denoted by an abrupt decline in glomerular
filtration rate (GFR) sufficient to decrease the
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elimination of nitrogenous waste products
(urea and creatinine) and other uremic toxins.
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EPIDEMIOLOGY
AKI complicates 5?7% of acute care hospital
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admissions and up to 30% of admissions to theintensive care unit, particularly in the setting
of diarrheal illnesses, infectious diseases like
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malaria
and
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leptospirosis,and
natural disasters such as earthquakes.
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Causes
The causes of AKI are usual y divided into three broad
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patho-physiologic categories:
1. Prerenal AKI--diseases characterized by effective
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hypoperfusion of the kidneys in which there is noparenchymal damage to the kidney
2. Intrinsic AKI--diseases involving the renal
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parenchyma
3. Postrenal (obstructive) AKI--diseases associated
with acute obstruction of the urinary tract
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Patho-physiology
Phases of Ischemic ATN
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1. Initiation Phase ? GFR declines, lasts for
hours- days
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2. Extension Phase ? continued damage3. Maintenance Phase ? GFR stabilises at nadir
of 5-10 ml/min, lasts for 1-2 wks
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4. Recovery Phase ? gradual return of GFRtowards normal, delay in recovery of tubular
function.
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Diagnosis
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