Renal. AKI+Nsaids+contrasAIN+IN+papil (07-23) (1) Flashcards
UW. Prerenal AKI.
etiology? main mechanism
Decreased renal perfusion
UW. Prerenal AKI.
etiology 5 that were in table
- True volume depletion
- Decreased EABV (eg. Hf, cirrhosis)
- Displacement of intravascular fluid (increased vascular permeability in sepsis, pancreatitis)
- Renal artery stenosis
- Afferent arteriole vasoconstriction (eg NSAIDs).
UW. Prerenal AKI.
What mechanism of nsaids etiology?
afferent arteriole vasoconstriction
UW. Prerenal AKI.
clinical? 5
incr. creatinine
Decr. urine output
BUN/Cr ratio > 20:1
Fract. Na < 1 proc.
Unremarkable urine sidement
UW. Prerenal AKI.
main treatment?
restoration of renal perfusion
UW. Prerenal AKI.
Presentation - oliguria. how much ml?
<500 ml day
OR < 0,5 ml/kg/h
UW. Prerenal AKI.
BUN/Cr ratio?
what if high urea?
> 20:1
anion gap metabolic acidosis
UW. Prerenal AKI.
FeNa?
< 1 proc.
UW. Prerenal AKI.
Urine sodium (uNa)?
<10 (kai kur raso <20)
UW. Prerenal AKI.
FeUrea?
< 35 proc.
UW. Prerenal AKI. treatment? 4
place catheter
if volume down -> iv fluids
if volume up (cardiorenal syndrome) –> diuresis
Avoid nephrotoxic drugs - metformin, ACEI, ARB.
UW. Prerenal AKI. Cardiorenal syndrome mechanism. Left heart failure?
LHF –> decr. Sv, CO –> decr. renal perfusion –> dec. GRF (renal injury) –> RAAS activation –> SNS tone and incr. Na and H2O absorption –> back to the first point ie LFH
UW. Prerenal AKI. Cardiorenal syndrome mechanism. Right heart failure?
RHF –> incr. CVP, RVP –> decr. glomerular capillary pressure gradient –> dec. GRF (renal injury) –> RAAS activation –> SNS tone and incr. Na and H2O absorption –> back to the first point ie RHF
UW. Postrenal AKI.
Causes?ureter
cancer and stones
UW. Postrenal AKI.
Causes?bladder
cancer, stones, neurogenic bladder (spinal cord injury, stroke)
UW. Postrenal AKI.
Causes?urethra
cancer, stones, BPH, Foley’s cath.
UW. Postrenal AKI.
Causes?
one very common case
what drug group?
postoperative urinary retention
First generation antihistamines (or drugs, containing anticholinergic activity) -> detrusor hypoactivity
UW. Postrenal AKI.
workup? 2
US or CT scan
look for hydroureter or hydronephrosis
UW. Postrenal AKI.
workup. what first thing to do in post-op?
check catheter
UW. Postrenal AKI.
treatment?
relieve obstruction - either Foley, surgery or nehrostomy
UW. Intrarenal AKI.
UW. Intrarenal AKI.
3 groups?
GN
Acute interstitial nephritis
Acute tubular necrosis
UW. Intrarenal AKI.
GN - UA finding.
What to rule out?
finding - RBC casts
rule out - nephrotic syndrom (> 3,5 g/dl, edema, inc. cholesterol)
UW. Intrarenal AKI.
acute interstitial nephritis. UA findings?
WBC casts, WBC, eosinophils.
UW. Intrarenal AKI.
acute interstitial nephritis - causes?
Drugs - sulfadrugs (TMP-SMX(, penicillin, cephalosporins, NSAIDS, allopurinol, PPIs)
UW. Intrarenal AKI.
acute interstitial nephritis presentation? 4
eosinophilia, eosinophiluria, fever, wbc casts, skin rash, hematuria
UW. Intrarenal AKI.
acute interstitial nephritis onset?
onset variable.
5 day to several weeks/month following exposure
UW. Intrarenal AKI.
ATN. 2 groups?
ischemia and exposure to toxins
UW. Intrarenal AKI.
ATN. what are toxins?
IV contrast,
AMG,
myoglobin (rhabdomyolysis)
GN
UW. Intrarenal AKI.
ATN. what to do prior radiologic procedures?
evaluate kidney function before administergin IV CONTRAST
UW. Intrarenal AKI.
ATN. what lab incr. in case of rabdomyolysis?
potassium and creatin kinase.
UW. Intrarenal AKI.
ATN. Multiple myeloma also cause (??)
.
UW. Acute interstitial neph. symptoms?
fever,
rash (DONT FORGET IT),
arthralgias,
eosinophilia,
hematuria, sterile pyuria, WBC casts,
eosinophiluria
renal: AKI, on byopsy inflammatory infiltrates in kidney interstitium
UW. Intrarenal AKI.
ATN. DIsease course? phases 4
prodrome - cr rises
oliguric phase
polyuric phase: urine output increases
recovery phase
UW. Intrarenal AKI.
ATN. treatment?
discontinue affending drug/toxin
vigorous IV fluids
UW. Intrarenal AKI.
ATN. BUN/cr?
typically normal
<15:1
UW. Intrarenal AKI.
ATN. UNa?
> 40
UW. Intrarenal AKI.
ATN. Na exc? proc.
> 2 proc.
UW. Intrarenal AKI.
ATN. urine osmolality?
~ 300
UW. prerenal AKI.
urine osmolality?
> 500
UW. Intrarenal AKI.
ATN. urine specific gravity?
<1.020
UW. prerenal AKI.
urine specific gravity?
> 1.020
UW. Intrarenal AKI.
ATN. Microscopy?
muddy brown casts
UW. prerenal AKI. Microscopy?
bland
UW. Contrast induced nephropathy.
4 risk factors?
Age > 75
CKD (esp. diabetic nephropathy)
Reduced renal perfusion (eg hypotension)
High contrast load
UW. Contrast induced nephropathy.
prevention? 3
periprocedural saline hydration
Lowest possible volume of agent
Hold NSAIDs
UW. Contrast induced nephropathy.
workup?
History and physical exam
Urinalysis
BUN/Cr ratio < 20:1 (jeigu pagal ATN lentele < 15)
sometimes need biopsy
UW. Contrast induced nephropathy.
treatment?
Disease specific.
Discontinue of nephrotoxic agent.
Supportive care.
Dialysis
UW. intrarenal. GN. what urinalysis?
RBC casts/RBC
UW. Analgesic nephropathy. it the most common cause of drug-inducec CKD.
.
UW. Analgesic nephropathy. 2 most common pathologies?
Chronic tubulointerstitial nephritis
Papillary necrosis
UW. Analgesic nephropathy. what 3 risk in general due to chronic analgetics use?
premature aging
atherosclerotic vascular disease
Urinary tract cancer
UW. Analgesic nephropathy.
what common scenario?
long term use of 1 or multiple anagetics for chronic headaches or other somatic complaints
UW. Analgesic nephropathy.
what usually symptoms?
usually asymptomatic
but can have chronic tubulointerstitial nephritis or hematuria due to papillary necrosis
UW. Analgesic nephropathy.
UW. Analgesic nephropathy. diagnosis. blood labs?
incr. creatinine
UW. Analgesic nephropathy. diagnosis. urinalysis?
hematuria
sterile pyuria
mild proteinuria (<1,5 g/d)
UW. Analgesic nephropathy. diagnosis. what shows CT?
small kidneys with bilateral renal papillary calcifications
UW. papillary necrosis.
rare cause of non-glomerular hematuria
.
UW. papillary necrosis. mechanism?
occurs due to sloughing of the renal papilla
UW. papillary necrosis. risk factors - mneumonic NSAID.
N - Nsaids (cause constriction of medullary blood vessels - vasa recta)
Sickle cell disease
Analgesic abuse
Infection (pyelonephritis)
DM
UW. Contrast induced nephropathy. when onset?
Acute rise in Cr within 24-48h post contrast administration, following gradual return to baseline
FA. prerenal mechanism?
decr. renal perfusion
FA. intrarenal mechanism?
injury within nephron
FA. posternal mechanism?
urinary outflow obstruction
FA. prerenal. what urine finding may be, but considered as normal (in volume depletion)?
hyaline casts