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Clin Med III > AKI > Flashcards

AKI Flashcards

1
Q

AKI

A
  • abrupt decline in renal function -> increased BUN and Cr over hours to weeks
  • AKI DOES NOT equal ARF
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2
Q

what is the RIFLE criteria

A
  • assessment of AKI
  • risk
  • injury
  • failure
  • loss of function
  • end stage renal disease (dialysis)
  • based on Cr elevation or decreased urine output
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3
Q

azotemia

A
  • increase in BUN andd Cr without sx
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4
Q

uremia

A
  • increase in BUN and Cr with sx
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5
Q

function of kidneys

A
  • acid base balance
  • water regulation
  • electrolyte balance
  • toxin excretion
  • BP
  • EPO
  • vit D regulation
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6
Q

pts at risk for AKI

A
  • HTN pts
  • CHF- low flow
  • diabetes
  • multiple myeloma
  • chronic infections
  • myeloproliferative disorders
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7
Q

multiple myeloma

A
  • bone marrow cancer
  • produces huge amounts of IgM
  • IgM antibodies clog up tubules
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8
Q

classification of AKI

A
  • pre-renal
  • intrinsic
  • post-renal
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9
Q

pre-renal causes of AKI

A
  • generally low flow states
  • NSAIDs
  • ACEI/ARBs
  • MAP < 80
  • hypovolemia, decreased CO
  • CHF, liver failure
  • sepsis
  • pancreatitis
  • nephrotic syndrome
  • hepatorenal syndrome
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10
Q

renal causes of AKI

A
  • glomerular
  • interstitial- ischemia, sepsis, nephrotoxins
  • vascular
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11
Q

post-renal causes of AKI

A
  • anything blocking urine from exiting
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12
Q

key factors to consider in AKI history taking

A
  • volume depletion
  • cardiac failure
  • radiocontrast exposure- sx usually 2-5 days later
  • rhabdo
  • vasculitis/ proliferative glomerulonephritis
  • hypotension/ shock
  • nephrotoxin exposure or any new meds
  • vascular/ cardiac surgery, anesthesia
  • any hx of liver disease, kidney disease, SLE, AIDs, MM, maligancy
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13
Q

why do NSAIDs cause impaired renal autoregulation

A
  • impair afferent arteriol dilation
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14
Q

why do ACEI/ARBs impair renal autoregulation

A
  • impair efferent arteriole constriction
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15
Q

what is the most common cause of renal failure

A
  • pre-renal
  • due to poor renal perfusion
  • reversed with reperfusion/ glomerular pressure
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16
Q

what does BUN:Cr ratio of 20:1 suggest

A
  • pre-renal injury
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17
Q

what is FeNa

A
  • fractional excretion of Na
  • aka % Na excreted in urine
  • < 1%= pre-renal azotemia
  • > 1%= intrinsic renal failure
  • > 4%= post-renal failure
  • not accurate if pt is on diuretics*
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18
Q

what is an alternative to FeNa

A
  • FeUrea or FeUA
  • not influenced by diuretics
  • FeUrea < 35% or FeUA <9-19% suggests prerenal
  • FeUrea > 50% or FeUA > 10-12% suggests ATN
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19
Q

what labs should you monitor for pre-renal injury

A
  • det volume depletion: H&H, albumin, Ca, Na, BUN, Cr
  • urine output- only half of pts will have oliguria
  • high specific gravity of urine
  • low urine Na < 20 meq/L
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20
Q

pre-renal injury treatment

A
  • fluid resuscitation
  • want to optimize effective circulating volume/ CO
  • diuretics if pt is fluid overloaded
  • nitrates, dobutamine if cardiac issue
  • avoid or dose adjust meds that are renally excreted
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21
Q

acute interstitial nephritis (AIN)

A
  • renal cause of AKI
  • usually allergic rxn
  • most commonly due to abx
  • can be post-infectious or autoimmune
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22
Q

presentation of acute interstitial nephritis

A
  • after recent drug exposure
  • fever, rash
  • peripheral eosinophilia
  • oliguria
  • more commonly found incidentally due to increasing Cr after new med
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23
Q

meds assoc with AIN

A
  • beta lactams*
  • sulfonamides*
  • vanco
  • erythromycin
  • rifampin
  • acyclovir/ valacyclovir
  • NSAIDs
  • anticonvulsants
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24
Q

UA findings for AIN

A
  • pyuria- WBC casts
  • hematuria- less common
  • if see WBC casts must also r/o pyelonephritis
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25
treatment for AIN
- d/c offending agent - steroids X 6 weeks - damage may be permanent if long duration of drug exposure
26
what is the most common cause of intrinsic renal failure
- acute tubular necrosis
27
acute tubular necrosis (ATN)
- due to ischemia, sepsis, or toxins | - usually reversible
28
exogenous toxins causing ATN
- NSAIDs - chemo- esp cisplatin - aminoglycosides - amphotericin - vanco - radioconstrast dye - poison- ethylene glycol, heavy metals
29
endogenous toxins causing ATN
- rhabdo - uric acid - multiple myeloma
30
lab findings for ATN
- pigmented or granular casts- muddy brown* - Cr and BUN elevated - FeNa> 2% - serum hyperK - serum hyperP - serum hyperuricemia
31
treatment for ATN
- aggressive volume replacement - if oliguria and extracellular volume normalized consider lasix- very controversial - protein restriction - d/c offending agent if due to nephrotoxin - dialysis- last line
32
acute glomerular diseases
- post-strep glomerulonephritis - nephrotic syndrome - minimal change disease - membranous glomerulonephritis - IgA nephropathy - henoch-schonlein purpura
33
post-strep glomerulonephritis (PSGN)
- immune complex with strep antigen gets deposited into glomerulus - 7-12 d after strep/ impetigo
34
sx of PSGN
- oliguria - cola colored urine - edema - HTN - malaise, anorexia, flank pain
35
treatment for PSGN
- abx - symptomatic - anti- HTN drugs - salt restriction - diuretics
36
prognosis for PSGN
- kids usually recover with treatment | - can be permanent damage in adults
37
UA findings for PSGN
- proteinuria - hematuria - pyuria - +/- RBC casts
38
diagnosis of PSGN
- clinical manifestations - kidney injury- elevated Cr - UA findings - MUST prove there was recent GABHS infection - cultures only pos 25% of time- get ab titers, usually ASO titer
39
IgA nephropathy
- IgA deposition into glomerulus - following URI - urine red or cola colored 1-2 days after onset - more of a chronic illness, most pts don't recover - usu require transplant
40
treatment for IgA nephropathy
- ACEI/ARB - steroids - renal transplant
41
Henoch schonlein purpura
- small vessel vasculitis PLUS IgA complex deposition | - usually in kids 6 y/o
42
presentation of henoch schonlein purpura
- rash- esp in LE and buttock - abd pain/ vomiting- severe - arthralgias - edema - elevated Cr and BUN - urine hematuria/ proteinuria
43
treatment for henoch schonlein purpura
- mostly supportive - excellent prognosis - steroids and/or plasmapheresis for worsening disease - skin biopsy can be considered for dx but not usually necessary
44
nephrotic syndrome
- heavy proteinuria 3.5 g/day - hypoalbuminemia > 3 g/dL - peripheral edema
45
other findings for nephrotic syndrome
- lipiduria- foamy urine - minimal hematuria - hypercholesterolemia - HTN - hypercoag states- DVT/PE may be first presentation - no cells or casts on UA
46
etiology of nephrotic syndrome
- membranous nephropathy - minimal change disease - amyloidosis - SLE - membranoproliferative glomerulonephritis - focal segmental glomerulosclerosis - IgA nephropathy
47
minimal change disease
- 70-90% of nephrotic syndrome in childhood - unknown cause - abrupt onset edema and nephrotic syndrome
48
dx of minimal change disease
- normal biopsy - urine protein 10 gm/day - hypoalbuminemia - HTN
49
treatment for minimal change disease
- some may spontaneously recover - all kids get treated with steroids - prednisone X 8 weeks, may need up to 16 weeks - ESRD is rare but may have relapses
50
causes of vascular AKI
- renal artery obstruction- rapid decline in fn - renal vein obstruction- more chronic presentation - microangiopathy- TTP, HUS, DIC - malignant HTN - scleroderma renal crisis - recent invasive vascular procedure or trauma
51
treatment for vascular AKI
- BP control and manage sx
52
causes of post-renal failure
- bladder outlet obstruction - neurogenic bladder - pregnancy - gyn surgery or abdominopelvic malignancy
53
sx of post-renal failure
- elevated BUN and Cr - flank pain - hematuria - possible renal calculi or papillary necrosis
54
medication induced post-renal failure
- acyclovir - mtx - triamterene - indinavir - sulfonamides - can cause collecting system/ ureteral obstruction by crystal formations
55
treatment for post-renal failure
- relieve obstruction - foley can or suprapubic cath - nephrostomy tube
56
polycystic kidney disease
- genetic disorder - cyst formation and enlargement of kidneys - affects multiple sys: pancreas, liver, spleen
57
prognosis of polycystic kidney disease
- 50% need transplant or dialysis by 60 - must screen families - intracranial aneurysm is 2X more common than general population
58
sx of polycystic kidney disease
- VERY painful- abd/ flank/ back pain - hemorrhage into cysts - perinephric hematoma - infections common- esp pyelonephritis - HTN* - palpable flank mass - nodular hepatomegaly - very susceptible to trauma
59
diagnosis of polycystic kidney disease
- classic appearance on US - elevated H&H - UA shows hematuria, possible microalbuminuria - elevated Cr
60
treatment for polycystic kidney disease
- manage BP with ACEI/ARB - pain control - very challenging, avoid NSAIDs - surgical cyst decompression - nephrectomy - treat recurrent infections - hydrate

Clin Med III (26 decks)

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