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Acute Kidney Injury AKI MAANTA 11 SAAC
Acute Kidney Injury AKI MAANTA 11 SAAC
(AKI)
Abdulsalam Halboup
M.Pharma (Clinical)
ACUTE KIDNEY INJURY
Acute kidney injury (AKI) is abrupt reduction in
kidney functions as evidence by changed in laboratory
values; serum creatinine, blood urea nitrogen(BUN)and
urine output.
1-prerenal AKI
2- intrinsic AKI
3- Postrenal AKI
PRERENAL AKI
Prerenal AKI: is characterized by reduced blood
delivery to the kidney.
A common causes are:
Volume depletion
hemorrhage
dehydration
GI fluid losses.
Decrease effective circulatory blood volume
Decrease cardiac output (CHF, MI, hypotension
Pulmonary hypertension
Liver failure
Sepsis
Functional
ACEIs, NSAIDs, ARBs, Cyclosporine and tacrolimus
Ureteral obstruction
Malignancy
Pelvic / renal obstruction
Postrenal AKI accounts for less than 10% of cases of AKI
Rapid resolution of Postrenal AKI without structural damage
restore kidney function
By monitoring Scr on a routine basis, it can be estimated
whether kidney function is improving or worsening.
Kidney function can also be evaluated based on urine
output. Oliguria and anuria
Oliguria is defined as urine outputs of less than 400 ml
over 24 hours
anuria is defined as urine output of less than 50 mL over
24 hours.
CLINICAL PRESENTATION AND DIAGNOSIS OF AKI
Peripheral edema
Weight gain
Nausea/vomiting/diarrhea/anorexia
Mental status changes
Fatigue
Shortness of breath
Pruritus
LABORATORY TESTS
Dose:
Initial iv loading dose equivalent to (40-60mg
furosemide )
Continuous infusion equivalent to 10-20mg/h
STRATEGY TO OVERCOME DIURETIC
RESISTANCE