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Clinical vignette VIII
Multi-organ failure
Reem Alyahya
212522156
introduction
Mona
Acute
abdominal
pain
Resuscitated
Day3:
deteriorated
Objective
 How to differentiate between renal and
pre-renal causes of AKI?
Acute kidney injury
 Abrupt deterioration in parenchymal renal
function, which is usually reversible over a
period of days or week.
Classification
Pre-
renal
Renal
Post-
renal
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
Causes include:
Volume depletion
Decreased
cardiac output
Systemic
vasodilatation
Renal
vasoconstriction
Drugs like NSAIDs
and ACEI
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)
Causes include:
Diseases
involving
renal
vessels
Glomerul-
onephritis
Tubular
(ischemic ,
nephrotoxic)
Interstitial
How to differentiate?
History
Physical
examination
Laboratory
criteria
History
Pre-renal
 Volume loss
 Heart failure
 sepsis
 Drug use
Renal
 Prolonged hypotension or
hypovolemia
 Nephrotoxic drugs
 Symptoms GN
Physical examination
Pre-renal
 tachycardia
 Low JVP
 Systemic/orthostatic
hypotension
 Manifestations of
hypovolemia
 Clinical picture of Heart
failure.
Renal
 Manifestations GN
 Manifestations of vascular
or interstitial disease
Laboratory criteria
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.
Reference
 Kumar p, Clark M. Clinical medicine. Eighth edition. 2012
Thank you
Any questions?

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Acute kidney injury

Editor's Notes

  1. 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.
  2. 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
  3. There’s nothing wrong with the kidney so it can….. But with prolonged impairment it may led to renal kidney injury
  4. Renal vasoconstriction NSAIDs, Hypercalcemia
  5. Leaving post renal as the leas common cause
  6. 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
  7. (Dry skin and mucous membrane, decreased skin turgor, oliguria)