10. AKI Flashcards
what is AKI
- clinical syndrome involving acute decrease in actual GFR (hrs-days)
- loss of kidney function results in:
i. ECF volume disruption
ii. electrolye and acid-base homeostasis disruption
iii. accumulation of nitrogenous waste products
how is kidney function measured in AKI - what are the limitations of this
- decreased GFR measured as increased serum creatinine
- not very sensitive as increase creatinine only detectable several days after kidney insult
- severe AKI also can be seen as decreased UO
what are the 3 types of AKI causes
- pre-renal: decreased renal perfusion in absence of any actual renal pathology
- intrinsic kidney disease: primary pathology within kidneys
- post-renal disease: obstruction to renal flow within urinary tract
explain the causes for pre-renal AKI
Sustained hypotension that decreases renal perfusion:
- true hypovolaemia, e.g. major haemorrhage, dehydration or hypovolaemic shock
- deranged haemodynamics, e.g.
- septic, anaphylactic or neurogenic shock (… systemic vasodilation)
- cardiogenic shock, MI or other causes of heart failure (… decreased CO)
- hepatorenal syndrome
what are the 2 outcomes of pre-renal AKI
- potentially reversible -
responds to fluid resuscitation - with sustained renal hypoperfusion, renal interstitium can become highly ischaemic… precipitates ATN
why should NSAIDs or ACE-I/ARBs be stopped during illness (eg vomiting, dehydration, AKI)
Can override intrinsic autoregulatory mechanisms, increasing risk of AKI:
- NSAIDs - prevent vasodilatory effects of prostaglandins on afferent arteriole
- ACE-I/ARB - prevent vasoconstriction effect of AngII on efferent arteriole
name the 4 main causes of intrinsic AKI
- vascular disease
- acute glomerulonephritis (i.e. causes of nephritic syndrome)
- acute (tubule)-interstitial nephritis: toxin-induced (antibiotics, NSAIDs and PPIs) or infection-induced (inflammatory response)
- acute tubular necrosis (most common cause)
how can vascular disease cause AKI - give 2 examples
- RENAL ATHEROEMBOLISM: thromboemboli from an atherosclerotic plaque reduce perfusion downstream of glomeruli
- THROMBOTIC MICROANGIOPATHY (haemolytic uraemic syndrome, malignant hypertension, scleroderma, pre-eclampsia): endothelial damage… platelet thrombi… RBC destruction (= microangiopathic haemolytic anaemia)… nephron vessel damage… AKI
suggest 3 causes of acute tubular necrosis
- renal interstitium ISCHAEMIA due to reduced perfusion… depletion of cellular ATP… cellular damage and loss of function
- NEPHROTOXINS - damage tubular epithelium causing cell death.
- SEPSIS
which parts of the nephron are most sensitive to ischaemia why
Terminal PCT and thick ascending loop of Henle:
- highly metabolically active - substantial amounts of reabsorption and secretion occur
- located in renal medulla - has relatively low O2 saturation at baseline due to geometry of vasa recta
give examples of nephrotoxins that can cause acute tubular necrosis
- endogenous, e.g. myoglobin, bilirubin, urate
2. exogenous, e.g. endotoxin, X-ray contrast, drugs such as NSAIDs and gentamicin, poisons
how can rhabdomyolysis cause acute tubular necrosis - what is a major sign of this
- occurs in cases of muscle necrosis, e.g. crush injuries, prolonged immobility, causing myoglobin release
- myoglobin filtered at glomerulus is toxic to tubule cells and can also cause obstruction
- signs: myoglobinuria (coca-cola urine)
how does post-renal AKI cause kidney damage - suggest different causes for this
- Significant urinary tract obstruction… increased intraluminal pressure… urine backup into kidneys… HYDRONEPROSIS (dilation of renal pelvis)… decreased GFR
- To cause AKI, obstruction must affect both kidneys (or single functioning kidney). Causes:
- within lumen (of kidney, ureter, bladder), e.g. stones, blood clots, tumours
- within wall (usually cause CKD)
- pressure from outside, e.g. enlarged prostate, tumour, aortic aneurysm
suggest 2 main symptoms of AKI
direct consequences of decreased GFR
- oliguria - decreased urine production
- generalised oedema - insufficient excretion of Na+ and water
which electrolyte and metabolic product changes would be detectable in serum analysis in AKI
- AZOTEMIA: build-up of metabolites such as creatinine and BUN
- HYPERKALAEMIA (decreased excretion of K+ in CT)
- HYPERPHOSPHATAEMIA (decreased excretion of plasma phosphate, + phosphate release from damaged cells, eg in rhabdomyolysis)
