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Clinical manifestation of ARF is decreased urine output (contrast with above: in CRF the patient will have increased urine output due to inability to concentrate, until the kidney totally gives up and scleroses.)
Causes of ARF: (remember our 3(or 4) major categories of renal diseases?):
glomerular
tubulo-interstitual
vascular
ATN is the most common cause of ARF (the most common cause of CRF was glomerulonephritis, remember?) ATN is caused by nephrotoxins or ischemia. More of this later . This is just a glimpse.
Clinical course of ARF (note, it’s opposite from CRF, as stated above):
A. Onset – after initial event (whatever the cause is), one has acute suppression of urine production and increase in K. This person will have hyperkalemia b/c he/she can’t excrete enough K.
B.Later stages: polyuric phase when patient can become dehydrated due to fluid loss (one eventually loses tubular function and ability to concentrate urine). It is essential to replace fluids.
Category: Nephrology Notes , Pathology Notes
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