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Regulatory: AKI - Coggle Diagram
Regulatory: AKI
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Treatment
Fluids are carefully maintained in AKI, administering more if the cause is hypoperfusion of kidneys r/t dehydration or restricting fluid if/when fluid overload occurs
Hemodialysis in more severe cases to remove fluids and waste build up, or CRRT
Identify and treat root causes, such as clearing obstructions, vascular volume restoration, DC nephrotoxic medications, restore cardiovascular function, treating sepsis ect...
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Diagnostic
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Urinalysis: specific gravity, proteinuria, hemoglobinuria, casts, fractional Na+
Labs: BUN, Cr, CBC, metabolic
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AKI can be caused by factors that affect the kidney pre/intra/postrenal. In the case of prerenal perfusion to the kidneys is disrupted. This causes a sharp decrease in UOP as adequate amounts of blood are not reaching the kidneys to be filtered. As they become ischemic GFR further decreases as afferent arteriolar constrict in a compensatory reaction to ease O2 demand of the tubules. This decrease in GFR results in the increased BUN and Cr. the increases can vary in amount depending on the source of the AKI. If blood flow is not restored the ischemia worsens and tubular cells begin to die off and form casts of the tubules and the injury is now an acute tubular necrosis and intrarenal. As the tubular cells die the kidney begins to lose the ability to concentrate urine and maintain F&E balances and functionally fail. ATN can result from hypoperfusion injury or drugs that are directly nephrotoxic. In the case of postrenal failure blockages have occurred that cause the kidney to swell and tissue damage occurs as pressure builds in the kidney and ultimately fails.