Risk factors
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chronic kidney disease = major risk factor for AKI
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DM
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HTN
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obestiy
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proteinuria
Causes
Pre-renal
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hypovoelaemia
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diarrhoea, vomiitng
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diuretics
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osmotic diuresis - from poorly controlled DM
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haemorrhage
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truama (shock)
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sepsis (shock)
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Decreased effective blood volume
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heart failure
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cirrhosis
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Vasoregulation
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NSAIDs
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ACEi or ARB
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Hypercalcaemia
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Intrinsic
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direct damage to nephron
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complex
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may be secondary to another illness
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Acute tubular necrosis = most common
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as result of pre-renal injury or
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direct toxicity
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hypotension
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hypovolaemia
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haemolysis
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rhabdomyolysis
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nephrotoxic meds
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NSAID
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lithium
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aminoglycosides
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pre rneal + ATN = 90% AKI
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Medication induced
- high mortality
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Acute glomerulonephritis
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small vessel vasculitis
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uncommon but improtamtn
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early diagnosis and appropriate treatment prevents end-stage CKD
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Post-renal
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blockage to flow of urine
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back-pressure to kidney: damage to nephrons
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obstructive nephropathy
- uncommon = 5%
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urinary tract sotnes
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prostatic hypertrophy
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intra-abdominal process encasing ureters
Prevention
CKD guidelines
- check renal function as per guideliens
medications
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Triple whammy
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NSAID
- blocks prostaglandin-mediated afferent arteriolar vasodilation
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ACEi
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blood flow to kidney can’t be reduced
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efferent arteriolar vasoconstriction prevented
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diuretics
- decrease GFR exacerbated
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Many cause intrinsic acute renal injuyr
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frusemide
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ppi
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beta lactam
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aminoglyucoside
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colchicine
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phenytoin
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History
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acute recent illness
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symptoms of outflow obstruction
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history of abdominal or pelvic malignancy
- obstruction/myeloma
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systemic symptoms
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rahs
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joint/muscle pain
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current prescribed and OTC medicine or recent contrast radiology
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pre-existing conditions
exam
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hydration
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systemic disease
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fever
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skin rashes
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joint swelling
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iriits
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vasuclar disases
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organomegaly
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AA
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bladder
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urinalysis
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ecg if K+ >5.5
Refer
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discuss especially if active sediment
- positive blood and protein
red flags
negligible UO for 6hrs or \<200mL over 12hrs
serum K+ >7 or \<5.5 with ECG changes
Volume overload
Cr >300 or change of 50%