subtypes of AKI - amboss Flashcards

1
Q

acute tubular necrosis

A

85% of intrinsic AKIs
injury occurs secondary to decreased renal blood flow, nephrotoxic substances, sepsis or infections

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2
Q

causes of decreased renal blood flow

A

severe hypotension, especially in the context shock, hypovolaemic (eg. haemorrhage severe dehydration) septic, cardiogenic (eg. heart failure) or neurogenic shock
thromboembolism
thrombotic microangiopathy
cholesterol embolism (atheroemboli)

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3
Q

causes of toxic damage to kidneys

A

injury occurs directly due to nephrotixic substances
contrast induced nephropathy
aminoglycosides, cisplatin, amphotericin, lead, ethylene glycol
pigment nephropathy: due to heme containing pigments eg. heamoglobin, myoglobin on proximal renal tubular cells
acute uric acid nephropathy

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4
Q

when might pigment nephropathy occur

A

due to heme containing pigments
eg
myoglobinuria due to rhabdomyolysis
hemoglobinuria associated with hemolysis

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5
Q

pathophysiology of acute tubular necrosis

A

necortic proximal tubular cells fall into the tubular lumen
debris obstructs tubules
decreased GFR
sequence of pathophysiological events similar to prerenal failure

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6
Q

blood findings of acute tubular necrosis

A

azotemia, hyperkalaemia and metabolic acidosis

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7
Q

urinary findings of acute tubular necrosis

A

increased fractional excretion of sodium
myoglobinuria
hemoglobinuria
urinary sediment - muddy brown granular casts, epithelial cell casts, free renal tubular epithelial cells (due to denudation of the tubular basement membrane)

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8
Q

muddy brown casts are typical of

A

acute tubular necrosis

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9
Q

prognosis of acute tubular necrosis

A

after 1-3 weeks, most patients with ATN will experience tubular re-epithelialization and spontenous full recovery is common
can be lethal if AKI is severe and not managed adequately eg. dialysis may be required for oliguric patients with volume overload or severe hyperkalemia

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10
Q

renal cortical necrosis

A

rare cause of AKI by acute generalised ischaemic necrosis of the renal cortex in both kidneys

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11
Q

aetiologies of renal cortical necrosis

A

septic shock
disseminated intravascular coagulation
hemolytic uremic syndrome (HUS)
obstetric complications

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12
Q

clinical features of renal cortical necrosis

A

flank pain, CVA tenderness and signs of AKI

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13
Q

management of renal cortical necrosis

A

dialysis can improve outcomes
high mortality rates without treatment

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14
Q

contrast induced nephropathy

A

AKI after IV administration of iodinated contrast medium

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15
Q

risk factors for contrast induced kidney injury

A

chronic kidney disease
congestive heart failure
nephrotoxic drugs esp. NSAIDs
anaemia
dehydration

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16
Q

course of contrast induced nephropathy

A

creatinine is highest 3-5 days after injury and usually falls back to the baseline level within 1 week
typically mild course because end stage renal disease usually onlu occurs in patients with pre existing CKD

17
Q
A