6. Pre- renal :
In pre-renal uremia, there is impaired blood
perfusion to the kidneys. Usually the kidney is able
to maintain GF close to normal despite wide
variation in renal perfusion.
The most common form of AKI
8. Renal :
Structural injury in the kidney is the hallmark of
renal AKI , it’s the second most common form of
AKI after pre-renal causes.
And its most commonly due to acute tubular
necrosis (ATN)
15. conclusion
AKI is an abrupt deterioration in parenchymal renal
function, which is usually reversible.
The causes can be classified into: pre-renal, renal and
post-renal
We can differentiate between these forms by the way of
: history, physical examination and laboratory criteria.
In prerenal failure, you have less renal blood flow, you will filter less and GFR will decrease.
When GFR decreases, it gives the proximal tubule more time to reabsorb urea.
Thus, there is an increase in serum urea.
Creatinine is not reabsorbed, but you do get rid of it through the kidneys.
When GFR is decreased, there is a back up of creatinine and will not be able to clear it as fast.
Therefore, there will be an increase in serum creatinine.
She present with acute abdominal pain , she was dynamically unstable, so she was resuscitated with saline , analgesia and AB, day 3 she worsened , tachypnea low ox and urine out put
There’s nothing wrong with the kidney so it can…..
But with prolonged impairment it may led to renal kidney injury
Renal vasoconstriction NSAIDs, Hypercalcemia
Leaving post renal as the leas common cause
Tubular etiologies may include ischemia or cytotoxicity. Cytotoxic etiologies include the following:
Heme pigment - Rhabdomyolysis, intravascular hemolysis
Crystals - Tumor lysis syndrome, seizures, ethylene glycol poisoning, megadose vitamin C, acyclovir, indinavir, methotrexate
Drugs - Aminoglycosides, lithium, amphotericin B, pentamidine, cisplatin, ifosfamide, radiocontrast agents
(Dry skin and mucous membrane, decreased skin turgor, oliguria)