UROLOGY / NEPHROLOGY - AKI, ATN
*AKI
- defined by 2 things
--> increased creatinine and BUN
--> or by oliguria/anuria - 3 types
--> pre renal
--> intrarenal
--> post renal obstructive
*Dirty USMLE
*AKI
*Causes of AKI and classification
- PRE INTRA and POST renal AKI
POST renal AKI
PRE renal AKI
INTRArenal AKI
*BUN/Creatinine ratio
- PRE AKI = Raised BUN/Creatinine >20:1
--> note creatinine NOT raised - INTRA AKI = Raised BUN/Creatinine < 10:1
--> half of PRE AKI
--> since the kidney is damaged itself so can't actually absorb that well - POST AKI
--> starts midway between PRE and INTRA = BUN creatinine ratio = 15:1
--> moves to INTRA renal as the stone/BPH blockage moves back into the kidney and causes damage
PHYS
- note the BUN/creatinine ratio measures two things for the kidney function
BUN
- measures the ability of kidney to concentrate urine with Blood urea nitrate
Creatinine
- recall that creatinine clearance estimates GFR and PAH estimates RPF
PAthophys of AKI
- "MAD HUNGER"
AKI MAD HUNGER = Uremia - high ADH response
- from response of increased BUN and urea reabsorption
AKI MAD HUNGER = Hyperkalemia
--> lose ROMK channels that leak K+ into the lumen at CD
(ROMK and ENaC (aldosterONE Na+) work in opposite directions at the CD)
*INTRA renal AKI
- RTA = renal tubular Acidosis
--> most common cause of INTRA kidney AKI - AIN = Acute interstital Nephritis
- almost always caused by drug reaction
--> happens few weeks after taking a drug
--> get diffuse MAC PAP rashes
--> AKI symptoms
--> eosinphilia in the interstitium of the kidney
--> type 2 hypersensitivity Rxn
*AIN - INTRA renal AKI
- AIN = Acute interstital Nephritis
- almost always caused by drug reaction
--> happens few weeks after taking a drug
--> get diffuse MAC PAP rashes
--> AKI symptoms
--> eosinphilia in the interstitium of the kidney
--> type 1 hypersensitivity Rxn (EOSINOPHILS and IgE)
CRISTAL AIN acute interstitial nephritis
- acyclovir is cleared rapidly by the liver so watch out for AIN INTRA renal AKI
*Acute Tubular Necrosis = ATN
Notes:
- Not that ATN happens when there is necrosis to the renal tubule secondary usually to infection or hemorrhage that leads to ischemia of the renal tubule
- 3 main stages of ATN --> think ATN = 3
- 1 = Initial damage = ischemia
- 2 = Maintenance with fluid overload and low urine output
--> this happens 24 hours later and last for a week - 3 = recovery phase
--> note the GFR recovers before the tubule reabsorption function
--> this means you get high urine output = polyuria
--> but you can lose a lot of electrolytes
--> recall that with high flow K+ uptake by
ALL Loop diuretics prior to CD that increase Na+ in tubule --> lead to hypokalemia (loss of K+)
- Na+ absorption through ENaC = epithelial sodium channel
--> always coupled with K+ excretion through ROMK - K+ excreted into lumen through ROMK channels
- ROMK = renal outer medullary K+ channels
--> coupled to ENaC channels
--> when ENaC absorbs Na in distal CT, ROMK excretes K+ back into the tubule - note that K+ is one of the few cations where it is excreted back into the tubule at the last second
--> think it is the largest cation so added in at end
Clinical Cases
Clinical Case
Clinical Case
Notes:
- note that
*DIRTY USMLE
*ATN = Acute tubular necrosis
FAT ASC BITCHES BARTER to GIT a LIDDLE love
- falconi,, ascending = Barter, Gitelman, liddle
