Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Renal Exam > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

acute kidney injury (AKI) - overview

A

*comprised of a wide spectrum of clinical syndromes characterized by an abrupt decrease in GFR
*resulting in the accumulation of nitrogenous waste products, including urea and creatinine, as well as other uremic middle molecules and inflammatory components
*decline in urine output can be variable
*no precise correlation exists between changes in sCr levels & GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

relationship of GFR to steady-state serum creatinine & BUN

A

*elevation in serum creatinine is apparent only when GFR falls to about 70 mL/min

*early renal disease: slight elevations in sCr → substantial decline in GFR
*late renal disease: large elevations in sCR → small declines in GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

most used indicators of renal function

A

*BUN and creatinine
*insensitive and late markers of renal dysfunction
*can also be affected by other confounding factors:
-elevated BUN: GI bleeding, steroids, etc
-elevated sCr: trimethoprim, rhabdomyolysis, etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

other conditions/medications that may increase serum creatinine

A

*rhabdomyolysis
*cimetidine
*trimethoprim
*probenacid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

other conditions/medications that may increase BUN

A

*GI bleeding
*catabolic states
*high protein diet
*amino acid infusion/TPN
*tetracycline
*steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

acute kidney injury (AKI) - definitions

A

*an acute or sustained increase in sCr by 0.5 (if baseline Cr < 2.5) OR an increase in sCr by 20% (if baseline Cr > 2.5)

*an abrupt (within 48 hrs) reduction of kidney function defined by an absolute increase sCr > 0.3 OR other

*RIFLE/AKIN criteria primarily used in research arena

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

RIFLE criteria for AKI

A
  1. renal risk
  2. renal injury
  3. renal failure
  4. renal LOSS
  5. ESRD (end-stage renal disease)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

diagnostic approach to AKI

A
  1. review old records (establish a baseline Cr, previous urinalysis/imaging; plot Cr/urine output trend)
  2. thorough HPI & physical
  3. examination of URINALYSIS and urine studies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

pre-renal acute kidney injury - defined

A

*clinical syndrome characterized by:
1. reduced renal perfusion
2. preserved renal parenchyma function
3. kidneys respond appropriately to reduced perfusion → Na+ and H2O retention, concentrated urine, LOW urine Na+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

pre-renal AKI - pathophysiological mechanisms

A

*true intravascular hypovolemia
*decreased effective circulatory volume
*intrarenal vasoconstriction
*renal artery disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

autoregulation of GFR: what happens when there is decreased renal perfusion?

A

*2 mechanisms by which the kidney is able to adapt in order to maintain normal GFR, despite decreased renal perfusion:

  1. decreased renal perfusion → release of NO and prostaglandins → VASODILATION of AFFERENT arteriole → increased renal blood flow → increased Pgc to maintain GFR
  2. decreased renal perfusion → release of Ang II → VASOCONSTRICTION of EFFERENT arteriole → maintained GFR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

effect of NSAIDs on autoregulation of GFR

A

*NSAIDs block prostaglandins → not able to vasodilate afferent arteriole → inability to increase renal blood flow to maintain GFR → DECREASE IN GFR

note - this is in patients with decreased renal perfusions on NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

effects of ACEi/ARBs on autoregulation of GFR

A

*ACEi/ARBs → inhibit the effect of Ang II on the efferent arteriole → inability to vasoconstrict the efferent arteriole → DECREASE IN GFR

note - this is in patients with decreased renal perfusions on ACEi or ARB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

causes of pre-renal AKI: true volume depletion

A

*renal: diuretic use, diabetes insipidus, osmotic diuresis
*extra-renal: diarrhea, vomiting, pancreatitis, GI bleeding, surgery/trauma, blood loss, burns, third spacing, surgical drains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

causes of pre-renal AKI: low effective circulation

A

*CHF
*cirrhosis
*shock/sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

causes of pre-renal AKI: intrarenal vasoconstriction

A

*hypercalcemia
*contrast dye
*cyclosporine
*tacrolimus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

causes of pre-renal AKI: pharmacological

A

*NSAIDs
*ACEi / ARBs

recall:
1. NSAIDs block prostaglands, preventing vasodilation of the afferent arteriole; effectively, constrict the afferent arteriole → decreased GFR
2. ACEi/ARBs block angiotensin II’s effects, preventing vasoconstriction of efferent arteriole; effectively, dilate the efferent arteriole → decreased GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

causes of pre-renal AKI: renal artery disease

A

*renal artery stenosis → decreased renal perfusion → decreased GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

pre-renal AKI due to true volume depletion - clinical presentation

A

*history: extracellular fluid loss from skin, GI or renal source
-inquire about recent infections, fever, diarrhea, diuretic use, decreased hydration, orthostatic lightheadedness, thirst
*PE: signs of hypovolemia such as:
-orthostatic hypotension
-tachycardia
-dry mucous membranes
-decreased skin turgor
-no axillary moisture
-oliguria or concentrated urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

pre-renal AKI due to low effective circulation - clinical presentation

A

*history: heart failure, low cardiac output, cirrhosis
-inquire about SOB, PND, orthopnea, change in weight, edema
*PE: edema, third heart sound (S3 or S4), JVD, pulmonary crackles/effusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

pre-renal AKI diagnosis: serum chemistry findings

A

*elevated BUN and Cr
*BUN/Cr ratio > 20:1 (low urinary flow allows for increased urea absorption)
*monitor for complications of AKI (hyperkalemia, acidosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

pre-renal AKI diagnosis: urinalysis

A

*normal/bland sediment (little to no protein, no blood, no WBCs, no other cellular elements)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

pre-renal AKI diagnosis: fractional excretion of sodium (FEna)

A

*amount of filtered sodium that is actually excreted
*expected to be VERY LOW: FEna < 1%
*note - not helpful if pt is on a diuretic (use FEurea; should be < 35%)

recall: FEna = (Una x Pcr) / (Ucr x Pna) x 100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

pre-renal AKI diagnosis: urine studies

A

*urine sodium: LOW (<20) due to increased proximal reabsorption of Na in response to hypovolemia

*urine Osm: HIGH (>500) due to increased concentration (reabsorption of water in effort to volume expand)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

pre-renal AKI - treatment

A

*key = normalize the effective renal blood flow

*expedient treatment will help minimize the risk of progression of intrinsic renal failure
*if true volume depletion, give fluids
*if CHF, diurese

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

intrinsic (renal) AKI - defined

A

*primary lesion is in the kidney
*renal parenchyma is NOT intact; can be:
-vascular/microvascular
-glomerular
-interstitial
-tubular
*unlike pre-renal and post-renal causes, recovery is not expected to be as dramatic with removal of the culprit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

acute tubular necrosis (ATN) - overview

A

*most common cause of intrinsic acute kidney injury in hospitalized patients
*a form of AKI described as acute damage to the renal tubules, usually due to ischemia associated with shock, IV contrast, or excess myoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

acute tubular necrosis (ATN) - clinical presentation

A

*nonspecific signs and symptoms of renal failure
*similar to prerenal symptoms (true volume depletion or low effective circulation)
*also look at:
-episodes of hypertension and recent surgeries
-recent contrast administration
-review meds for nephrotoxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

pre-renal AKI and ATN spectrum

A

*pre-renal AKI and ATN are two extremes of the same clinical spectrum

*3 causes that can lead to progression from pre-renal AKI to ATN:
1. ischemia: prolonged hypoperfusion, crush injury & trauma, septic shock, pancreatitis
2. endotoxins: uric acid, hemoglobin & myoglobin, immunoglobulin light chains
3. exotoxins: heavy metals (lead), ethylene glycol, contrast dye, antibiotics (ex. ampho)

30
Q

pathophysiology of ischemic acute tubular necrosis (ATN)

A

*ischemic ATN is a progression of the prerenal state to a point at which compensatory mechanisms decompensate
1. overwhelming levels of AngII and endothelin-1 causes intense vasoconstriction → further reduction of perfusion
2. increase in inflammatory cytokines potentiates endothelial injury
3. congestion & obstruction of capillaries
4. disruption of actin cytoskeleton → loss of brush border
5. loss of polarity of epithelial cells → failure of tight junctions → backleak of tubular fluid, detached BM
6. apoptosis and necrosis of tubular epithelium

31
Q

acute tubular necrosis (ATN) - phases

A
  1. initiation (OLIGURIC phase):
    -inciting event damages tubular epithelial necrosis → blockage of tubular lumen by necrotic debris → reduction in GFR, vasoconstriction, resulting in prolonged ischemia
  2. maintenance:
    -ongoing renal failure
    -creatinine usually increases slightly per day
    *conversion from oliguria → nonoliguria does not improve mortality
  3. recovery (POLYURIC PHASE):
    -regeneration of tubular epithelium, but unable to reabsorb H2O and electrolytes
    -gradual return of BUN/Cr to baseline or near-normal levels
32
Q

ATN diagnosis: serum chemistries

A

*elevated BUN and creatinine
*BUN/Cr ratio < 20:1 (contrast to pre-renal, where ratio is greater than 20)

33
Q

ATN diagnosis: urine studies

A

*FEna > 2%

*urine sodium > 40

*urine osmolarity < 350

34
Q

ATN diagnosis: urine sediment

A

*classic “muddy brown cast” (GRANULAR CASTS)

35
Q

ATN diagnosis: renal biopsy

A

*tubular injury
*flattened tubular epithelium
*sloughed cells

note - we typically do NOT biopsy these patients

36
Q

acute tubular necrosis (ATN) - treatment

A

*largely supportive:
-attempt to improve renal perfusion, maintain SBP > 100, avoid nephrotoxic agents, remember to adjust doses of meds for Cr clearance < 10-15

*medical therapy:
-correct volume status, treat electrolyte disturbances, treat acidosis, consider dialysis

37
Q

contrast urine and serum studies in pre-renal AKI vs. acute tubular necrosis (ATN)

A

*urine osmolarity (mOsm/kg)
-prerenal AKI: > 500
-ATN: < 350

*urine Na+ (mEq/L):
-prerenal AKI: < 20
-ATN: > 40

*FENa:
-prerenal AKI: < 1%
-ATN: > 2%

*serum BUN/Cr ratio:
-prerenal AKI: > 20:1
-ATN: < 20:1

38
Q

contrast-induced nephropathy - overview

A

*subset of ATN injury frequently seen in hospital settings
*pathogenesis: IV contrast → vasoconstriction of renal arteries & direct tubular injury

*risk factors:
-underlying renal insufficiency
-diabetic nephropathy with renal insufficiency
-advanced heart failure
-states of hypoperfusion
-percutaneous coronary interventrions
-high total dose of contrast agent

39
Q

contrast-induced nephropathy - clinical presentation

A

*AKI apparent within the first 24-48 hours after contrast study
*non-oliguric with mild decline in renal function
*patients occasionally require dialysis

40
Q

differentiating contrast-induced nephropathy from atheroembolic disease

A

ATHEROEMBOLIC DISEASE has the following:
*presence of other embolic lesions (as on the toes) or livedo reticularis
*transient eosinophilia and hypocomplementemia
*onset of renal failure that may be delayed for days to weeks after the procedure
*protracted course with frequently little or no recovery of renal function

41
Q

contrast-induced nephropathy - diagnosis

A

*similar to ATN (FENa > 2%, urine Osm < 350, urine Na+ > 40, serum BUN/Cr ratio < 20:1)
*history of recent contrast administration and characteristic rise in creatinine 24-48 hrs later

42
Q

contrast-induced nephropathy - prevention

A

*avoid contrast, if possible, in high-risk individuals
*use of nonionic, low osmolal agents
*use lower doses of contrast
*avoid repetitive, closely spaced studies
*avoid volume depletion and NSAIDs

43
Q

contrast-induced nephropathy - treatment

A

*VOLUME EXPAND:
-fluids prior to/during/after contrast administration
-ANY type of fluid suffices (saline)
-if volume expansion contraindicated (i.e. CHF), just hold diuretic

44
Q

atheroembolic disease - overview

A

*cholesterol crystal embolization occurs when portions of an atherosclerotic plaque break off and embolize distally
*resulting in partial or total occlusion of multiple small arteries (or glomerular arterioles)
*leading to tissue or organ ischemia
*seen after manipulation of the aorta or other large arteries

45
Q

atheroembolic disease - clinical presentation

A

*blue toe syndrome
*livedo reticularis
*GI manifestations
*renal failure
*CVA

46
Q

atheroembolic disease - renal manifestations

A

*occurs primarily in older patients
*marked AKI with an acute onset, seen within 1-2 weeks of event
*sub-acute presentation: renal dysfunction occurs in staggered steps separated by periods of stable kidney function

47
Q

atheroembolic disease - diagnosis

A

*urine: bland urine sediment
-eosinophiluria during active phase
-proteinuria is usually not a prominent feature

*eosinophilia & hypocomplementemia

*definitive dx: biopsy
-skin lesion (if present)
-kidney

48
Q

pigment-induced ATN - overview

A

*subset of ATN injury
*seen with rhabdomyolysis:
-associated with marked elevations in CPK
-seen with trauma or statin therapy

49
Q

pigment-induced ATN - clinical findings

A

*rapid rise in creatinine, often > 2 mg/L/day
*hyperkalemia
*hyperphosphatemia
*hyperuricemia
*urine dipstick positive for blood BUT NO RBC on urinalysis (picks up myoglobin)

50
Q

causes of nephrotoxin drug-induced ATN

A
  1. aminoglycosides (gentamicin, tobramycin, amikacin)
  2. amphotericin B
  3. vancomycin
51
Q

nephrotoxin drug-induced ATN due to aminoglycosides

A

*NON-OLIGURIC AKI [5-10 days post-exposure to drug]
*hypomagnesemia
*mechanism of injury: non-protein bound drug filters into glomerulus & cationic properties allow it to be taken into PT → accumulate in lysosomes and interfere with normal cells functions → cell death
*risk factors: high peak serum levels, cumulative dose

52
Q

nephrotoxin drug-induced ATN due to amphotericin B

A

*mechanism of injury:
-direct binding to tubular epithelial cells creates PORES → Na+, K+, Mag wasting (directly)
-indirect mech: afferent arteriolar vasoconstriction

53
Q

nephrotoxin drug-induced ATN due to vancomycin

A

*synergistic nephrotoxicity (worse when in conjunction with other nephrotoxic meds)
*independent risk factors for nephrotoxicity:
-use of concomitant nephrotoxic agents, age, duration of therapy, etc

54
Q

acute interstitial nephritis (AIN) - overview

A

*defines a pattern of renal injury characterized histopathologically by inflammation and edema of the renal interstitium
*a type of intrinsic (renal) AKI
*most commonly caused by:
-drugs (antibiotics, NSAIDs, etc)
-infections (bacterial & viral)
-autoimmune disorders (sarcoid, TINU syndrome)
-idiopathic

55
Q

acute interstitial nephritis (AIN) - clinical presentations

A

*nonspecific symptoms (except for drug-induced):
-malaise, anorexia, N/V
-acute or subacute onset
-s/s of AKI

*drug-induced AKI:
-onset within 3 weeks of first exposure or 3-5 days after second exposure
-classic symptoms: RASH, FEVER, EOSINOPHILIA

56
Q

acute interstitial nephritis (AIN) - diagnosis

A

*clinical symptoms
*AKI improves with removal of offending agent
*peripheral eosinophilia
*urine is VARIABLE:
-white cells, white cells casts
-urine eosinophils
-sterile pyuria
*definitive = biopsy

57
Q

acute interstitial nephritis (AIN) - treatment

A
  1. drug-induced:
    *discontinue offending agent (expect improvement in 3-7 days)
    *trial of corticosteroids
  2. non-drug induced:
    -treat underlying disease
58
Q

acute glomerulonephritis & vasculitis - overview

A

*another cause of intrinsic AKI (rare)
*look at URINE:
-active sediment? RBC casts? proteinuria, hematuria?
-nephrotic vs. nephritic

59
Q

3 causes of intrinsic (renal) AKI

A
  1. acute tubular necrosis (ATN)
  2. acute interstitial nephritis (AIN)
  3. acute glomerulonephritis & vasculitis
60
Q

post-renal AKI - overview

A

*an impediment of urine flow due to structural or functional obstruction
*resulting in an increase in pressure proximal to obstruction
*obstruction can occur anywhere from the renal pelvis to the tip of the urethra

61
Q

post-renal AKI - obstructive nephropathy

A

*when the kidney parenchyma itself if damaged
*functional or pathological changes in the kidney that results from urinary tract obstruction
*obstruction classified based on:
-duration (acute vs. chronic)
-level of obstruction (upper vs. lower tract)
-degree of obstruction (complete vs. partial)
-unilateral vs. bilateral

62
Q

ureteral causes of post-renal AKI

A

*intrinsic: crystals, light chain casts, stones, blood clots, papillary necrosis, fungus balls, edema
*extrinsic: gravida uterus, uterine prolapse, uterine tumors, RP fibrosis, RP tumor, radiation therapy

63
Q

bladder causes of post-renal AKI

A

*diabetes mellitus
*multiple sclerosis
*spinal cord injury
*anticholinergic agents

64
Q

urethral causes of post-renal AKI

A

*posterior urethral valves
*BPH
*diverticula
*strictures
*tumors
*obstructed foley catheters

65
Q

post-renal AKI - clinical presentation

A

*VARIABLE, depending on site, duration, and severity
*common symptoms:
-pain
-change in urine output
-palpable mass
-bladder symptoms

66
Q

diagnosis of post-renal AKI - serum chemistries

A

*elevated BUN/Cr > 15:1
*FEna > 2-4%
*hyponatremia
*hyperkalemia

note - VARIABLE!!

67
Q

diagnosis of post-renal AKI - urine studies

A

*bland sediment
*hematuria (stones, tumors)
*crystals

68
Q

post-renal AKI - treatment

A

*relieve obstruction
*depends on level of obstruction & cause

69
Q

post obstructive diuresis

A

*commonly seen after relief of severe bilateral obstruction
*polyuria:
-osmotic diuresis caused by retained urea
-volume overload
-tubular concentration defect

70
Q

compare serum chemistries of pre-renal, intrinsic, and post-renal AKI

A

*BUN/Cr > 20:1 = prerenal
*BUN/Cr < 20:1 = intrinsic
*BUN/Cr > 25:1 and variable in post-renal

71
Q

compare urinalysis of pre-renal, intrinsic, and post-renal AKI

A

*bland sediment: prerenal or post-renal
*epithelial cells & muddy brown casts: ATN
*RBC casts: glomerulonephritis
*WBCs, WBC casts, sterile pyuria: AIN

Renal Exam (44 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions