AKI Flashcards
AKI
- abrupt decline in renal function -> increased BUN and Cr over hours to weeks
- AKI DOES NOT equal ARF
what is the RIFLE criteria
- assessment of AKI
- risk
- injury
- failure
- loss of function
- end stage renal disease (dialysis)
- based on Cr elevation or decreased urine output
azotemia
- increase in BUN andd Cr without sx
uremia
- increase in BUN and Cr with sx
function of kidneys
- acid base balance
- water regulation
- electrolyte balance
- toxin excretion
- BP
- EPO
- vit D regulation
pts at risk for AKI
- HTN pts
- CHF- low flow
- diabetes
- multiple myeloma
- chronic infections
- myeloproliferative disorders
multiple myeloma
- bone marrow cancer
- produces huge amounts of IgM
- IgM antibodies clog up tubules
classification of AKI
- pre-renal
- intrinsic
- post-renal
pre-renal causes of AKI
- generally low flow states
- NSAIDs
- ACEI/ARBs
- MAP < 80
- hypovolemia, decreased CO
- CHF, liver failure
- sepsis
- pancreatitis
- nephrotic syndrome
- hepatorenal syndrome
renal causes of AKI
- glomerular
- interstitial- ischemia, sepsis, nephrotoxins
- vascular
post-renal causes of AKI
- anything blocking urine from exiting
key factors to consider in AKI history taking
- 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
why do NSAIDs cause impaired renal autoregulation
- impair afferent arteriol dilation
why do ACEI/ARBs impair renal autoregulation
- impair efferent arteriole constriction
what is the most common cause of renal failure
- pre-renal
- due to poor renal perfusion
- reversed with reperfusion/ glomerular pressure
what does BUN:Cr ratio of 20:1 suggest
- pre-renal injury
what is FeNa
- 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*
what is an alternative to FeNa
- FeUrea or FeUA
- not influenced by diuretics
- FeUrea < 35% or FeUA <9-19% suggests prerenal
- FeUrea > 50% or FeUA > 10-12% suggests ATN
what labs should you monitor for pre-renal injury
- 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
pre-renal injury treatment
- 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
acute interstitial nephritis (AIN)
- renal cause of AKI
- usually allergic rxn
- most commonly due to abx
- can be post-infectious or autoimmune
presentation of acute interstitial nephritis
- after recent drug exposure
- fever, rash
- peripheral eosinophilia
- oliguria
- more commonly found incidentally due to increasing Cr after new med
meds assoc with AIN
- beta lactams*
- sulfonamides*
- vanco
- erythromycin
- rifampin
- acyclovir/ valacyclovir
- NSAIDs
- anticonvulsants
UA findings for AIN
- pyuria- WBC casts
- hematuria- less common
- if see WBC casts must also r/o pyelonephritis
treatment for AIN
- d/c offending agent
- steroids X 6 weeks
- damage may be permanent if long duration of drug exposure
what is the most common cause of intrinsic renal failure
- acute tubular necrosis
acute tubular necrosis (ATN)
- due to ischemia, sepsis, or toxins
- usually reversible
exogenous toxins causing ATN
- NSAIDs
- chemo- esp cisplatin
- aminoglycosides
- amphotericin
- vanco
- radioconstrast dye
- poison- ethylene glycol, heavy metals
endogenous toxins causing ATN
- rhabdo
- uric acid
- multiple myeloma
lab findings for ATN
- pigmented or granular casts- muddy brown*
- Cr and BUN elevated
- FeNa> 2%
- serum hyperK
- serum hyperP
- serum hyperuricemia
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
acute glomerular diseases
- post-strep glomerulonephritis
- nephrotic syndrome
- minimal change disease
- membranous glomerulonephritis
- IgA nephropathy
- henoch-schonlein purpura
post-strep glomerulonephritis (PSGN)
- immune complex with strep antigen gets deposited into glomerulus
- 7-12 d after strep/ impetigo
sx of PSGN
- oliguria
- cola colored urine
- edema
- HTN
- malaise, anorexia, flank pain
treatment for PSGN
- abx
- symptomatic
- anti- HTN drugs
- salt restriction
- diuretics
prognosis for PSGN
- kids usually recover with treatment
- can be permanent damage in adults
UA findings for PSGN
- proteinuria
- hematuria
- pyuria
- +/- RBC casts
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
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
treatment for IgA nephropathy
- ACEI/ARB
- steroids
- renal transplant
Henoch schonlein purpura
- small vessel vasculitis PLUS IgA complex deposition
- usually in kids 6 y/o
presentation of henoch schonlein purpura
- rash- esp in LE and buttock
- abd pain/ vomiting- severe
- arthralgias
- edema
- elevated Cr and BUN
- urine hematuria/ proteinuria
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
nephrotic syndrome
- heavy proteinuria 3.5 g/day
- hypoalbuminemia > 3 g/dL
- peripheral edema
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
etiology of nephrotic syndrome
- membranous nephropathy
- minimal change disease
- amyloidosis
- SLE
- membranoproliferative glomerulonephritis
- focal segmental glomerulosclerosis
- IgA nephropathy
minimal change disease
- 70-90% of nephrotic syndrome in childhood
- unknown cause
- abrupt onset edema and nephrotic syndrome
dx of minimal change disease
- normal biopsy
- urine protein 10 gm/day
- hypoalbuminemia
- HTN
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
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
treatment for vascular AKI
- BP control and manage sx
causes of post-renal failure
- bladder outlet obstruction
- neurogenic bladder
- pregnancy
- gyn surgery or abdominopelvic malignancy
sx of post-renal failure
- elevated BUN and Cr
- flank pain
- hematuria
- possible renal calculi or papillary necrosis
medication induced post-renal failure
- acyclovir
- mtx
- triamterene
- indinavir
- sulfonamides
- can cause collecting system/ ureteral obstruction by crystal formations
treatment for post-renal failure
- relieve obstruction
- foley can or suprapubic cath
- nephrostomy tube
polycystic kidney disease
- genetic disorder
- cyst formation and enlargement of kidneys
- affects multiple sys: pancreas, liver, spleen
prognosis of polycystic kidney disease
- 50% need transplant or dialysis by 60
- must screen families
- intracranial aneurysm is 2X more common than general population
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
diagnosis of polycystic kidney disease
- classic appearance on US
- elevated H&H
- UA shows hematuria, possible microalbuminuria
- elevated Cr
treatment for polycystic kidney disease
- manage BP with ACEI/ARB
- pain control - very challenging, avoid NSAIDs
- surgical cyst decompression
- nephrectomy
- treat recurrent infections
- hydrate
