AKI Flashcards
Acute vs Chronic Kidney Disease?
Chronic - irreversible loss, and persisting for longer than 90 days
Acute - sudden onset and abrupt loss of kidney function occurring in less than 7 days, and with damage that may or may not be reversible
Pre-renal causes of AKI
Caused by a decrease in renal perfusion can be caused by:
Hypovolemic state (or 3rd spacing)
Vasodilation (sepsis, anaphylaxis)
Decreased cardiac output
Intra-renal AKI causes?
Direct damage to the kidney. This can be of the glomerulus, tubules or interstitial spaces.
Post-renal causes of AKI?
Obstruction due to:
- stones, BPH
- cancer
- neurogenic bladder
Work up for AKI?
Figure out if pre-renal or post renal - because intra-renal needs a nephrologist…
Labs - BUN/Cr, U/A, C&S, Blood cultures, LFTs, CBC, Calcium + Phosphate, CK,
Imaging - Ultrasound, or non-contrast CT
Tx for AKI
Give NS or other fluids that will stay in vascular space
Stop ACE/ARBs, NSAIDs, renal-toxic drugs
Treat pre-renal causes - and monitor electrolytes
If obstruction - catheter and find way to remove obstruction
Factors effecting GFR
Hydrostatic - pressure of blood on the blood vessel walls (causes water to exit the vessel into the the interstitial space - aka Bowman’s space) - high blood pressure and high volume states
Oncotic - the pull of proteins with in the blood vessels (causes water to return to vessels) - would be reduced in low protein states (liver disease, nephrotic syndrome)
What causes afferent dilation and constriction in the kidney?
Dilation is caused by:
- Prostaglandins (which is why NSAIDs are contraindication in AKI)
- NO, Dopamine
Constriction:
- NSAIDs
- ADH
- Norepinephrine
Efferent arteriole dilation and constriction?
Constriction is caused by:
- Angiotensin II (ACE and ARB will cause dilation)
- Norepinephrine
ACE/ARB are contraindicated in bilateral renal artery stenosis and low volume status because the vasodilation will cause drop in pressure and perfusion in the afferents leading to inadequate renal perfusion
Signs and Sx of AKI
Azotemia - too much nitrogen (high BUN) High Cr - if both BUN and Cr are elevated = kidney if only BUN then more likely dehydration LOC/ confusion Hematuria Flank pain Abnormal urine output Thirst Nausea/Vomiting/ Weakness
Based on the Cr determine if acute, chronic or acute on chronic
Acute: serum Cr increases equal or >2-3 times baseline, GFR >50% decrease, less than 0.5ml/kg/hr for greater than 12 hours
Chronic: GFR less than 60, markers of kidney damage - could not find anything about serum Cr…
Acute on chronic: serum Cr is at baseline >25
What is Alport disease?
Genetic, x-linked disease, characterized by kidney disease (nephritis), eye and hearing abnormalities
Creatine vs BUN - what are they measuring?
BUN - waste product of amino acid and protein breakdown
Cr - from the breakdown of muscle proteins
Uraemic syndrome
Progressive weakness, nausea/ vomiting, confusion, loss of weight, tremors, fatigue
HyperCa+ major causes
PTH high (hyperPTH - primary or tertiary, FHH), , or PTH low (malignancy (bone mets, SSC lung/ breast via PTHRP ), milk-alkali syndrome, sarcoidosis, TB, vasculitis, lymphoma)
