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Renal > SM_195a: AKI: Pre, Post, and Intrinsic > Flashcards

SM_195a: AKI: Pre, Post, and Intrinsic Flashcards

1
Q

AKI is _______

A

AKI is deterioration of renal function over hours to days resulting in the kidney’s inability to excrete nitrogenous waste products, maintain fluid balance, and maintain electrolyte balance

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2
Q

AKI occurs due to _____ in developing nations

A

AKI occurs due to hypovolemic shock from diarrhea in developing nations

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3
Q

AKI occurs due to _____ in industrialized nations

A

AKI occurs due to bypass cardiac surgery in industrialized nations

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4
Q

There is a higher risk of AKI if ________

A

There is a higher risk of AKI if pre-existing chronic kidney disease

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5
Q

Prognosis of AKI is worse if _____ or _____

A

Prognosis of AKI is worse if elderly or pre-existing CKD

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6
Q

AKI is observed clinically as ______ or ______

A

AKI is observed clinically as rise in creatinine or reduction in urine output

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7
Q

Oliguria is 24 hour urine output ______

A

Oliguria is 24 hour urine output < 500 mL

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8
Q

Anuria is 24 hour urine output _____

A

Anuria is 24 hour urine output < 50 mL

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9
Q

Describe the systemic manifestations of AKI

A

Systemic manifestations of AKI

  • Extracellular volume expansion manifesting as HTN, CHF, pulm or peripheral edema
  • Hyperkalemia
  • Metabolic acidosis
  • Hyperphosphatemia
  • Anemia due to a decrease in the production of erythropoietin
  • Uremia (toxic metabolic state)
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10
Q

Describe the natural history of AKI

A
  • Full recovery (best)
  • AKI to CKD
  • Acute-on-chronic kidney disease
  • AKI to ESRD (worst)
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11
Q

Types of AKI are _____, _____, and _____

A

Types of AKI are pre-renal, intrinsic, and post-renal

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12
Q

Describe the etiology of pre-renal AKI

A

Pre-renal AKI

  • Occurs when kidney hypoperfusion
  • Due to true volume depletion or ineffective arterial blood volume
  • No structural injury to kidney
  • Generally prompt recovery of glomerular filtration when hemodynamics are restored
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13
Q

Describe causes of pre-renal AKI

A

Causes of pre-renal AKI

  • Hypovolemia: intravascular volume depletion, third spacing, decreased cardiac output
  • Hypotension
  • Pharmacologic
  • Large vessel compromise
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14
Q

Pre-renal AKI is most common in ______

A

Pre-renal AKI is most common in outpatients

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15
Q

Glomerular filtration depends on sufficient _____ to provide adequate blood flow to glomerulus and adequate filtration pressure

A

Glomerular filtration depends on sufficient effective circulating blood volume to provide adequate blood flow to glomerulus and adequate filtration pressure

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16
Q

Normally, autoregulation of GFR ____ over a wide range of systemic blood pressures

A

Normally, autoregulation of GFR is constant over a wide range of systemic blood pressures

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17
Q

As blood pressure falls, _____ progressively dilates due to ______, while ______ progressively constricts due to ______

A

As blood pressure falls, afferent arteriole progressively dilates due to prostaglandins, while efferent arteriole progressively constricts due to angiotesin II

  • Prostaglandins preferentially vasodilate afferent arteriole to increase blood flow into glomerulus
  • Angiotesin II causes greater constriction of efferent than afferent arteriole to preserve ultrafiltration pressure
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18
Q

When effective circulating blood volume decreases, GFR ______ due to ______ and ______

A

When effective circulating blood volume decreases, GFR stays constant due to afferent arteriole vasodilation via prostaglandins and efferent arteriole vasoconstriction via angiotensin II

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19
Q

When effective circulating blood volume decreases and person takes NSAIDs, GFR ______ because ______

A

When effective circulating blood volume decreases and person takes NSAIDs, GFR decreases because vasodilatory effect of prostaglandins on afferent arteriole is blocked

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20
Q

When effective circulating blood volume decreases and person takes an ACE-i/ARB, GFR ______ because ______

A

When effective circulating blood volume decreases and person takes an ACE-i/ARB, GFR decreases because ACE-i/ARB inhibit vasoconstrictive effect of angiotensin II on efferent arteriole

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21
Q

In pre-renal AKI, what occurs when glomerular filtration is reduced?

A

In pre-renal AKI, when glomerular filtration is reduced

  • Aldosterone release increased -> increased distal nephron Na+ reabsorption
  • ADH increased -> decreased free water clearance

Leads to concentrated urine with low urine sodium

22
Q

Describe diagnosis of pre-renal AKI

A

Diagnosis of pre-renal AKI

  • Diarrhea, diuretic use, dizziness
  • Signs of dehydration or heart failure
  • Lab: urinalysis, urine sodium (FENA < 1% suggestive but not exclusive), BUN/creatinine (> 20:1)
23
Q

Describe management of pre-renal AKI

A

Management of pre-renal AKI

  • Rapid and reversal of underlying process
  • Volume expansion of hypovolemic
  • Blood pressure support (vasopressors, inotropes)
24
Q

Pre-renal AKI is _____ to volume repletion, while hepatorenal syndrome is _____ to volume repletion

A

Pre-renal AKI is responsive to volume repletion, while hepatorenal syndrome is NOT responsive to volume repletion

25
Q

Post-renal AKI is _______

A

Post-renal AKI is obstruction anywhere in urinary tract, causing AKI

(increase in hydrostatic pressure -> decrease in GFR)

26
Q

Post-renal causes of AKI are _____, _____, and _____

A

Post-renal causes of AKI are ureteral (bilateral in setting of 2 functional kidneys), bladder neck, and urethral

27
Q

In post-renal AKI, severe or complete obstruction causes increased ______ in renal pelvis, leading to ______

A

In post-renal AKI, severe or complete obstruction causes increased hydrostatic pressure in renal pelvis, leading to decreased GFR

28
Q

Describe diagnosis of post-renal AKI

A

Diagnosis of post-renal AKI

  • Physical exam: distended bladder, enlarged prostate
  • BUN/Cr > 20:1 - enhanced urea reabsorption in decreased urine flow state
  • Post-void residual bladder volume (lower tract obstruction)
  • Renal ultrasound (upper tract obstruction)
  • Foley catheter placement
  • Non-contrast CT
29
Q

Management of post-renal AKI necessitates _____ and _____ to preserve kidney function

A

Management of post-renal AKI necessitates rapid diagnosis and relief of obstruction to preserve kidney function

30
Q

In intrinsic renal AKI, _____, _____, _____, and _____ are affected

A

In intrinsic renal AKI, tubules (acute tubular necrosis), interstitium (interstitial nephritis), glomeruli (glomerulonephritis), and vasculature (vascular disorders) are affected

31
Q

Causes of acute renal AKI are _____, _____, _____, and _____

A

Causes of acute renal AKI are tubules, interstitium, glomeruli, and vascular (small vessels)

32
Q

Describe diagnosis of intrinsic AKI

A

Diagnosis of intrinsic AKI

  • Medications (can cause interstitial or tubular damage)
  • Labs: urinalysis (proteinuria, hematuria), urine sediment
  • Renal ultrasound (vascular)
33
Q

Urine sediment of intrinsic AKI would reveal _____, _____, _____, or _____

A

Urine sediment of intrinsic AKI would reveal renal tubular epithelial cells, muddy brown casts, RBC casts, or WBC casts

34
Q

The tubular etiology of intrinsic AKI is ______

A

The tubular etiology of intrinsic AKI is acute tubular necrosis (ATN)

  • Most common cause of hospital AKI
  • Etiology: ischemic (pre-renal, sepsis), nephrotoxic (exogenous, endogenous), intra-tubular obstruction (myeloma, tumor lysis syndrome, drugs)
  • Does not resolve immediately after restoration of renal blood flow
35
Q

Describe acute tubular necrosis

A

Acute tubular necrosis

  • Most common cause of hospital AKI
  • Etiology: ischemic (pre-renal, sepsis), nephrotoxic (exogenous, endogenous), intra-tubular obstruction (myeloma, tumor lysis syndrome, drugs)
  • Does not resolve immediately after restoration of renal blood flow
36
Q

The interstitial etiology of intrinsic AKI is ______

A

The interstitial etiology of intrinsic AKI is acute interstitial nephritis

  • Drug-induced, infection, autoimmune disease, malignancy, sarcoidosis, idiopathic
37
Q

The glomerular etiology of intrinsic AKI is ______

A

The glomerular etiology of intrinsic AKI is glomerulonephritis

  • RPGN, IgA nephropathy, post-infectious glomerulonephritis, MPGN, FSGS, MCD, MGN
38
Q

The vascular etiology of intrinsic AKI is ______ or ______

A

The vascular etiology of intrinsic AKI is small/medium vssel inflammation resulting in vasculitis or vascular obstruction/occlusion

  • Prinicipal vessels: bilateral renal artery thrombosis or embolism
  • Bilateral renal vein thrombosis
  • Small vessels
39
Q

Describe the urinalysis and urine chemistry findings in different types of AKI

A
40
Q

Pre-renal AKI has urine osmolality _____

A

Pre-renal AKI has urine osmolality > 500

41
Q

Describe AKI in tropical countries

A

AKI in tropical countries

  • Bimodal pattern: spike during rainy season and after rainy season
  • Lots of infectious, insect, obstetric causes
42
Q

Post-renal AKI has urine osmolality _____

A

Post-renal AKI has urine osmolality < 350

43
Q

Describe conservative and immediate management for AKI

A

Conservative and immediate management for AKI

  • Adjust fluids: volume depletion, volume overload
  • Adjust dose and frequency of meds at minimum daily
  • Review electrolytes, BUN, creatinine, urine output closely
44
Q

Risk factors for developing AKI include _____, _____, and _____

A

Risk factors for developing AKI include hypovolemia, older age, and underlying chronic kidney disease

45
Q

Urine sodium / fractional excretion of sodium is low in pre-renal AKI because ______

A

Urine sodium / fractional excretion of sodium is low in pre-renal AKI because there is decreased kidney perfusion, which results in reduction in GFR, prompting reabsorption of nearly all the filtered sodium

46
Q

Diagnostic tests/maneuvers used to rule out post-renal problems as the cause of AKI include _____ and _____

A

Diagnostic tests/maneuvers used to rule out post-renal problems as the cause of AKI include renal ultrasound and Foley catheter placement

47
Q

All of the following findings would be suggestive of pre-renal AKI EXCEPT

A. orthostatic hypotension

B. urine sodium of 75

C. BUN/Cr ratio of 30

D. urine osmolality of 500

A

All of the following findings would be suggestive of pre-renal AKI EXCEPT

A. orthostatic hypotension

B. urine sodium of 75 - should be < 20 in pre-renal

C. BUN/Cr ratio of 30

D. urine osmolality of 500

48
Q

There is a mismatch between ____ and ____

A

There is a mismatch between GFR and urinary flow rate

49
Q

What should you do?

A. start IV fluids (e.g. normal saline)

B. stop ACE inhibitor

C. stop ibuprofen

D. check for post-void residual urine, place catheter in bladder

E. all of the above

A

What should you do?

A. start IV fluids (e.g. normal saline)

B. stop ACE inhibitor

C. stop ibuprofen

D. check for post-void residual urine, place catheter in bladder

E. all of the above

50
Q

Describe common causes of AKI

A
51
Q

AKI is defined as ______ or _______

A

AKI is defined as rise in serum creatinine or decreased urine output (oliguria)

  • Creatinine increase by >0.3 mg/dL in 48 hours or rise to above 1.5x baseline in preceding 7 days
  • Urine output of <0.5 mL/kg/hr for ≥6 hours

Renal (31 decks)

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