subtypes of AKI - amboss

Question 1

acute tubular necrosis

Answer 1

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

Question 2

causes of decreased renal blood flow

Answer 2

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)

Question 3

causes of toxic damage to kidneys

Answer 3

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

Question 4

when might pigment nephropathy occur

Answer 4

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

Question 5

pathophysiology of acute tubular necrosis

Answer 5

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

Question 6

blood findings of acute tubular necrosis

Answer 6

azotemia, hyperkalaemia and metabolic acidosis

Question 7

urinary findings of acute tubular necrosis

Answer 7

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

Question 8

prognosis of acute tubular necrosis

Answer 8

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

Question 9

renal cortical necrosis

Answer 9

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

Question 10

aetiologies of renal cortical necrosis

Answer 10

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

Question 11

pathophysiology of renal cortical necrosis

Answer 11

vasospasms and microvascular injury with vascular thrombosis
prolonged severe renal ischaemia
diffuse or patchy destruction of the renal cortex

Question 12

clinical features of renal cortical necrosis

Answer 12

flank pain, CVA tenderness and signs of AKI

Question 13

management of renal cortical necrosis

Answer 13

dialysis can improve outcomes
high mortality rates without treatment

Question 14

contrast induced nephropathy

Answer 14

AKI after IV administration of iodinated contrast medium

Question 15

risk factors for contrast induced kidney injury

Answer 15

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

Question 16

course of contrast induced nephropathy

Answer 16

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