18
Q

How does urine output correlate with GFR?

A

Urine output does NOT correlate well with changes in GFR

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19
Q

How does urine output present in most cases of AKI?

A

50-60% of all causes of AKI are nonoliguric (urine output does not change)

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20
Q

If serum Cr is greater than or equal to 1.5 mg/dL/day, what must be ruled out?

A

Rhabdomyolysis

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21
Q

What is a quick way to determine furosemide dose?

22
Q

How does AKI MC present in children?

A

Prerenal - hypovolemia due to gastroenteritis (profuse vomiting)

23
Q

What should be suspected when bladder pressure is over 25 mm Hg?

A

Suspect AKI as a result of abdominal compartment syndrome

24
Q

What is the hallmark of intrinsic failure?

A

Structural injury in the kidney (either ischemic or cytotoxic)

25
What causes most cases of intrinsic failure AKI?
Acute tubular necrosis (ATN)
26
Where is the main site of cell death in ATN?
Distal nephron
27
What causes the reduced GFR in ATN?
Intrarenal vasoconstriction
28
What is found on urinalysis that indicates ATN?
Urine sediment with pigmented granular casts and renal tubular epithelial cells
29
What are the major causes of ATN?
Ischemic (inadequate GFR/RBF) | Exogenous nephrotoxins
30
How to treat ATN?
- Avoid volume overload and hyperkalemia - Loop diuretics, IV thiazides - Nutrition support preventing excessive catabolism
31
What causes interstitial nephritis?
70% of cases caused by hypersensitivity to drugs (penicillins, cephalosporins, sulfas, NSAIDs, PPIs, etc.)
32
How does interstitial nephritis present?
- Fever - Transient rash - Acute/chronic kidney injury - Pyuria
33
Treatment of interstitial nephritis?
- Supportive including removal of inciting agent | - Short course of steroids if necessary
34
Prognosis of interstitial nephritis?
Good prognosis, rarely progresses to ESRD
35
Describe glomerulonephritis
- Intrinsic failure AKI | - Caused by immune reaction
36
What is the universal finding of glomerulonephritis?
Hematuria
37
What does urinalysis show for GN?
RBC casts
38
What causes postrenal AKI?
- Tubular obstruction from crystals - BPH, prostate cancer - Renal vein thrombosis - Intra-abdominal HTN
39
Classic presentation of vascular AKI?
- Lower extremity rash - Livedo reticularis - Eosinophils in urine
40
Treatment of vascular AKI?
BP should be controlled and further intra-arterial procedures should be limited
41
How does vascular AKI occur?
1 day to several weeks after undergoing invasive vascular procedure or major trauma
42
Causes of renal artery stenosis
- Athero (80-90%) - Fibromuscular dysplasia (rare) - HTN - Patients starting ACEI
43
How does renal artery stenosis present?
- Refractory or new onset HTN - Pulm edema w/poorly controlled BP - AKI upon starting ACEI
44
How is renal artery stenosis diagnosed?
Renal angiography
45
How does fibromuscular dysplasia present?
"Beads on a string" on renal angiography
46
Treatment of renal artery stenosis?
- Medical management | - Angioplasty with or w/o stenting
47
What are the nephritic glomerular diseases?
- Postinfectious GN - IgA nephropathy - Henoch Schonlein Purpura - Pauci-Immune GN - Anti-GBM GN (Goodpasture) - Cryoglobulin GN - Idiopathic MPGN - HCV and SLE
48
What are the nephrotic glomerular diseases classified into?
Primary renal disorders | Systemic disorders
49
What are the primary renal nephrotic glomerular diseases?
- Minimal Change Disease - Membranous nephropathy - Focal segmental glomerulosclerosis
50
What are the systemic nephrotic glomerular diseases?
- Amyloidosis - Diabetic nephropathy - HIV associated nephropathy