2. INCIDENCE :
Acute kidney injury (AKI) is a :
life-threatening disease
5% of all hospitalized patients .
30% of the admissions to ICU.
5-fold increased mortality Rate
3.
4. THE CONCEPT OF AKI
DEFINITION
Acute kidney injury (AKI) is defined as :functional or
structural abnormalities or markers of kidney
damage including abnormalities in blood, urine or
tissue tests or imaging studies present for less than
three months.
5.
6. CONSIDERATIONS :
1- SERUM Createnine Does not differentiate:
the nature and type of renal insult
site of renal insult
Prognosis of AKI
2- Changes in SCr may lag changes in GFR
and may be a very late indicator of renal injury
3- There is a direct relationship between duration of
renal failure and mortality.
4- Early diagnosis will enable timely institution of
measures for treatment of renal injuries and
prevention of progression.
7. ACUTE VS. CHRONIC
Previous values of BUN and Cr.
Previous images of the kidneys.
Anemia.
Electrolytes’ derangements.
Manifestations.
8. CLASSIFICATION OF ARF
ARF
Pre-renal
No kidney damage
Bland sediment
Reversible
Intrinsic renal
There is kidney damage
Sediment depends upon the
Affected part of the
Kidney
+/- reversibility
Post-renal
+/- kidney damage (depends
On for how long)
Sediment depends on the
Obstructing cause
+/- reversibility (depends on
For how long
17. ACUTE TUBULAR NECROSIS :
Golden role :
كلوي قصور كل
ماقبل
طالت كلوي
لنخر يؤدي شدته وزادت مدته
حاد أنبوبي
Prolonged Pre renal
azotemia will lead to
ATN .
18. PATHOPHYSIOLOGY
ATP depletion resulting in proximal tubule,
endothelial, and smooth muscle injury and apoptosis
Vascular congestion, and ongoing hypoxia
increase in permeability, which increases interstitial
pressure
decreases capillary blood flow.
apoptosis in this area.
25. Sepsis
SIRS Severe Sepsis Septic Shock
Infection
Early Goal Directed Therapy
Antibiotics and Source Control
TREATEMENT:
EARLY GOAL-DIRECTED THERAPY (EGDT): INVOLVES
ADJUSTMENTS OF CARDIAC PRELOAD, AFTERLOAD, AND
CONTRACTILITY TO BALANCE O2 DELIVERY WITH O2 DEMAND:
FLUIDS, BLOOD, AND INOTROP
es
Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. NEJM 2001;345:1368.
CVP > 8-12 mm Hg
MAP > 65 mm Hg
Urine Output > 0.5 ml/kg/hr
ScvO2 > 70%
SaO2 > 93%
Hct > 30%
*
26. B. NEPHROTOXINS
Exogenous :
Antibiotics and chemotherapy :
Aminoglycosides
Use once daily
Adjusted to IBW
VANCOMYCIN
should be utilized
only when medically
necessary
27. AMPHOTERICIN B, CISPLATIN AND
CARBOPLATIN :
Repetitive courses of amphotericin B may cause
permanent impairment of renal function
hypokalemia.
renal tubular acidosis,
impaired urinary concentrating capacity.
magnesium-wasting syndrome
Prevention :
2-3 L NS
LIPOSOMAL amphotericin B
28. ACE INHIBITORS & ANGIOTENSIN
:
RECEPTOR BLOCKERS
Pathogenesis :
Several conditions including :
volume depletion
(NSAIDs, cyclosporine)
chronic renal insufficiency
congestive heart failure,hypertension.
patients depend on efferent arteriolar vasoconstriction to
maintain adequate glomerular filtration. Initiation of ACE
inhibitors or ARBs may result in a rapid fall in the GFR
and a rise in serum creatinine.
GFR
A
N
G
PG
29. :
PREVENTION & TREATMENT
A chemistry panel should be obtained on all patients
prior to and within
5–7 days of initiation of drug therapy.
If the rise in serum creatinine does not exceed
20%, the ACE inhibitor or ARB should be continued
32. TREATMENT :
discontinuation of the NSAID.
Additional measures include correction of the underlying
process that predisposed to nephrotoxicity.
In general, renal function returns to baseline within 2–5
days
35. (2) ENDOGENOUS NEPHROTOXINS :
Myoglobinuria as a consequence of
rhabdomyolysis is a frequent cause of AKI.
Massive intravascular hemolysis can be seen in
severe transfusion reactions and snake bites
and may cause significant hemoglobinuria and
ATN.
37. TREATMENT :
Eliminate Potential Nephrotoxins or Confounders
Intravenous hydration (eg, 3 L/m2/day) should be initiated 48
hours prior to administration
of chemotherapy
brisk diuresis (100–150 mL/m2/hour), which can inhibit
intratubular uric acid crystallization and
obstruction.
an alkaline diuresis using intravenous sodium
bicarbonate (eg, 50–100 mEq of sodium bicarbonate
diluted in 1 L of D5 0.45% saline) to maintain a urine pH7.0–7.5
should help prevent ARF beyond
Allopurinol should be started 24–48 hours prior to chemotherapy
Recently a recombinant form of urate oxidase, rasburicase (Elitek)
has been approved in the United States.
39. :
2. GLOMERULAR DISEASE
less than 5% of AKI cases:
Glomerulonephritis that causes AKI is referred to as
rapidly progressive glomerulonephritis (RPGN). RPGN
can occur in :
systemic lupus nephritis,
Wegener’s granulomatosis, PAN,
Goodpasture’s syndrome,
Henoch–Schonlein purpura,
immunologic glomerulonephritis due to infection,
hemolytic uremic syndrome.
40. 3. INTERSTITIAL NEPHRITIS :
This is often associated with fever, maculopapular
rash, and eosinophils in the urine.
Many drugs can cause AIN but the most common
are NSAIDs, penicillins, cephalosporins,
sulfonamides, diuretics, and allopurinol.
AIN should be considered in any patients with a
rising serum creatinine but little or no evidence of
glomerular or arterial disease, no prerenal factors,
and no dilatation of the urinary collecting system on
ultransonography
42. C. POSTRENAL ACUTE KIDNEY INJURY
قاعدة
:
توجد لم ولو حاد كلوي قصور كل أمام االنسداد نفي يجب
انسدادية أعراض
Rule out the obstruction
43. A. SYMPTOMS AND SIGNS :
The symptoms of AKI include those related to
azotemia generally and those due to underlying
cause
Decrease in urine output and dark and cola-
colored urine. Azotemic
anorexia, nausea, malaise, metallic
taste in the mouth, itching, confusion, fluid
retention,
hypertension
44. LABORATORY FINDINGS :
THE DIAGNOSIS OF AKI IS MADE BY DOCUMENTING
ELEVATIONS OFTHE BUN AND SERUM CREATININE.
49. :
COMPLICATIONS
A. Hyperkalemia :
In patients with AKI the serum potassium rises rapidly,
especially in the presence of cell lysis such as occurs with :
muscle injury, hemolysis, gastrointestinal ischemia, tumor
lysis syndrome, high fever, or blood transfusion
is further aggravated by metabolic acidosis as potassium is
shifted from the intracellular to the extracellular
compartment.
50. TREATMENT :
temporarily lowered by :
the administration of
glucose and insulin,
bicarbonate,
inhaled 2-agonists, and
potassiumbinding
resins.
renal replacement
therapy
51. B. METABOLIC ACIDOSIS :
No role for bicarbonate infusion unless arterial
blood PH is less than 7.15.
